"Anorexic" redirects here. For the use of the term as an appetite suppressant, see
Anorectic.
Anorexia nervosa is an eating disorder characterized by excessive food restriction and irrational fear of gaining weight, and a distorted body self-perception. It typically involves excessive weight loss. Anorexia nervosa usually develops during adolescence and early adulthood.[1] Due to the fear of gaining weight, people with this disorder restrict the amount of food they consume. This restriction of food intake causes metabolic and hormonal disorders.[2] Outside of medical literature, the terms anorexia nervosa and anorexia are often used interchangeably; however, anorexia is simply a medical term for lack of appetite. However, people with anorexia nervosa do not lose their appetites.[3]
People suffering from anorexia have extremely high levels of ghrelin, the hunger hormone that tells the brain when it is time to eat, in their blood. The high levels of ghrelin suggests that their bodies are trying desperately to switch hunger on but that hunger’s call is being suppressed, ignored, or overridden. Nevertheless, one small single-blind study found that intravenous administration of ghrelin to anorexia nervosa patients increased food intake by 12-36% over the trial period.[4]
Anorexia nervosa has many complicated implications and may be thought of as a lifelong illness that may never be truly cured, but only managed over time. Anorexia nervosa is characterized by low body weight, inappropriate eating habits and obsession with having a thin figure. Individuals suffering from it may also practice repeated weighing, measuring, and mirror gazing, alongside other obsessive actions, to make sure they are still thin, a common practice known as "body checking".[5]
Anorexia nervosa is often coupled with a distorted self image[6][7] which may be maintained by various cognitive biases[8] that alter how the affected individual evaluates and thinks about her or his body, food and eating.[9] Anorexia nervosa is characterized by the fear of gaining weight. Those suffering from this disorder often view themselves as "too fat" even if they are already underweight.[10] Persons with anorexia nervosa continue to feel hunger, but deny themselves all but very small quantities of food.[9] The average caloric intake of a person with anorexia nervosa is 600–800 calories per day, but extreme cases of complete self-starvation are known. It is a serious mental illness with a high incidence of comorbidity and similarly high mortality rates to serious psychiatric disorders.[10]
Anorexia nervosa most often has its onset in adolescence and is more prevalent among adolescent girls than adolescent males.[11] However, more recent studies show the onset age has decreased from an average of 13 to 17 years of age to 9 to 12.[12] While it can affect men and women of any age, race, and socioeconomic and cultural background,[13] anorexia nervosa occurs in 10 times more females than males.[14]
The term anorexia nervosa was established in 1873 by Sir William Gull, one of Queen Victoria's personal physicians.[15] The term is of Greek origin: an- (ἀν-, prefix denoting negation) and orexis (ὄρεξις, "appetite"), thus meaning a lack of desire to eat.[16] However, while the term "anorexia nervosa" literally means "neurotic loss of appetite", the literal meaning of the term is somewhat misleading. Many anorexics do enjoy eating and have certainly not lost their appetites as the term "loss of appetite" is normally understood; it is better to regard anorexia nervosa as a self-punitive addiction to fasting, rather than a literal loss of appetite.
Schneer suggested anorexia nervosa patients who have "difficulties in identifying, containing and articulating emotions resort to food as a symbolic expression of the inability to establish subjective limits in their relationships with others".[17]
Anorexia nervosa is an eating disorder characterized by attempts to lose weight, sometimes to the point of starvation. A person with anorexia nervosa may exhibit a number of signs and symptoms, the type and severity of which may vary in each case and may be present but not readily apparent. Anorexia nervosa, and the associated malnutrition that results from self-imposed starvation, can cause severe complications in every major organ system in the body.[18][19][20]
Hypokalaemia, a drop in the level of potassium in the blood, is a symptom of anorexia nervosa. A significant drop in potassium can cause abnormal heart rhythms, constipation, fatigue, muscle damage and paralysis.
50-75% of individuals with an eating disorder experience depression. In addition, 1 in 4 individuals who are diagnosed with anorexia nervosa also exhibit obsessive compulsive disorder.[21]
Symptoms for a typical patient include:
- Refusal to maintain a normal body mass index for their age[22]
- Amenorrhea, the absence of three consecutive menstrual cycles [22]
- Fearful of even the slightest weight gain and takes all precautionary measures to avoid weight gain and becoming overweight [22]
- Obvious, rapid, dramatic weight loss
- Lanugo: soft, fine hair growing on the face and body[23]
- Obsession with calories and fat content of food
- Preoccupation with food, recipes, or cooking; may cook elaborate dinners for others, but not eat the food themselves[24]
- Dieting despite being thin or dangerously underweight
- Rituals: cuts food into tiny pieces; refuses to eat around others; hides or discards food
- Purging: uses laxatives, diet pills, ipecac syrup, or water pills; may engage in self-induced vomiting; may run to the bathroom after eating in order to vomit and quickly get rid of the calories[25][26] (see also bulimia nervosa).
- May engage in frequent, strenuous exercise[27]
- Perception of self to be overweight despite being told by others they are too thin and, in most cases, underweight.
- Becomes intolerant to cold and frequently complains of being cold from loss of insulating body fat or poor circulation resulting from extremely low blood pressure; body temperature lowers (hypothermia) in effort to conserve energy[28]
- Depression: may frequently be in a sad, lethargic state[29]
- Solitude: may avoid friends and family; becomes withdrawn and secretive
- Cheeks may become swollen because of enlargement of the salivary glands caused by excessive vomiting[30]
- Swollen joints[31]
- Abdominal distension
- Bad breath (from vomiting or starvation-induced ketosis)
- Hair loss or thinning[32]
- Fatigue [33]
Anorexia nervosa can have serious implications when onset occurs before the completion of growth, pubertal maturation and prior to attaining peak bone mass.[52]Complications specific to adolescents and children with anorexia nervosa can include:
-
- Growth retardation - height gain slows and can stop completely with severe weight loss. Growth in height can commence a few months after weight restoration.[53]
- Pubertal delay or arrest - both height gain and pubertal development are dependent on the release of growth hormone and gonadotrophins (LH and FSH) from the pituitary gland. Suppression of gonadotrophins in patients with anorexia nervosa has been frequently documented.[54]
- Reduction of Peak Bone Mass - bone accretion is the highest during adolescence, and if onset of anorexia nervosa occurs during this time and stalls puberty, bone mass may remain low.[52]
- Hepatic steatosis - fatty infiltration of the liver, is an indicator of malnutrition in children.[52]
- More information on symptoms and complications of anorexia nervosa in children and adolescents can be found at Yale Medical Group.
Studies have hypothesized the continuance of disordered eating patterns may be epiphenomena of starvation. The results of the Minnesota Starvation Experiment showed normal controls exhibit many of the behavioral patterns of anorexia nervosa (AN) when subjected to starvation. This may be due to the numerous changes in the neuroendocrine system, which results in a self-perpetuating cycle.[55][56][57][58] Studies have suggested the initial weight loss such as dieting may be the triggering factor in developing AN in some cases, possibly because of an already inherent predisposition toward AN. One study reported cases of AN resulting from unintended weight loss that resulted from varied causes, such as a parasitic infection, medication side effects, and surgery. The weight loss itself was the triggering factor.[59][60]
- Obstetric complications: various prenatal and perinatal complications may factor into the development of AN, such as maternal anemia, diabetes mellitus, preeclampsia, placental infarction, and neonatal cardiac abnormalities. Neonatal complications may also have an influence on harm avoidance, one of the personality traits associated with the development of AN.[61][62]
- Genetics: anorexia nervosa is believed to be highly heritable, with estimated inheritance rates ranging from 56% to 84%.[63][64][65] Association studies have been performed, studying 128 different polymorphisms related to 43 genes including genes involved in regulation of eating behavior, motivation and reward mechanics, personality traits and emotion. Consistent associations have been identified for polymorphisms associated with agouti-related peptide, brain derived neurotrophic factor, catechol-o-methyl transferase, SK3 and opioid receptor delta-1.[66] In one study, variations in the norepinephrine transporter gene promoter were associated with restrictive anorexia nervosa, but not binge-purge anorexia.[67] Recent studies have advanced the theory that the sex difference in incidence and the common onset at the age of puberty may reflect an abnormal response of the brain to anorexic (feeding suppressing) effects of the female sex hormone, estrogen.[68] This viewpoint has been recently supported by a report that abnormal forms of the estrogen receptor are more common in women with anorexia nervosa of the restricting type.[69]
- epigenetics: Epigenetic mechanisms: are means by which genetic mutations are caused by environmental effects that alter gene expression via methods such as DNA methylation, these are independent of and do not alter the underlying DNA sequence. They are heritable, as was shown in the Överkalix study, but also may occur throughout the lifespan, and are potentially reversible. Dysregulation of dopaminergic neurotransmission and Atrial natriuretic peptide homeostasis resulting from epigenetic mechanisms has been implicated in various eating disorders.[70] "We conclude that epigenetic mechanisms may contribute to the known alterations of ANP homeostasis in women with eating disorders."[70][71]
- serotonin dysregulation;[76] particularly high levels in those areas in the brain with the 5HT1A receptor – a system particularly linked to anxiety, mood and impulse control. Starvation has been hypothesized to be a response to these effects, as it is known to lower tryptophan and steroid hormone metabolism, which might reduce serotonin levels at these critical sites and ward off anxiety. Other studies of the 5HT2A serotonin receptor (linked to regulation of feeding, mood, and anxiety), suggest that serotonin activity is decreased at these sites. There is evidence that both personality characteristics associated with AN, and disturbances to the serotonin system are still apparent after patients have recovered from anorexia.[77]
- Brain-derived neurotrophic factor (BDNF) is a protein that regulates neuronal development and neuroplasticity, it also plays a role in learning, memory and in the hypothalamic pathway that controls eating behavior and energy homeostasis. BDNF amplifies neurotransmitter responses and promotes synaptic communication in the enteric nervous system. Low levels of BDNF are found in patients with AN and some comorbid disorders such as major depression.[78][79] Exercise increases levels of BDNF[80]
- leptin and ghrelin; leptin is a hormone produced primarily by the fat cells in white adipose tissue of the body it has an inhibitory (anorexigenic) effect on appetite, by inducing a feeling of satiety. Ghrelin is an appetite inducing (orexigenic) hormone produced in the stomach and the upper portion of the small intestine. Circulating levels of both hormones are an important factor in weight control. While often associated with obesity both have been implicated in the pathophysiology of anorexia nervosa and bulimia nervosa.[81]
- cerebral blood flow (CBF); neuroimaging studies have shown reduced CBF in the temporal lobes of anorectic patients, which may be a predisposing factor in the onset of AN.[82]
- autoimmune system; Autoantibodies against neuropeptides such as melanocortin have been shown to affect personality traits associated with eating disorders such as those that influence appetite and stress responses.[83]
- Infections: Some people are hypothesized to have developed anorexia abruptly as a reaction to a streptococcus or mycoplasma infection. PANS is an acronym for Pediatric acute-onset neuropsychiatric syndrome, a hypothesis describing children who have abrupt, dramatic onset of obsessive-compulsive disorder (OCD) or anorexia nervosa coincident with the presence of two or more neuropsychiatric symptoms.[84]
- Nutritional deficiencies
- Zinc deficiency may play a role in anorexia. It is not thought responsible for causation of the initial illness but there is evidence that it may be an accelerating factor that deepens the pathology of the anorexia. A 1994 randomized, double-blind, placebo-controlled trial showed that zinc (14 mg per day) doubled the rate of body mass increase compared to patients receiving the placebo.[85]
Sociocultural studies have highlighted the role of cultural factors, such as the promotion of thinness as the ideal female form in Western industrialized nations, particularly through the media.[86] A change in culture can cause anorexia nervosa in teenage girls who live in a Western culture and are from immigrant families.[87] A recent epidemiological study of 989,871 Swedish residents indicated that gender, ethnicity and socio-economic status were large influences on the chance of developing anorexia, with those with non-European parents among the least likely to be diagnosed with the condition, and those in wealthy, white families being most at risk.[88] People in professions where there is a particular social pressure to be thin (such as models and dancers) were much more likely to develop anorexia during the course of their career,[89] and further research has suggested that those with anorexia have much higher contact with cultural sources that promote weight-loss.[90]
Anorexia nervosa is more likely to occur in a person’s pubertal years, especially for girls.[91] Female students are 10 times more likely to suffer from anorexia nervosa than male students. According to a survey of 1799 Japanese female high school students, “85% who were a normal weight wanted to be thinner and 45% who were 10–20% underweight wanted to be thinner.”[92] Teenage girls concerned about their weight and who believe that slimness is more attractive among peers trend to weight-control behaviors. Teen girls are learning from each other to consume low-caloric, low-fat foods and diet pills. This results in lack of nutrition and a greater chance of developing anorexia nervosa.[93]
It has also been noted that anorexia nervosa is more likely to occur in populations in which obesity is more prevalent. It has been suggested that anorexia nervosa results from a sexually selected evolutionary drive to appear youthful in populations in which size becomes the primary indicator of age.[94]
There is also evidence to suggest that patients who have anorexia nervosa can be characterised by alexithymia[95] and also a deficit in certain emotional functions. A research study showed that this was the case in both adult and adolescent anorexia nervosa patients.[96]
There is a high rate of reported child sexual abuse experiences in clinical groups of who have been diagnosed with anorexia. The connection between eating disorders and abuse has been convincingly evidenced by a number of studies, including one published in Epidemiology (and strengthened by blind hypothesis survey), which showed in a comparison of women with no history of eating disorders, women with a history of eating disorders were twice as likely to have reported childhood sexual abuse.[97] While the joint effect of both physical and sexual abuse resulted in a nearly 4-fold risk of eating disorders that met DSM-IV criteria.[97] It is thought that links between childhood abuse and sexual abuse are complex, such as by influencing psychologic processes that increase a woman's susceptibility to the development of an eating disorder, or perhaps by producing changes in psychobiologic process and neurotransmitting function, associated with eating behaviour.[97]
Recent efforts have been made to dispel some of the myths around anorexia nervosa and eating disorders, such as the misconception that families, in particular mothers, are responsible for their daughter developing an eating disorder.[98]
File:Anorexia-autism2.png
A summary of the strategy Zucker
et al. (2007) used to assess the relationship between anorexia nervosa and the autism spectrum.
[99]
Since Gillberg's (1983 & 1985)[100][101] and others' initial suggestion of relationship between anorexia nervosa and autism,[102][103] a large-scale longitudinal study into teenage-onset anorexia nervosa conducted in Sweden confirmed that 23% of people with a long-standing eating disorder are on the autism spectrum.[104][105][106][107][108][109][110] Those on autism spectrum tend to have a worse outcome,[111] but may benefit from the combined use of behavioural and pharmacological therapies tailored to ameliorate autism rather than anorexia nervosa per se.[112][113] Other studies, most notably research conducted at the Maudsley Hospital, UK, furthermore suggest that autistic traits are common in people with anorexia nervosa; shared traits include, e.g., poor executive function, autism quotient score, central coherence, theory of mind, cognitive-behavioural flexibility, emotion regulation and understanding facial expressions.[114][115][116][117][118][119]
Zucker et al. (2007) proposed that conditions on the autism spectrum make up the cognitive endophenotype underlying anorexia nervosa and appealed for increased interdisciplinary collaboration (see figure to right).[99] A pilot study into the effectiveness Cognitive Behaviour Therapy, which based its treatment protocol on the hypothesised relationship between anorexia nervosa and an underlying autistic like condition, reduced perfectionism and rigidity in 17 out of 19 participants.[120]
The initial diagnosis should be made by a competent medical professional. There are multiple medical conditions, such as viral or bacterial infections, hormonal imbalances, neurodegenerative diseases and brain tumors which may mimic psychiatric disorders including anorexia nervosa. According to an in depth study conducted by psychiatrist Richard Hall as published in the Archives of General Psychiatry:
- Medical illness often presents with psychiatric symptoms.
- It is difficult to distinguish physical disorders from functional psychiatric disorders on the basis of psychiatric symptoms alone.
- Detailed physical examination and laboratory screening are indicated as a routine procedure in the initial evaluation of psychiatric patients.
- Most patients are unaware of the medical illness that is causative of their psychiatric symptoms.
- The conditions of patients with medically induced symptoms are often initially misdiagnosed as a functional psychosis.[121][122]
- Complete Blood Count (CBC): a test of the white blood cells. red blood cells and platelets used to assess the presence of various disorders such as leukocytosis, leukopenia, thrombocytosis and anemia which may result from malnutrition.[123]
- urinalysis: a variety of tests performed on the urine used in the diagnosis of medical disorders, to test for substance abuse, and as an indicator of overall health[124]
- ELISA: Various subtypes of ELISA used to test for antibodies to various viruses and bacteria such as Borrelia burgdoferi (Lyme Disease)[125]
- Western Blot Analysis: Used to confirm the preliminary results of the ELISA[126]
- Chem-20: Chem-20 also known as SMA-20 a group of twenty separate chemical tests performed on blood serum. Tests include cholesterol, protein and electrolytes such as potassium, chlorine and sodium and tests specific to liver and kidney function.[127]
- glucose tolerance test: Oral glucose tolerance test (OGTT) used to assess the body's ability to metabolize glucose. Can be useful in detecting various disorders such as diabetes, an insulinoma, Cushing's Syndrome, hypoglycemia and polycystic ovary syndrome[128][129]
- Secritin-CCK Test: Used to assess function of pancreas and gall bladder[130][131]
- Serum cholinesterase test: a test of liver enzymes (acetylcholinesterase and pseudocholinesterase) useful as a test of liver function and to assess the effects of malnutrition[132]
- Liver Function Test: A series of tests used to assess liver function some of the tests are also used in the assessment of malnutrition, protein deficiency, kidney function, bleeding disorders, Crohn's Disease[133]
- Lh response to GnRH: Luteinizing hormone (Lh) response to gonadotropin-releasing hormone (GnRH): Tests the pituitary glands' response to GnRh a hormone produced in the hypothalumus. Central hypogonadism is often seen in anorexia nervosa cases.[134]
- Creatine Kinase Test (CK-Test): measures the circulating blood levels of creatine kinase an enzyme found in the heart (CK-MB), brain (CK-BB) and skeletal muscle (CK-MM).[135][136]
- Blood urea nitrogen (BUN) test: urea nitrogen is the byproduct of protein metabolism first formed in the liver then removed from the body by the kidneys. The BUN test is used primarily to test kidney function. A low BUN level may indicate the effects of malnutrition.[137]
- BUN-to-creatinine ratio: A BUN to creatinine ratio is used to predict various conditions. High BUN/creatinine ratio can occur in severe hydration, acute kidney failure, congestive heart failure, intestinal bleeding. A low BUN/creatinine can indicate a low protein diet, celiac disease rhabdomyolysis, cirrhosis of the liver.[138][139][140]
- echocardiogram: utilizes ultrasound to create a moving picture of the heart to assess function[141]
- electrocardiogram (EKG or ECG): measures electrical activity of heart can be used to detect various disorders such as hyperkalemia[142]
- electroencephalogram (EEG): measures the electrical activity of the brain. Can be used to detect abnormalities such as those associated with pituitary tumors[143][144]
- Upper GI Series: test used to assess gastrointestinal problems of the middle and upper intestinal tract[145]
- Thyroid Screen TSH, t4, t3 :test used to assess thyroid functioning by checking levels of thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3)[146]
- Parathyroid hormone (PTH) test: tests the functioning of the parathyroid by measuring the amount of (PTH) in the blood. Test is used to diagnose parahypothyroidism. PTH also controls the levels of calcium and phosphorus in the blood (homeostasis).[147]
- barium enema: an x-ray examination of the lower gastrointestinal tract[148]
- neuroimaging; via the use of various techniques such as PET scan, fMRI, MRI and SPECT imaging should be included in the diagnostic procedure for any eating disorder 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.[citation needed]
Not only does starvation result in physical complications, but mental complications as well [149] . It has been shown that eating disorders such as anorexia nervosa are reinforced by reward and attention. P. Sodersten and colleagues suggest that effective treatment of this disorder depends on re-establishing reinforcement for normal eating behaviours instead of unhealthy weight loss. [150]
Anorexia nervosa is classified as an Axis I[151] disorder in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM-IV), published by the American Psychiatric Association. The DSM-IV should not be used by laypersons to diagnose themselves.
- DSM-IV-TR: diagnostic criteria for AN includes intense fear of gaining weight, a refusal to maintain body weight above 85% of the expected weight for a given age and height, and three consecutive missed periods and either refusal to admit the seriousness of the weight loss, or undue influence of shape or weight on one's self image, or a disturbed experience in one's shape or weight. There are two types: the binge-eating/purging type is characterized by overeating or purging, and the restricting type is not.[152]
- Criticism of DSM-IV There has been criticisms over various aspects of the diagnostic criteria utilized for anorexia nervosa in the DSM-IV. Including the requirement of maintaining a body weight below 85% of the expected weight and the requirement of amenorrhea for diagnosis; some women have all the symptoms of AN and continue to menstruate.[153] Those who do not meet these criteria are usually classified as eating disorder not otherwise specified; this may affect treatment options and insurance reimbursments.[154] The validity of the AN subtype classification has also been questioned because of the considerable diagnostic overlap between the binge-eating/purging type and the restricting type and the propensity of the patient to switch between the two.[155][156]
- Criticisms of DSM-IV and Diagnosing Adolescents with Anorexia Nervosa- There have been criticisms over the diagnostic criteria utilized for anorexia nervosa in the DSM- IV and it’s applicability in diagnosing adolescents with anorexia nervosa. Several criticisms of the DSM-IV in diagnosing adolescents with anorexia nervosa are:
-
- Fulfillment of DSM- IV criteria B and C for anorexia nervosa are dependent on complex abstract reasoning, the capacity to describe internal experiences, and the ability to perceive risk[157]. While formal thought emerges between ages 11–13, complex abstract reasoning continues to develop late into adolescence. The ability to perceive risk also continues to develop through adolescence, as some preadolescents have difficult perceiving the relative risk of alternative outcomes.[157] Adolescents and children must first develop these internal thought processes in order to then endorse fear of weight gain or distortion of body image, and deny the seriousness of low body weight despite their behaviors that contribute to harmful weight loss, which are necessary to fulfill criteria B and C[158]. These developmental factors may impede an adolescent or child from receiving a diagnosis of anorexia nervosa. It is the hope of certain professionals that the DSM-V will take the unique developmental stages of children and adolescents into account when revising the current criteria. One proposed amendment would be to allow behavioral indicators as a means of substituting internally referenced cognitive criteria.[157]
- Another criticism focuses on the current weight criteria specified to receive a diagnosis of anorexia nervosa. Critics state that there is wide variability in the rate, timing and magnitude of both height and weight gain during normal puberty.[159] Physical development varies greatly during puberty, making it a challenge to define an optimal weight range for a growing child or adolescents. [158]
- ICD-10: The criteria are similar, but in addition, specifically mention:
- The ways that individuals might induce weight-loss or maintain low body weight (avoiding fattening foods, self-induced vomiting, self-induced purging, excessive exercise, excessive use of appetite suppressants or diuretics).
- If onset is before puberty, that development is delayed or arrested.
- Certain physiological features, including "widespread endocrine disorder involving hypothalamic-pituitary-gonadal axis is manifest in women as amenorrhoea and in men as loss of sexual interest and potency. There may also be elevated levels of growth hormones, raised cortisol levels, changes in the peripheral metabolism of thyroid hormone and abnormalities of insulin secretion".
Dr. Hilde Burch, in her 1973 book, Eating Disorders: Obesity, Anorexia Nervosa, and the Person Within, explains that Anorexia Nervosa is "not a static condition," but one that continually provokes new problems with its various stages. She writes, "The state of starvation is associated by marked psychological changes... camouflaged by rationalizations." She identifies the family interaction becomes difficult, marked by rising anxiety, annoyance and resentment. It also brings about social isolation. (Burch 215).
Dr. Burch believed that anorexia, which is simply not eating enough, as a result from schizophrenia, depression, or esophageal problems often were misdiagnosed as anorexia nervosa. In her assessment, this blurred the definition of anorexia nervosa. For this reason, she distinguished between, what she calls "atypical" and "primary" cases of anorexia nervosa. The atypical cases of anorexia were brought about by a range of stimuli (from schizophrenia to depression, as noted above). (Burch 227).
In contrast to the atypical group, Burch observed primary, or genuine anorexia nervosa, "amazingly uniform". The first outstanding symptom is "disturbance of delusional proportions in the body image". The second outstanding characteristic is "disturbance in the accuracy of their perception or cognitive interpretation of stimuli arising from the body... failure to recognize hunger and denial of fatigue". The third outstanding characteristic is a "paralyzing sense of ineffectiveness". "Anorexics struggle against a feeling of enslaved, exploited, and not being permitted to lead a life of their own. They would rather starve than continue a life of accommodation. In this blind search for a sense of identity and selfhood they will not accept anything that their parents, or the world around them, has to offer." It is a "desperate struggle for a self respecting identity". She understood that the personality disorder (struggle for control, for a sense of identity, competence, and effectiveness) precedes the somatic disorders (such as emaciation, amenorrhea, constipation, etc.) (Burch 250–255).
There are various medical and psychological conditions that have been misdiagnosed as anorexia nervosa, in some cases the correct diagnosis was not made for more than ten years. In a reported case of achalasia misdiagnosed as AN, the patient spent two months confined to a psychiatric hospital.[160]
There are various other psychological issues that may factor into anorexia nervosa, some fulfill the criteria for a separate Axis I diagnosis or a personality disorder which is coded Axis II and thus are considered comorbid to the diagnosed eating disorder. Axis II disorders are subtyped into 3 "clusters", A, B and C.The causality between personality disorders and eating disorders has yet to be fully established.[161] Some people have a previous disorder which may increase their vulnerability to developing an eating disorder.[162][163][164] Some develop them afterwards.[165] The severity and type of eating disorder symptoms have been shown to affect comorbidity.[166]
- Body dysmorphic disorder (BDD) is listed as a somatoform disorder that affects up to 2% of the population. BDD is characterized by excessive rumination over an actual or perceived physical flaw. BDD has been diagnosed equally among men and women. While BDD has been misdiagnosed as anorexia nervosa, it also occurs comorbidly in 25% to 39% of AN cases.[181]
BDD is a chronic and debilitating condition which may lead to social isolation, major depression, suicidal ideation and attempts. Neuroimaging studies to measure response to facial recognition have shown activity predominately in the left hemisphere in the left lateral prefrontal cortex, lateral temporal lobe and left parietal lobe showing hemispheric imbalance in information processing. There is a reported case of the development of BDD in a 21 year old male following an inflammatory brain process. Neuroimaging showed the presence of new atrophy in the frontotemporal region.[182][183][184][184][185]
The distinction between the diagnoses of anorexia nervosa, bulimia nervosa and eating disorder not otherwise specified (EDNOS) is often difficult to make as there is considerable overlap between patients diagnosed with these conditions. Seemingly minor changes in a patient's overall behavior or attitude can change a diagnosis from "anorexia: binge-eating type" to bulimia nervosa. It is not unusual for a person with an eating disorder to "move through" various diagnoses as his or her behavior and beliefs change over time.[99]
Treatment for anorexia nervosa tries to address three main areas. 1) Restoring the person to a healthy weight; 2) Treating the psychological disorders related to the illness; 3) Reducing or eliminating behaviours or thoughts that originally led to the disordered eating.[186] Although restoring the person's weight is the primary task at hand, optimal treatment also includes and monitors behavioral change in the individual as well[187]. As treatment can prove to be difficult, "as many as 6 percent of people with the disorder die from causes related to it. [188]If anorexia nervosa is not treated, serious complications such as heart conditions and kidney failure can initiate and eventually lead to death.
-
- Zinc supplementation has been shown in various studies to be beneficial in the treatment of AN even in patients not suffering from zinc deficiency, by helping to increase weight gain.[189][190][191]
- Essential fatty acids:The omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) have been shown to benefit various neuropsychiatric disorders. There was reported rapid improvement in a case of severe AN treated with ethyl-eicosapentaenoic acid (E-EPA) and micronutrients.[192] DHA and EPA supplementation has been shown to be a benefit in many of the comorbid disorders of AN including: attention deficit/hyperactivity disorder (ADHD), autism, major depressive disorder (MDD),[193] bipolar disorder, and borderline personality disorder. Accelerated cognitive decline and mild cognitive impairment (MCI) correlate with lowered tissue levels of DHA/EPA, and supplementation has improved cognitive function.[194][195]
- Nutrition counseling[196][197]
- Medical Nutrition Therapy;(MNT) also referred to as Nutrition Therapy is the development and provision of a nutritional treatment or therapy based on a detailed assessment of a person's medical history, psychosocial history, physical examination, and dietary history.[198][199][200]
-
- Olanzapine: has been shown to be effective in treating certain aspects of AN including to help raise the body mass index and reduce obsessionality, including obsessional thoughts about food.[201][202] However, its primary usefulness is that it is one of the most potent appetite stimulants known, and causes the body to preferentially store fat.
-
- Cognitive behavioral therapy (CBT) CBT is an evidence based approach which in studies to date has shown to be useful in adolescents and adults with anorexia nervosa.[203][204][205]Components of using CBT with adults and adolescents with anorexia nervosa have been outlined by several professionals as:
-
- the therapist focuses on using cognitive restructuring to modify distorted beliefs and attitudes about the meaning of weight, shape and appearance[206]
- specific behavioral techniques addressing the normalization of eating patterns and weight restorations, examples of this include the use of a food diary, meal plans, and incremental weight gain[206]
- cognitive techniques such as restructuring, problem solving, and identification and expression of affect[206]
-
- When using CBT with adolescents and children with AN, several professionals have expressed concerns about the minimum age and level of cognition necessary for implementing cognitive behavioral techniques.[206] Modified versions and elements of CBT can be implemented with children and adolescents with AN. Such modifications may include the use of behavioral experiments to disconfirm distorted beliefs and absolutistic thinking in children and adolescents.[206]
- Acceptance and commitment therapy: A type of CBT, has shown promise in the treatment of AN" participants experienced clinically significant improvement on at least some measures; no participants worsened or lost weight even at 1-year follow-up."[207]
- Cognitive Remediation Therapy (CRT): is a cognitive rehabilitation therapy developed at King's College in London designed to improve neurocognitive abilities such as attention, working memory, cognitive flexibility and planning, and executive functioning which leads to improved social functioning. Neuropsychological studies have shown that patients with AN have difficulties in cognitive flexibility. In studies conducted at Kings College[208] and in Poland with adolescents CRT was proven to be beneficial in treating anorexia nervosa,[208] in the United States clinical trials are still being conducted by the National Institute of Mental Health[209] on adolescents age 10–17 and Stanford University in subjects over 16 as a conjunctive therapy with Cognitive behavioral therapy.[210]
-
- Family therapy: The most effective form of therapy for adolescents with anorexia is family therapy.[211] There are various forms of family-based therapy that have been proven to work in the treatment of adolescent AN including "conjoint family therapy" (CFT), in which the parents and child are seen together by the same therapist, "separated family therapy" (SFT) in which parents and child attend therapy separately with different therapists. "Eisler's cohort show that, irrespective of the type of FBT, 75% of patients have a good outcome, 15% an intermediate outcome... ".[212][213] Proponents of Family Therapy for adolescents with AN assert that it is important to include parents in the adolescent's treatment.[214] Several components of using Family Therapy with Children and Adolescents are:
-
- the family is seen as a resource for the adolescent[215]
- anorexia nervosa is reframed in benign, non blaming terms[215]
- directives are provided to parents so that they may take charge of their child or adolescent's eating routine[215]
- a structured behavioral weight gain program is implemented[215]
- after weight gain, control over eating is gradually returned to the child or adolescent[215]
- as the child or adolescent begins to eat and gain weight, the theraputic focus broadens to include family interaction problems, growth and autonomy issues and parent child conflicts[215]
- Maudsley Family Therapy: A 4 to 5 year follow up study of the Maudsley approach, a manualized model, that shows full recovery at rates up to 90%.[216]
-
- Yoga: In preliminary studies indivualized yoga treatment has shown positive results for use as an adjunctive therapy to standard care. The treatment was shown to reduce eating disorder symptoms, including food preoccupation, which decreased immediately after each session. Scores on the Eating Disorder Examination decreased consistently over the course of treatment.[217]
The long term prognosis of anorexia is more on the favorable side. The National Comorbidity Replication Survey was conducted among more than 9,282 participants throughout the United States, the results found that the average duration of anorexia nervosa is 1.7 years. "Contrary to what people may believe, anorexia is not necessarily a chronic illness; in many cases, it runs its course and people get better..."[218]
In cases of adolescent anorexia nervosa that utilize family-based treatment 75% of patients have a good outcome and an additional 15% show an intermediate yet more positive outcome.[212] In a five year post treatment follow-up of Maudsley Family Therapy the full recovery rate was between 75% and 90%.[219] Even in severe cases of AN, despite a noted 30% relapse rate after hospitalization, and a lengthy time to recovery ranging from 57 to 79 months, the full recovery rate was still 76%. There were minimal cases of relapse even at the long term follow-up conducted between 10–15 years.[220] The long-term prognosis of anorexia nervosa is changeable: a fifth of patients stay severely ill, another fifth of patients recover fully and three fifths of patients have a fluctuating and chronic course (Gelder, Mayou and Geddes 2005).
Anorexia has an average prevalence of 0.3–1% in women and 0.1% in men for the diagnosis in developed countries.[221] The condition largely affects young adolescent women, with between 15 and 19 years old making up 40% of all cases. Approximately 75% of people with anorexia are female.[222] Anorexia nervosa is more prevalent in the upper social classes and it is declared to be rare in less developed countries (Gelder, Mayou and Geddes 2005). Anorexia is more prevalent in females and males born after 1945 ( Attia and Walsh 2007). [223]
The history of anorexia nervosa begins with descriptions of religious fasting dating from the Hellenistic era [224] and continuing into the medieval period. A number of well known historical figures, including Catherine of Siena and Mary, Queen of Scots are believed to have suffered from the condition.[225][226]
Of interest in terms of anorexia nervosa is the medieval practice of self-starvation by women, including some young women, in the name of religious piety and purity. This is sometimes referred to as anorexia mirabilis. By the thirteenth century, it was increasingly common for women to participate in religious life . Many women who ultimately became saints engaged in self-starvation, including Saint Hedwig of Andechs in the thirteenth century and Catherine of Siena in the fourteenth century. By the time of Catherine of Siena, however, the Church became concerned about extreme fasting as an indicator of spirituality and as a criterion for sainthood. Indeed, Catherine of Siena was told by Church authorities to pray that she would be able to eat again, but was unable to give up fasting.[225]
The earliest medical descriptions of anorexic illnesses are generally credited to English physician Richard Morton, in 1689.[224]
However it was not until the late 19th century that anorexia nervosa was to be widely accepted by the medical profession as a recognised condition. In 1873, Sir William Gull, one of Queen Victoria’s personal physicians, published a seminal paper which established the term anorexia nervosa and provided a number of detailed case descriptions and treatments. In the same year, French physician Ernest-Charles Lasègue similarly published details of a number of cases in a paper entitled De l’Anorexie Histerique.
Awareness of the condition was largely limited to the medical profession until the latter part of the 20th century, when German-American psychoanalyst Hilde Bruch published her popular work The Golden Cage: the Enigma of Anorexia Nervosa in 1978. This book created a wider awareness of anorexia nervosa among lay readers. A further important event was the death of the popular singer drummer Karen Carpenter in 1983, which prompted widespread ongoing media coverage of eating disorders.
- ^ Hockenbury,Don and Sandra (2008). Psychology, p. 593. Worth Publishers, New York. ISBN 978-1-4292-0143-8.
- ^ Nogal, Powel; Lewiński,Andrzej (01.03.2008). "Anorexia Nervosa". Endokrynologia Polska/Polish Journal of Endocrinology 59 (2): 148–155. ISSN 0423–104X.
- ^ Carlson, N.; Heth C., Miller Harold, Donahoe John, Buskist William, Martin G., Schmaltz Rodney (2007). Psychology: the science of behaviour-4th Canadian ed. Toronto, ON: Pearson Education Canada. pp. 414-415. ISBN 978-0-205-64524-4.
- ^ Hotta M, Ohwada R, Akamizu T, Shibasaki T, Takano K, Kangawa K (2009). "Ghrelin increases hunger and food intake in patients with restricting-type anorexia nervosa: a pilot study". Endocrine Journal 56 (9): 1119–28. DOI:10.1507/endocrj.K09E-168. PMID 19755753.
- ^ WHO. International statistical classification of diseases and related health problems, 10th revision. Geneva: WHO, 1992
- ^ Rosen JC, Reiter J, Orosan P (1995). "Assessment of body image in eating disorders with the body dysmorphic disorder examination". Behaviour Research and Therapy 33 (1): 77–84. DOI:10.1016/0005-7967(94)E0030-M. PMID 7872941.
- ^ Cooper MJ (2005). "Cognitive theory in anorexia nervosa and bulimia nervosa: progress, development and future directions". Clinical Psychology Review 25 (4): 511–31. DOI:10.1016/j.cpr.2005.01.003. PMID 15914267.
- ^ Brooks S, Prince A, Stahl D, Campell IC, Treasure J (2010). "A systematic review & meta-analysis of cognitive bias to food stimuli in people with disordered eating behaviour". Clinical Psychology 31 (1): 37. DOI:10.1016/j.cpr.2010.09.006.
- ^ a b Neil Frude (1998). Understanding abnormal psychology. Wiley-Blackwell. ISBN 978-0-631-16195-0. http://books.google.com/books?id=rVMMj4Y7Xm8C. Retrieved 4 February 2012.
- ^ a b Attia E (2010). "Anorexia Nervosa: Current Status and Future Directions". Annual Review of Medicine 61 (1): 425–35. DOI:10.1146/annurev.med.050208.200745. PMID 19719398.
- ^ "Society of Clinical Child and Adolescent Psychology – What is Anorexia Nervosa?". http://www.abct.org/sccap/?m=sPublic&fa=pub_AnorexiaNervosa.
- ^ The scary trend of tweens with anorexia. CNN.com (2011-08-08). Retrieved on 2012-02-04.
- ^ Bennett J (2008). "It's not just white girls. Anorexics can be male, old, Latino, black or pregnant. A new book undercuts old stereotypes". Newsweek 152 (11): 96. PMID 18800573.
- ^ Woodside, DB; Garfinkel, PE; Lin, E; Goering, P; Kaplan, AS; Goldbloom, DS; Kennedy, SH (2001). "Comparisons of Men With Full or Partial Eating Disorders, Men Without Eating Disorders, and Women With Eating Disorders in the Community". The American Journal of Psychiatry 158 (4): 570–4. PMID 11282690. http://homepage.psy.utexas.edu/homepage/class/Psy394Q/Behavior%20Therapy%20Class/Assigned%20Readings/Eating%20Disorders/Woodside2001.pdf.
- ^ Gull WW (1997). "Anorexia nervosa (apepsia hysterica, anorexia hysterica). 1868". Obesity Research 5 (5): 498–502. PMID 9385628.
- ^ Costin, Carolyn (1999). The Eating Disorder Sourcebook. Linconwood: Lowell House. p. 6. ISBN 0-585-18922-6.
- ^ Rojo-Moreno, L., Plumed, J. J., Fons, M. B., Gonzalez-Piqueras, J. C., Rojo-Bofill, L. and Livianos, L. (2011), "Auditory hallucinations in anorexia nervosa". Eur. Eat. Disorders Rev. (19): 494–500. doi:10.1002/erv.1084"
- ^ Abell, TL; Malagelada, JR; Lucas, AR; Brown, ML; Camilleri, M; Go, VL; Azpiroz, F; Callaway, CW et al. (1987). "Gastric electromechanical and neurohormonal function in anorexia nervosa". Gastroenterology 93 (5): 958–65. PMID 3653645.
- ^ Ulger Z, Gürses D, Ozyurek AR, Arikan C, Levent E, Aydoğdu S (2006). "Follow-up of cardiac abnormalities in female adolescents with anorexia nervosa after refeeding". Acta Cardiologica 61 (1): 43–9. DOI:10.2143/AC.61.1.2005139. PMID 16485732.
- ^ Støving RK, Hangaard J, Hagen C; Hangaard; Hagen (2001). "Update on endocrine disturbances in anorexia nervosa". Journal of Pediatric Endocrinology & Metabolism 14 (5): 459–80. DOI:10.1515/JPEM.2001.14.5.459. PMID 11393567.
- ^ Anorexia, Bulimia. 1. 2003. pp. 86-92.
- ^ a b c Attia, E. and Walsh, B. T. (2007). "Anorexia Nervosa". American Journal of Psychiatry 164 (12): 1805–1810. DOI:10.1176/appi.ajp.2007.07071151. PMID 18056234.
- ^ Walsh JM, Wheat ME, Freund K (2000). "Detection, Evaluation, and Treatment of Eating Disorders: The Role of the Primary Care Physician". Journal of General Internal Medicine 15 (8): 577–90. DOI:10.1046/j.1525-1497.2000.02439.x. PMC 1495575. PMID 10940151. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1495575.
- ^ Pietrowsky R, Krug R, Fehm HL, Born J (2002). "Food deprivation fails to affect preoccupation with thoughts of food in anorexic patients". The British Journal of Clinical Psychology 41 (Pt 3): 321–6. DOI:10.1348/014466502760379172. PMID 12396259.
- ^ Kovacs D, Palmer RL (2004). "The associations between laxative abuse and other symptoms among adults with anorexia nervosa". The International Journal of Eating Disorders 36 (2): 224–8. DOI:10.1002/eat.20024. PMID 15282693.
- ^ Friedman EJ (1984). "Death from ipecac intoxication in a patient with anorexia nervosa". The American Journal of Psychiatry 141 (5): 702–3. PMID 6143508.
- ^ Peñas-Lledó E, Vaz Leal FJ, Waller G (2002). "Excessive exercise in anorexia nervosa and bulimia nervosa: relation to eating characteristics and general psychopathology". The International Journal of Eating Disorders 31 (4): 370–5. DOI:10.1002/eat.10042. PMID 11948642.
- ^ Haller E (1992). "Eating disorders. A review and update". The Western Journal of Medicine 157 (6): 658–62. PMC 1022101. PMID 1475950. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1022101.
- ^ Lucka I (2004). "[Depression syndromes in patients suffering from anorexia nervosa]" (in Polish). Psychiatria Polska 38 (4): 621–9. PMID 15518310.
- ^ Bozzato A, Burger P, Zenk J, Uter W, Iro H (2008). "Salivary gland biometry in female patients with eating disorders". European Archives of Oto-rhino-laryngology 265 (9): 1095–102. DOI:10.1007/s00405-008-0598-8. PMID 18253742.
- ^ "Signs of Anorexia". http://anorexia.emedtv.com/anorexia/signs-of-anorexia.html.
- ^ "Noticing the Signs and Symptoms". http://www.something-fishy.org/isf/signssymptoms.php.
- ^ McClure, G.M.; Timimi, Westman (1995). "Anorexia nervosa in early adolescence following illness — the importance of the sick role". Journal of Adolescence 18 (3): 359. http://search.proquest.com/docview/61418456?accountid=14771.
- ^ Strumia R (2005). "Dermatologic signs in patients with eating disorders". American Journal of Clinical Dermatology 6 (3): 165–73. DOI:10.2165/00128071-200506030-00003. PMID 15943493.
- ^ Chiarioni, Giuseppe; Bassotti, Gabrio; Monsignori, Antonella; Menegotti, Monica; Salandini, Lara; Di Matteo, Giorgio; Vantini, Italo; Whitehead, William E. (2000). "Anorectal dysfunction in constipated women with anorexia nervosa". Mayo Clinic Proceedings 75 (10): 1015–9. DOI:10.4065/75.10.1015. PMID 11040849.
- ^ Waldholtz BD, Andersen AE (1990). "Gastrointestinal symptoms in anorexia nervosa. A prospective study". Gastroenterology 98 (6): 1415–9. PMID 2338185.
- ^ Olson AF (2005). "Outpatient management of electrolyte imbalances associated with anorexia nervosa and bulimia nervosa". Journal of Infusion Nursing 28 (2): 118–22. DOI:10.1097/00129804-200503000-00005. PMID 15785332.
- ^ van Nieuw Amerongen A, Vissink A (2001). "[Oral complications of anorexia nervosa, bulimia nervosa and other metabolic disorders]" (in Dutch). Nederlands Tijdschrift Voor Tandheelkunde 108 (6): 242–7. PMID 11441717.
- ^ de Moor RJ (2004). "Eating disorder-induced dental complications: a case report". Journal of Oral Rehabilitation 31 (7): 725–32. DOI:10.1111/j.1365-2842.2004.01282.x. PMID 15210036.
- ^ García-Rubira JC, Hidalgo R, Gómez-Barrado JJ, Romero D, Cruz Fernández JM (1994). "Anorexia nervosa and myocardial infarction". International Journal of Cardiology 45 (2): 138–40. DOI:10.1016/0167-5273(94)90270-4. PMID 7960253.
- ^ Golden NH, Shenker IR (1994). "Amenorrhea in anorexia nervosa. Neuroendocrine control of hypothalamic dysfunction". The International Journal of Eating Disorders 16 (1): 53–60. DOI:10.1002/1098-108X(199407)16:1<53::AID-EAT2260160105>3.0.CO;2-V. PMID 7920581.
- ^ Demaerel P, Daele MC, De Vuysere S, Wilms G, Baert AL (1996). "Orbital fat edema in anorexia nervosa: a reversible finding". American Journal of Neuroradiology 17 (9): 1782–4. PMID 8896638. http://www.ajnr.org/cgi/pmidlookup?view=long&pmid=8896638.
- ^ Joyce JM, Warren DL, Humphries LL, Smith AJ, Coon JS (1990). "Osteoporosis in women with eating disorders: comparison of physical parameters, exercise, and menstrual status with SPA and DPA evaluation". Journal of Nuclear Medicine 31 (3): 325–31. PMID 2308003. http://jnm.snmjournals.org/cgi/pmidlookup?view=long&pmid=2308003.
- ^ Golden NH (2003). "Osteopenia and osteoporosis in anorexia nervosa". Adolescent Medicine 14 (1): 97–108. PMID 12529194.
- ^ Bahia A, Chu ES, Mehler PS (2010). "Polydipsia and hyponatremia in a woman with anorexia nervosa". The International Journal of Eating Disorders 44 (2): 186–8. DOI:10.1002/eat.20792. PMID 20127934.
- ^ Bonne OB, Bloch M, Berry EM (1993). "Adaptation to severe chronic hypokalemia in anorexia nervosa: a plea for conservative management". The International Journal of Eating Disorders 13 (1): 125–8. DOI:10.1002/1098-108X(199301)13:1<125::AID-EAT2260130115>3.0.CO;2-4. PMID 8477271.
- ^ Mroczkowski MM, Redgrave GW, Miller NR, McCoy AN, Guarda AS (2010). "Reversible vision loss secondary to malnutrition in a woman with severe anorexia nervosa, purging type, and alcohol abuse". The International Journal of Eating Disorders 44 (3): 281–3. DOI:10.1002/eat.20806. PMID 20186722.
- ^ Drevelengas A, Chourmouzi D, Pitsavas G, Charitandi A, Boulogianni G (2001). "Reversible brain atrophy and subcortical high signal on MRI in a patient with anorexia nervosa". Neuroradiology 43 (10): 838–40. DOI:10.1007/s002340100589. PMID 11688699.
- ^ Addolorato G, Taranto C, Capristo E, Gasbarrini G (1998). "A case of marked cerebellar atrophy in a woman with anorexia nervosa and cerebral atrophy and a review of the literature". The International Journal of Eating Disorders 24 (4): 443–7. DOI:10.1002/(SICI)1098-108X(199812)24:4<443::AID-EAT13>3.0.CO;2-4. PMID 9813771.
- ^ Hütter G, Ganepola S, Hofmann WK (2009). "The hematology of anorexia nervosa". The International Journal of Eating Disorders 42 (4): 293–300. DOI:10.1002/eat.20610. PMID 19040272.
- ^ Allende, LM; Corell, A; Manzanares, J; Madruga, D; Marcos, A; Madrono, A; Lopez-Goyanes, A; Garcia-Perez, MA et al. (1998). "Immunodeficiency associated with anorexia nervosa is secondary and improves after refeeding". Immunology 94 (4): 543–51. DOI:10.1046/j.1365-2567.1998.00548.x. PMC 1364233. PMID 9767443. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1364233.
- ^ a b c Nicholls, D. & Stanhope, R. "Medical Complications of Anorexia Nervosa in Children and Young Adolescents". European Disorders Review,2000,p.171
- ^ Nicholls, D. & Stanhope, R. "Medical Complications of Anorexia Nervosa in Children and Young Adolescents". European Eating Disorders Review, 2000, p.173
- ^ Nicholls, D. & Stanhope, R. "Medical Complications of Anorexia Nervosa in Children and Young Adolescents". European Eating Disorders Review, 2000, p.174
- ^ Zandian M, Ioakimidis I, Bergh C, Södersten P (2007). "Cause and treatment of anorexia nervosa". Physiology & Behavior 92 (1–2): 283–90. DOI:10.1016/j.physbeh.2007.05.052. PMID 17585973.
- ^ Thambirajah, M. S. (2007). Case Studies in Child and Adolescent Mental Health. Radcliffe Publishing. p. 145. ISBN 978-1-85775-698-2. OCLC 84150452.
- ^ Kaye W (2008). "Neurobiology of Anorexia and Bulimia Nervosa Purdue Ingestive Behavior Research Center Symposium Influences on Eating and Body Weight over the Lifespan: Children and Adolescents". Physiology & Behavior 94 (1): 121–35. DOI:10.1016/j.physbeh.2007.11.037. PMC 2601682. PMID 18164737. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2601682.
- ^ Støving RK, Hansen-Nord M, Hangaard J, Hagen C (1996). "[Neuroendocrine disorders in anorexia nervosa—primary or secondary?]" (in Danish). Ugeskrift for Laeger 158 (49): 7052–6. PMID 8999610.
- ^ Brandenburg BM, Andersen AE (2007). "Unintentional onset of anorexia nervosa". Eating and Weight Disorders 12 (2): 97–100. PMID 17615494. http://www.kurtis.it/abs/index.cfm?id_articolo_numero=3749.
- ^ Nygaard JA (1990). "Anorexia nervosa. Treatment and triggering factors". Acta Psychiatrica Scandinavica. Supplementum 361: 44–9. PMID 2291425.
- ^ Favaro A, Tenconi E, Santonastaso P (2006). "Perinatal factors and the risk of developing anorexia nervosa and bulimia nervosa". Archives of General Psychiatry 63 (1): 82–8. DOI:10.1001/archpsyc.63.1.82. PMID 16389201.
- ^ Favaro A, Tenconi E, Santonastaso P (2008). "The relationship between obstetric complications and temperament in eating disorders: a mediation hypothesis". Psychosomatic Medicine 70 (3): 372–7. DOI:10.1097/PSY.0b013e318164604e. PMID 18256341.
- ^ Klump KL, Miller KB, Keel PK, McGue M, Iacono WG (2001). "Genetic and environmental influences on anorexia nervosa syndromes in a population-based twin sample". Psychological Medicine 31 (4): 737–40. DOI:10.1017/S0033291701003725. PMID 11352375.
- ^ Kortegaard LS, Hoerder K, Joergensen J, Gillberg C, Kyvik KO (2001). "A preliminary population-based twin study of self-reported eating disorder". Psychological Medicine 31 (2): 361–365. DOI:10.1017/S0033291701003087. PMID 11232922.
- ^ Wade TD, Bulik CM, Neale M, Kendler KS (2000). "Anorexia nervosa and major depression: shared genetic and environmental risk factors". Am J Psychiatry 157 (3): 469–71. DOI:10.1176/appi.ajp.157.3.469. PMID 10698830.
- ^ Rask-Andersen M, Olszewski PK, Levine AS, Schiöth HB (2009). "Molecular mechanisms underlying anorexia nervosa: Focus on human gene association studies and systems controlling food intake". Brain Res Rev 62 (2): 147–64. DOI:10.1016/j.brainresrev.2009.10.007. PMID 19931559.
- ^ Urwin, R E; Bennetts, B; Wilcken, B; Lampropoulos, B; Beumont, P; Clarke, S; Russell, J; Tanner, S et al. (2002). "Anorexia nervosa (restrictive subtype) is associated with a polymorphism in the novel norepinephrine transporter gene promoter polymorphic region". Molecular Psychiatry 7 (6): 652–7. DOI:10.1038/sj.mp.4001080. PMID 12140790.
- ^ Young JK (2010). "Anorexia nervosa and estrogen: current status of the hypothesis". Neuroscience and Biobehavioral Reviews 34 (8): 1195–1200. DOI:10.1016/j.neubiorev.2010.01.015. PMID 20138911.
- ^ Versini, Audrey; Ramoz, Nicolas; Le Strat, Yann; Scherag, Susann; Ehrlich, Stefan; Boni, Claudette; Hinney, Anke; Hebebrand, Johannes et al. (2010). "Estrogen Receptor 1 Gene (ESR1) is Associated with Restrictive Anorexia Nervosa". Neuropsychopharmacology 35 (8): 1–8. DOI:10.1038/npp.2010.49. PMC 3055492. PMID 20375995. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3055492.
- ^ a b Frieling, Helge; Römer, Konstanze D.; Scholz, Sarah; Mittelbach, Franziska; Wilhelm, Julia; De Zwaan, Martina; Jacoby, Georg E.; Kornhuber, Johannes et al. (2009). "Epigenetic dysregulation of dopaminergic genes in eating disorders". The International Journal of Eating Disorders 43 (7): 577–83. DOI:10.1002/eat.20745. PMID 19728374.
- ^ Epigenetic Downregulation of Atrial Natriuretic Peptide but not Vasopressin mRNA Expression in Females with Eating Disorders is Related to Impulsivity
- ^ Kaye WH, Frank GK, Bailer UF, Henry SE (2005). "Neurobiology of anorexia nervosa: clinical implications of alterations of the function of serotonin and other neuronal systems". The International Journal of Eating Disorders. 37 Suppl (S1): S15–9; discussion S20–1. DOI:10.1002/eat.20109. PMID 15852312.
- ^ Bergen, Andrew W; Yeager, Meredith; Welch, Robert A; Haque, Kashif; Ganjei, J Kelly; Van Den Bree, Marianne B M; Mazzanti, Chiara; Nardi, Irma et al. (2005). "Association of multiple DRD2 polymorphisms with anorexia nervosa". Neuropsychopharmacology 30 (9): 1703–10. DOI:10.1038/sj.npp.1300719. PMID 15920508.
- ^ Kaye, W; Bailer, U; Frank, G; Wagner, A (2006). "Persistent alterations of serotonin and dopamine activity after recovery from anorexia and bulimia nervosa". Psychosomatic Medicine 1287: 45–48. DOI:10.1016/j.ics.2005.12.038.
- ^ Bosanac P, Norman T, Burrows G, Beumont P (2005). "Serotonergic and dopaminergic systems in anorexia nervosa: a role for atypical antipsychotics?". The Australian and New Zealand Journal of Psychiatry 39 (3): 146–53. DOI:10.1111/j.1440-1614.2005.01536.x. PMID 15701063.
- ^ Kaye, W; Frank, G; Bailer, U; Henry, S; Meltzer, C; Price, J; Mathis, C; Wagner, A (2005). "Serotonin alterations in anorexia and bulimia nervosa: new insights from imaging studies". Physiology & Behavior 85 (1): 73–81. DOI:10.1016/j.physbeh.2005.04.013. PMID 15869768.
- ^ Kaye WH, Bailer UF, Frank GK, Wagner A, Henry SE (2005). "Brain imaging of serotonin after recovery from anorexia and bulimia nervosa". Physiology & Behavior 86 (1–2): 15–7. DOI:10.1016/j.physbeh.2005.06.019. PMID 16102788.
- ^ Monteleone P, Fabrazzo M, Martiadis V, Serritella C, Pannuto M, Maj M (2005). "Circulating brain-derived neurotrophic factor is decreased in women with anorexia and bulimia nervosa but not in women with binge-eating disorder: relationships to co-morbid depression, psychopathology and hormonal variables". Psychological Medicine 35 (6): 897–905. DOI:10.1017/S0033291704003368. PMID 15997610.
- ^ Wang C, Bomberg E, Billington C, Levine A, Kotz CM (2007). "Brain-derived neurotrophic factor in the hypothalamic paraventricular nucleus increases energy expenditure by elevating metabolic rate". American Journal of Physiology. Regulatory, Integrative and Comparative Physiology 293 (3): R992–1002. DOI:10.1152/ajpregu.00516.2006. PMID 17567712.
- ^ Ferris LT, Williams JS, Shen CL (2007). "The effect of acute exercise on serum brain-derived neurotrophic factor levels and cognitive function". Medicine and Science in Sports and Exercise 39 (4): 728–34. DOI:10.1249/mss.0b013e31802f04c7. PMID 17414812.
- ^ Frederich R, Hu S, Raymond N, Pomeroy C (2002). "Leptin in anorexia nervosa and bulimia nervosa: importance of assay technique and method of interpretation". The Journal of Laboratory and Clinical Medicine 139 (2): 72–9. DOI:10.1067/mlc.2002.121014. PMID 11919545.
- ^ Lask B, Gordon I, Christie D, Frampton I, Chowdhury U, Watkins B (2005). "Functional neuroimaging in early-onset anorexia nervosa". The International Journal of Eating Disorders. 37 Suppl (S1): S49–51; discussion S87–9. DOI:10.1002/eat.20117. PMID 15852320.
- ^ Fetissov, S. O.; Harro, J; Jaanisk, M; Järv, A; Podar, I; Allik, J; Nilsson, I; Sakthivel, P 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. DOI:10.1073/pnas.0507204102. PMC 1253594. PMID 16195379. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1253594.
- ^ Swedo SE, Leckman JF, Rose NR (Feb 2012). "From Research Subgroup to Clinical Syndrome: Modifying the PANDAS Criteria to Describe PANS (Pediatric Acute-onset Neuropsychiatric Syndrome)". Pediatr Therapeut. 2 (2). DOI:10.4172/2161-0665.1000113. http://pandasnetwork.org/wp-content/uploads/2012/02/2161-0665-2-113.pdf.
- ^ Shay NF, Mangian HF (2000). "Neurobiology of zinc-influenced eating behavior". The Journal of Nutrition 130 (5S Suppl): 1493S–9S. PMID 10801965. http://jn.nutrition.org/cgi/pmidlookup?view=long&pmid=10801965.
- ^ Psychiatrists call for new ‘editorial code’ to end media promotion of a thin body ideal. Rcpsych.ac.uk (2010-02-23). Retrieved on 2012-02-04.
- ^ DiNicola, V. (1990). Anorexia Multiforme: Self-Starvation in Historical and Cultural Context.Part II: Anorexia Nervosa as a Culture-Reactive Syndrome . Transcultural Psychiatric Research Review, 27(4), 245-286. Retrieved April 9, 2012, doi: 10.1177/136346159002700401
- ^ Lindberg L, Hjern A (2003). "Risk factors for anorexia nervosa: a national cohort study". The International Journal of Eating Disorders 34 (4): 397–408. DOI:10.1002/eat.10221. PMID 14566927.
- ^ Garner DM, Garfinkel PE (1980). "Socio-cultural factors in the development of anorexia nervosa". Psychological Medicine 10 (4): 647–56. DOI:10.1017/S0033291700054945. PMID 7208724.
- ^ Toro J, Salamero M, Martinez E (1994). "Assessment of sociocultural influences on the aesthetic body shape model in anorexia nervosa". Acta Psychiatrica Scandinavica 89 (3): 147–51. DOI:10.1111/j.1600-0447.1994.tb08084.x. PMID 8178671.
- ^ Schmidt U, Treasure J. Anorexia nervosa: valued and visible. A cognitive-interpersonal maintenance model and its implications for research and practice. Br J Clin Psychol 2006
- ^ Mukai, T; Crago, M; Shisslak, CM (1994). "Eating attitudes and weight preoccupation among female high school students in Japan". Journal of child psychology and psychiatry, and allied disciplines 35 (4): 677–88. PMID 8040220.
- ^ Levine et al. 1994, Shisslak et al. 1998, Stice 1998, Wertheim et al. 1997
- ^ Lozano, GA (2008). "Obesity and sexually selected anorexia nervosa". Medical Hypotheses 71 (6): 933–940. DOI:10.1016/j.mehy.2008.07.013. PMID 18760541.
- ^ Harrison, A.; Sullivan, S.; Tchanturia, K.; Treasure, J. (2009). "Emotion recognition and regulation in anorexia nervosa". Clinical Psychology & Psychotherapy 16 (4): 348–356. DOI:10.1002/cpp.628. PMID 19517577. edit
- ^ Zonnevijlle-Bender, M. J.; Van Goozen, S. H.; Cohen-Kettenis, P. T.; Van Elburg, A.; Van Engeland, H. (2002). "Do adolescent anorexia nervosa patients have deficits in emotional functioning?". European Child & Adolescent Psychiatry 11 (1): 38–42. DOI:10.1007/s007870200006. PMID 11942427. edit
- ^ a b c Rayworth, B. B.; Wise, L. A.; Harlow, B. L. (2004). "Childhood Abuse and Risk of Eating Disorders in Women". Epidemiology 15 (3): 271–278. JSTOR 20485891. PMID 15097006.
- ^ "Lessons for Parents of Anorexics" (2005) in BBC Health News, 22 October 2005 viewable at http://news.bbc.co.uk/1/hi/health/4363304.stm (Accessed 22 Aug, 2011)
- ^ a b c Zucker NL, Losh M, Bulik CM, LaBar KS, Piven J, Pelphrey KA (2007). "Anorexia nervosa and autism spectrum disorders: guided investigation of social cognitive endophenotypes". Psychological Bulletin 133 (6): 976–1006. DOI:10.1037/0033-2909.133.6.976. PMID 17967091. http://www.duke.edu/web/mind/level2/faculty/labar/pdfs/Zucker_et_al_2007.pdf.
- ^ Gillberg, C. (1983). "Are autism and anorexia nervosa related?". The British Journal of Psychiatry 142 (4): 428b. DOI:10.1192/bjp.142.4.428b.
- ^ Gillberg, C. (1985). "Autism and anorexia nervosa: Related conditions". Nordisk Psykiatrisk Tidskrift 39 (4): 307–312. DOI:10.3109/08039488509101911. http://informahealthcare.com/doi/abs/10.3109/08039488509101911.
- ^ Rothery, D.J.; D.M.F. Garden (1988-01-11). "Anorexia nervosa and infantile autism". The British journal of psychiatry : the journal of mental science 153 (5): 714. DOI:10.1192/bjp.153.5.714. PMID 3255470.
- ^ Gillberg, C.; M. Rastam (1992). "Do some cases of anorexia nervosa reflect underlying autistic-like conditions?". Behavioural neurology 5 (1): 27–32. http://psycnet.apa.org/?fa=main.doiLanding&uid=1993-02071-001.
- ^ Gillberg, I. Carina; Maria Råstam, Christopher Gillberg (1995-02). "Anorexia nervosa 6 years after onset: Part I. Personality disorders". Comprehensive Psychiatry 36 (1): 61–69. DOI:10.1016/0010-440X(95)90100-A. PMID 7705090.
- ^ Gillberg, I. Carina; Christopher Gillberg, Maria Råstam, Maria Johansson (1996-02). "The cognitive profile of anorexia nervosa: A comparative study including a community-based sample". Comprehensive Psychiatry 37 (1): 23–30. DOI:10.1016/S0010-440X(96)90046-2. PMID 8770522.
- ^ Råstam, M.; C. Gillberg, I. C. Gillberg (1996). "A six-year follow-up study of anorexia nervosa subjects with teenage onset". Journal of Youth and Adolescence 25 (4): 439–453. DOI:10.1007/BF01537541.
- ^ Nilsson, E. W; C. Gillberg, I. C Gillberg (1999-11). "Ten-year follow-up of adolescent-onset anorexia nervosa: personality disorders". Journal of the American Academy of Child and Adolescent Psychiatry 38 (11): 1389–95. DOI:10.1097/00004583-199911000-00013. PMID 10560225.
- ^ Wentz, Elisabet; Christopher Gillberg, I. Carina Gillberg, Maria Råstam (2001). "Ten-Year Follow-up of Adolescent-Onset Anorexia Nervosa: Psychiatric Disorders and Overall Functioning Scales". The Journal of Child Psychology and Psychiatry and Allied Disciplines 42 (5): 613–622. DOI:10.1017/S0021963001007284.
- ^ Råstam, Maria; Christopher Gillberg, Elisabet Wentz (2003-01-01). "Outcome of teenage-onset anorexia nervosa in a Swedish community-based sample". European Child & Adolescent Psychiatry 12 (1): I78–90. DOI:10.1007/s00787-003-1111-y. PMID 12567219.
- ^ Wentz, Elisabet; J. Lacey, Glenn Waller, Maria Råstam, Jeremy Turk, Christopher Gillberg (2005-12-01). "Childhood onset neuropsychiatric disorders in adult eating disorder patients". European Child & Adolescent Psychiatry 14 (8): 431–437. DOI:10.1007/s00787-005-0494-3. PMID 16341499.
- ^ Wentz, Elisabet; I. Carina Gillberg, Henrik Anckarsater, Christopher Gillberg, Maria Rastam (2009-02-01). "Adolescent-onset anorexia nervosa: 18-year outcome". The British Journal of Psychiatry 194 (2): 168–174. DOI:10.1192/bjp.bp.107.048686. PMID 19182181.
- ^ Fisman, S; M Steele, J Short, T Byrne, C Lavallee (1996-07). "Case study: anorexia nervosa and autistic disorder in an adolescent girl". Journal of the American Academy of Child and Adolescent Psychiatry 35 (7): 937–940. DOI:10.1097/00004583-199607000-00021. ISSN 0890-8567. PMID 8768355.
- ^ Kerbeshian, Jacob; Larry Burd (2008). "Is anorexia nervosa a neuropsychiatric developmental disorder? An illustrative case report". World Journal of Biological Psychiatry 10 (4 Pt 2): 648–57. DOI:10.1080/15622970802043117. ISSN 1562-2975. PMID 18609437.
- ^ Gillberg, I. C; M. Raastam, E. Wentz, C. Gillberg (2007). "Cognitive and executive functions in anorexia nervosa ten years after onset of eating disorder". Journal of Clinical and Experimental Neuropsychology 29 (2): 170–178. DOI:10.1080/13803390600584632. PMID 17365252.
- ^ Hambrook, D.; K. Tchanturia, U. Schmidt, T. Russell, J. Treasure (2008). "Empathy, systemizing, and autistic traits in anorexia nervosa: a pilot study". The British journal of clinical psychology/the British Psychological Society 47 (Pt 3): 335–9. DOI:10.1348/014466507X272475. PMID 18208640. http://openurl.ingenta.com/content?genre=article&issn=0144-6657&volume=47&issue=3&spage=335&epage=339.
- ^ Lopez, C.; K. Tchanturia, D. Stahl, R. Booth, J. Holliday, J. Treasure (2008). "An examination of the concept of central coherence in women with anorexia nervosa". International Journal of Eating Disorders 41 (2): 143–152. DOI:10.1002/eat.20478. PMID 17937420.
- ^ Russell, Tamara Anne; Ulrike Schmidt, Liz Doherty, Vicky Young, Kate Tchanturia (2009). "Aspects of social cognition in anorexia nervosa: Affective and cognitive theory of mind". Psychiatry Research 168 (3): 181–185. DOI:10.1016/j.psychres.2008.10.028. ISSN 01651781. PMID 19467562.
- ^ Zastrow, Arne; Kaiser; Kaiser, Christoph Stippich, Stephan Walther, Wolfgang Herzog, Kate Tchanturia, Aysenil Belger, Matthias Weisbrod, Janet Treasure, Hans-Christoph Friederich (2009-05-01). "Neural Correlates of Impaired Cognitive-Behavioral Flexibility in Anorexia Nervosa". Am J Psychiatry 166 (5): 608–616. DOI:10.1176/appi.ajp.2008.08050775. PMID 19223435.
- ^ Harrison, Amy; Sarah Sullivan, Kate Tchanturia, Janet Treasure (2009). "Emotion recognition and regulation in anorexia nervosa". Clinical Psychology & Psychotherapy 16 (4): 348–356. DOI:10.1002/cpp.628. PMID 19517577.
- ^ Whitney, Jenna; Abigail Easter, Kate Tchanturia (2008). "Service users' feedback on cognitive training in the treatment of anorexia nervosa: A qualitative study". International Journal of Eating Disorders 41 (6): 542–550. DOI:10.1002/eat.20536. PMID 18433016.
- ^ Hall RC, Popkin MK, Devaul RA, Faillace LA, Stickney SK (1978). "Physical illness presenting as psychiatric disease". Archives of General Psychiatry 35 (11): 1315–20. DOI:10.1001/archpsyc.1978.01770350041003. PMID 568461. http://archpsyc.ama-assn.org/cgi/pmidlookup?view=long&pmid=568461.
- ^ Hall RC, Gardner ER, Stickney SK, LeCann AF, Popkin MK (1980). "Physical illness manifesting as psychiatric disease. II. Analysis of a state hospital inpatient population". Archives of General Psychiatry 37 (9): 989–95. DOI:10.1001/archpsyc.1980.01780220027002. PMID 7416911.
- ^ CBC at Medline. Nlm.nih.gov. Retrieved on 2012-02-04.
- ^ Urinalysis at Medline. Nlm.nih.gov (2012-01-26). Retrieved on 2012-02-04.
- ^ Kawabata M, Kubo N, Arashima Y, Yoshida M, Kawano K (1991). "[Serodiagnosis of Lyme disease by ELISA using Borrelia burgdorferi flagellum antigen]" (in Japanese). Rinsho Byori 39 (8): 891–4. PMID 1920889.
- ^ Western Blot use in Lyme Disease. CDC
- ^ Chem-20 at Medline. Nlm.nih.gov. Retrieved on 2012-02-04.
- ^ Lee H, Oh JY, Sung YA, Chung H, Cho WY (2009). "The prevalence and risk factors for glucose intolerance in young Korean women with polycystic ovary syndrome". Endocrine 36 (2): 326–32. DOI:10.1007/s12020-009-9226-7. PMID 19688613.
- ^ Takeda, N; Yasuda, K; Horiya, T; Yamada, H; Imai, T; Kitada, M; Miura, K (1986). "[Clinical investigation on the mechanism of glucose intolerance in Cushing's syndrome]" (in Japanese). Nippon Naibunpi Gakkai Zasshi 62 (5): 631–48. PMID 3525245.
- ^ Rolny P, Lukes PJ, Gamklou R, Jagenburg R, Nilson A (1978). "A comparative evaluation of endoscopic retrograde pancreatography and secretin-CCK test in the diagnosis of pancreatic disease". Scandinavian Journal of Gastroenterology 13 (7): 777–81. DOI:10.3109/00365527809182190. PMID 725498.
- ^ Glasbrenner, B; Malfertheiner, P; Pieramico, O; Klatt, S; Riepl, R; Friess, H; Ditschuneit, H (1993). "Gallbladder dynamics in chronic pancreatitis. Relationship to exocrine pancreatic function, CCK, and PP release". Digestive Diseases and Sciences 38 (3): 482–9. PMID 8444080.
- ^ Montagnese C, Scalfi L, Signorini A, De Filippo E, Pasanisi F, Contaldo F (2007). "Cholinesterase and other serum liver enzymes in underweight outpatients with eating disorders". The International Journal of Eating Disorders 40 (8): 746–50. DOI:10.1002/eat.20432. PMID 17610252.
- ^ Narayanan V, Gaudiani JL, Harris RH, Mehler PS (2010). "Liver function test abnormalities in anorexia nervosa—cause or effect". The International Journal of Eating Disorders 43 (4): 378–81. DOI:10.1002/eat.20690. PMID 19424979.
- ^ Sherman BM, Halmi KA, Zamudio R (1975). "LH and FSH response to gonadotropin-releasing hormone in anorexia nervosa: Effect of nutritional rehabilitation". The Journal of Clinical Endocrinology and Metabolism 41 (1): 135–42. DOI:10.1210/jcem-41-1-135. PMID 1097461.
- ^ Salvadori A, Fanari P, Ruga S, Brunani A, Longhini E (1992). "Creatine kinase and creatine kinase-MB isoenzyme during and after exercise testing in normal and obese young people". Chest 102 (6): 1687–9. DOI:10.1378/chest.102.6.1687. PMID 1446472.
- ^ Walder A, Baumann P (2008). "Increased creatinine kinase and rhabdomyolysis in anorexia nervosa". The International Journal of Eating Disorders 41 (8): 766–7. DOI:10.1002/eat.20548. PMID 18521917.
- ^ BUN at Medline. Nlm.nih.gov (2012-01-26). Retrieved on 2012-02-04.
- ^ Ernst AA, Haynes ML, Nick TG, Weiss SJ (1999). "Usefulness of the blood urea nitrogen/creatinine ratio in gastrointestinal bleeding". The American Journal of Emergency Medicine 17 (1): 70–2. DOI:10.1016/S0735-6757(99)90021-9. PMID 9928705.
- ^ Sheridan AM, Bonventre JV (2000). "Cell biology and molecular mechanisms of injury in ischemic acute renal failure". Current Opinion in Nephrology and Hypertension 9 (4): 427–34. DOI:10.1097/00041552-200007000-00015. PMID 10926180.
- ^ Nelsen DA (2002). "Gluten-sensitive enteropathy (celiac disease): more common than you think". American Family Physician 66 (12): 2259–66. PMID 12507163. http://www.aafp.org/link_out?pmid=12507163.
- ^ Pascual, M; Pascual, DA; Soria, F; Vicente, T; Hernández, AM; Tébar, FJ; Valdés, M (2003). "Effects of isolated obesity on systolic and diastolic left ventricular function". Heart 89 (10): 1152–6. DOI:10.1136/heart.89.10.1152. PMC 1767886. PMID 12975404. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1767886.
- ^ Esposito C, Bellotti N, Fasoli G, Foschi A, Plati AR, Dal Canton A (2004). "Hyperkalemia-induced ECG abnormalities in patients with reduced renal function". Clinical Nephrology 62 (6): 465–8. PMID 15630907.
- ^ Electroencephalogram at Medline. Nlm.nih.gov (2012-01-26). Retrieved on 2012-02-04.
- ^ Kameda K, Itoh N, Nakayama H, Kato Y, Ihda S (1995). "Frontal intermittent rhythmic delta activity (FIRDA) in pituitary adenoma". Clinical EEG 26 (3): 173–9. PMID 7554305.
- ^ Mashako, Mamba Nyenya Léonard; Cezard, Jean Pierre; Navarro, Jean; Mougenot, Jean Francois; Sonsino, Elise; Gargouri, Abdellatif; Maherzi, Ahmed (1989). "Crohn's disease lesions in the upper gastrointestinal tract: correlation between clinical, radiological, endoscopic, and histological features in adolescents and children". Journal of Pediatric Gastroenterology and Nutrition 8 (4): 442–6. DOI:10.1097/00005176-198905000-00004. PMID 2723935.
- ^ Kumar MS, Safa AM, Deodhar SD, Schumacher OP (1977). "The relationship of thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3) in primary thyroid failure". American Journal of Clinical Pathology 68 (6): 747–51. PMID 579717.
- ^ Nilsson P, Melsen F, Malmaeus J, Danielson BG, Mosekilde L (1985). "Relationships between calcium and phosphorus homeostasis, parathyroid hormone levels, bone aluminum, and bone histomorphometry in patients on maintenance hemodialysis". Bone 6 (1): 21–7. DOI:10.1016/8756-3282(85)90402-8. PMID 2581596.
- ^ Barium Enema at Medline. Nlm.nih.gov (2012-01-26). Retrieved on 2012-02-04.
- ^ Schleimer, Kari (February 1981). "Anorexia Nervosa". Nutrition Reviews 39 (2): 99. http://journals1.scholarsportal.info.myaccess.library.utoronto.ca/tmp/14631477129826646045.pdf. Retrieved February.
- ^ Carlson, Neil (2010). Psychology: the Science of Behaviour. New Jersey, USA: Pearson Education. pp. 414–415. ISBN 978-0-205-64524-4.
- ^ 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. DOI:10.1176/appi.ajp.158.4.547. PMID 11282688.
- ^ American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th, text revision (DSM-IV-TR) ed. 2000. ISBN 0-89042-025-4. Anorexia Nervosa.
- ^ Gendall KA, Joyce PR, Carter FA, McIntosh VV, Jordan J, Bulik CM (2006). "The psychobiology and diagnostic significance of amenorrhea in patients with anorexia nervosa". Fertility and Sterility 85 (5): 1531–5. DOI:10.1016/j.fertnstert.2005.10.048. PMID 16600234.
- ^ Smith, A. T.; Wolfe, B. E. (2008). "Amenorrhea as a Diagnostic Criterion for Anorexia Nervosa: A Review of the Evidence and Implications for Practice". Journal of the American Psychiatric Nurses Association 14 (3): 209–15. DOI:10.1177/1078390308320288. PMID 21665766.
- ^ Eddy KT, Dorer DJ, Franko DL, Tahilani K, Thompson-Brenner H, Herzog DB (2008). "Diagnostic crossover in anorexia nervosa and bulimia nervosa: implications for DSM-V". The American Journal of Psychiatry 165 (2): 245–50. DOI:10.1176/appi.ajp.2007.07060951. PMID 18198267.
- ^ Marlene Busko Diagnostic Criteria for Eating Disorders May Be Too Stringent. Medscape.com (2007-05-30). Retrieved on 2012-02-04.
- ^ a b c Workgroup for Classification of Eating Disorders in Children and Adolescents. "Classifications of Eating Disturbance in Children and Adolescents: Proposed Changes for the DSM-V". European Eating Disorders Review, 2010,p.81
- ^ a b Knoll, S., Bulik, C., & Hebebrand, J. "Do the currently proposed DSM-5 criteria for anorexia nervosa adequately consider developmental aspects in children and adolescents?". Early Adolescent Psychiatry, 2011,p.96
- ^ Journal of Adolescent Health. "Eating Disorders in Adolescents: Position Paper of the Society for Adolescent Medicine". 2003,33,p.496
- ^ Marshall JB, Russell JL (1993). "Achalasia mistakenly diagnosed as eating disorder and prompting prolonged psychiatric hospitalization". Southern Medical Journal 86 (12): 1405–7. DOI:10.1097/00007611-199312000-00019. PMID 8272922.
- ^ Rosenvinge JH, Martinussen M, Ostensen E (2000). "The comorbidity of eating disorders and personality disorders: a meta-analytic review of studies published between 1983 and 1998". Eating and Weight Disorders 5 (2): 52–61. PMID 10941603.
- ^ Kaye WH, Bulik CM, Thornton L, Barbarich N, Masters K (2004). "Comorbidity of anxiety disorders with anorexia and bulimia nervosa". The American Journal of Psychiatry 161 (12): 2215–21. DOI:10.1176/appi.ajp.161.12.2215. PMID 15569892.
- ^ Thornton C, Russell J (1997). "Obsessive compulsive comorbidity in the dieting disorders". The International Journal of Eating Disorders 21 (1): 83–7. DOI:10.1002/(SICI)1098-108X(199701)21:1<83::AID-EAT10>3.0.CO;2-P. PMID 8986521.
- ^ Vitousek K, Manke F (1994). "Personality variables and disorders in anorexia nervosa and bulimia nervosa". Journal of Abnormal Psychology 103 (1): 137–47. DOI:10.1037/0021-843X.103.1.137. PMID 8040475.
- ^ Braun DL, Sunday SR, Halmi KA (1994). "Psychiatric comorbidity in patients with eating disorders". Psychological Medicine 24 (4): 859–67. DOI:10.1017/S0033291700028956. PMID 7892354.
- ^ Spindler A, Milos G (2007). "Links between eating disorder symptom severity and psychiatric comorbidity". Eating Behaviors 8 (3): 364–73. DOI:10.1016/j.eatbeh.2006.11.012. PMID 17606234.
- ^ Casper RC (1998). "Depression and eating disorders". Depression and Anxiety 8 (Suppl 1): 96–104. DOI:10.1002/(SICI)1520-6394(1998)8:1+<96::AID-DA15>3.0.CO;2-4. PMID 9809221.
- ^ Serpell L, Livingstone A, Neiderman M, Lask B (2002). "Anorexia nervosa: obsessive-compulsive disorder, obsessive-compulsive personality disorder, or neither?". Clinical Psychology Review 22 (5): 647–69. DOI:10.1016/S0272-7358(01)00112-X. PMID 12113200.
- ^ Bulik, Cynthia M.; Klump, Kelly L.; Thornton, Laura; Kaplan, Allan S.; Devlin, Bernie; Fichter, Manfred M.; Halmi, Katherine A.; Strober, Michael et al. (2004). "Alcohol use disorder comorbidity in eating disorders: a multicenter study". The Journal of Clinical Psychiatry 65 (7): 1000–6. DOI:10.4088/JCP.v65n0718. PMID 15291691.
- ^ Larsson JO, Hellzén M (2004). "Patterns of personality disorders in women with chronic eating disorders". Eating and Weight Disorders 9 (3): 200–5. PMID 15656014.
- ^ Swinbourne JM, Touyz SW (2007). "The co-morbidity of eating disorders and anxiety disorders: a review". European Eating Disorders Review : the Journal of the Eating Disorders Association 15 (4): 253–74. DOI:10.1002/erv.784. PMID 17676696.
- ^ Ronningstam E (1996). "Pathological narcissism and narcissistic personality disorder in Axis I disorders". Harvard Review of Psychiatry 3 (6): 326–40. DOI:10.3109/10673229609017201. PMID 9384963.
- ^ Anderluh MB, Tchanturia K, Rabe-Hesketh S, Treasure J (2003). "Childhood obsessive-compulsive personality traits in adult women with eating disorders: defining a broader eating disorder phenotype". The American Journal of Psychiatry 160 (2): 242–7. DOI:10.1176/appi.ajp.160.2.242. PMID 12562569.
- ^ Pinto A, Mancebo MC, Eisen JL, Pagano ME, Rasmussen SA (2006). "The Brown Longitudinal Obsessive Compulsive Study: clinical features and symptoms of the sample at intake". The Journal of Clinical Psychiatry 67 (5): 703–11. DOI:10.4088/JCP.v67n0503. PMID 16841619.
- ^ Lucka I, Cebella A (2004). "[Characteristics of the forming personality in children suffering from anorexia nervosa]" (in Polish). Psychiatria Polska 38 (6): 1011–8. PMID 15779665.
- ^ Dukarm CP (2005). "Bulimia nervosa and attention deficit hyperactivity disorder: a possible role for stimulant medication". Journal of Women's Health 14 (4): 345–50. DOI:10.1089/jwh.2005.14.345. PMID 15916509.
- ^ Mikami, Amori Yee; Hinshaw, Stephen P.; Arnold, L. Eugene; Hoza, Betsy; Hechtman, Lily; Newcorn, Jeffrey H.; Abikoff, Howard B. (2010). "Bulimia nervosa symptoms in the multimodal treatment study of children with ADHD". The International Journal of Eating Disorders 43 (3): 248–59. DOI:10.1002/eat.20692. PMID 19378318.
- ^ Biederman J, Ball SW, Monuteaux MC, Surman CB, Johnson JL, Zeitlin S (2007). "Are girls with ADHD at risk for eating disorders? Results from a controlled, five-year prospective study". Journal of Developmental and Behavioral Pediatrics 28 (4): 302–7. DOI:10.1097/DBP.0b013e3180327917. PMID 17700082.
- ^ Cortese S, Bernardina BD, Mouren MC (2007). "Attention-deficit/hyperactivity disorder (ADHD) and binge eating". Nutrition Reviews 65 (9): 404–11. DOI:10.1111/j.1753-4887.2007.tb00318.x. PMID 17958207.
- ^ 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. DOI:10.1017/S003329170300864X. PMID 14971632.
- ^ Grant JE, Kim SW, Eckert ED (2002). "Body dysmorphic disorder in patients with anorexia nervosa: Prevalence, clinical features, and delusionality of body image". International Journal of Eating Disorders 32 (3): 291–300. DOI:10.1002/eat.10091. PMID 12210643.
- ^ Gabbay V, Asnis GM, Bello JA, Alonso CM, Serras SJ, O'Dowd MA (2003). "New onset of body dysmorphic disorder following frontotemporal lesion". Neurology 61 (1): 123–5. PMID 12847173.
- ^ Phillips, KA; McElroy, SL; Keck Jr, PE; Hudson, JI; Pope Jr, HG (1994). "A comparison of delusional and nondelusional body dysmorphic disorder in 100 cases". Psychopharmacol Bull. 30 (2): 179–86. PMID 7831453.
- ^ a b Feusner JD, Townsend J, Bystritsky A, Bookheimer S (2007). "Visual Information Processing of Faces in Body Dysmorphic Disorder". Archives of General Psychiatry 64 (12): 1417–25. DOI:10.1001/archpsyc.64.12.1417. PMID 18056550.
- ^ Feusner JD, Yaryura-Tobias J, Saxena S (2008). "The pathophysiology of body dysmorphic disorder". Body Image 5 (1): 3–12. DOI:10.1016/j.bodyim.2007.11.002. PMID 18314401.
- ^ National Institute of Mental Health. http://www.nimh.nih.gov/health/publications/eating-disorders/anorexia-nervosa.shtml.
- ^ Attia E, Walsh BT. "Anorexia nervosa". The American Journal of Psychiatry 164 (12). http://bf4dv7zn3u.search.serialssolutions.com.myaccess.library.utoronto.ca/?ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info:sid/summon.serialssolutions.com&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Anorexia+Nervosa&rft.jtitle=The+American+journal+of+psychiatry&rft.au=Attia%2C+Evelyn&rft.au=Walsh%2C+B+Timothy&rft.date=2007-12-01&rft.pub=AMER+PSYCHIATRIC+PUBLISHING%2C+INC&rft.issn=0002-953X&rft.volume=164&rft.issue=12&rft.spage=1805&rft.epage=1810&rft_id=info:doi/10.1176%2Fappi.ajp.2007.07071151&rft.externalDBID=GPSI&rft.externalDocID=18056234.
- ^ Carlson N. & Heth C., "Psychology: The Science of Behaviour" p.297, Retrieved April 8, 2012.
- ^ Safai-Kutti S (1990). "Oral zinc supplementation in anorexia nervosa". Acta Psychiatrica Scandinavica. Supplementum 361: 14–7. PMID 2291418.
- ^ Su JC, Birmingham CL (2002). "Zinc supplementation in the treatment of anorexia nervosa". Eating and Weight Disorders 7 (1): 20–2. PMID 11930982.
- ^ Birmingham CL, Gritzner S (2006). "How does zinc supplementation benefit anorexia nervosa?". Eating and Weight Disorders 11 (4): e109–11. PMID 17272939. http://www.kurtis.it/abs/index.cfm?id_articolo_numero=3347.
- ^ Ayton AK, Azaz A, Horrobin DF (2004). "Rapid improvement of severe anorexia nervosa during treatment with ethyl-eicosapentaenoate and micronutrients". European Psychiatry 19 (5): 317–9. DOI:10.1016/j.eurpsy.2004.06.002. PMID 15276668.
- ^ Lucas M, Asselin G, Mérette C, Poulin MJ, Dodin S (2009). "Ethyl-eicosapentaenoic acid for the treatment of psychological distress and depressive symptoms in middle-aged women: a double-blind, placebo-controlled, randomized clinical trial". The American Journal of Clinical Nutrition 89 (2): 641–51. DOI:10.3945/ajcn.2008.26749. PMID 19116322.
- ^ McNamara, R. K; Able, J.; Jandacek, R.; Rider, T.; Tso, P.; Eliassen, J. C; Alfieri, D.; Weber, W. et al. (2010). "Docosahexaenoic acid supplementation increases prefrontal cortex activation during sustained attention in healthy boys: a placebo-controlled, dose-ranging, functional magnetic resonance imaging study". The American Journal of Clinical Nutrition 91 (4): 1060–7. DOI:10.3945/ajcn.2009.28549. PMC 2844685. PMID 20130094. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2844685.
- ^ Kidd PM (2007). "Omega-3 DHA and EPA for cognition, behavior, and mood: clinical findings and structural-functional synergies with cell membrane phospholipids". Alternative Medicine Review 12 (3): 207–27. PMID 18072818. http://www.thorne.com/altmedrev/.fulltext/12/3/207.pdf.
- ^ Latner JD, Wilson GT (2000). "Cognitive-behavioral therapy and nutritional counseling in the treatment of bulimia nervosa and binge eating". Eating Behaviors 1 (1): 3–21. DOI:10.1016/S1471-0153(00)00008-8. PMID 15001063.
- ^ Breen HB, Espelage DL (2004). "Nutrition expertise in eating disorders". Eating and Weight Disorders 9 (2): 120–5. PMID 15330079.
- ^ Perelygina L, Patrusheva I, Manes N, Wildes MJ, Krug P, Hilliard JK (2003). "Quantitative real-time PCR for detection of monkey B virus (Cercopithecine herpesvirus 1) in clinical samples". Journal of Virological Methods 109 (2): 245–51. DOI:10.1016/S0166-0934(03)00078-8. PMID 12711069.
- ^ Whisenant SL, Smith BA (1995). "Eating disorders: current nutrition therapy and perceived needs in dietetics education and research". Journal of the American Dietetic Association 95 (10): 1109–12. DOI:10.1016/S0002-8223(95)00301-0. PMID 7560681.
- ^ American Dietetic, Association (2006). "Position of the American Dietetic Association: Nutrition intervention in the treatment of anorexia nervosa, bulimia nervosa, and other eating disorders". Journal of the American Dietetic Association 106 (12): 2073–82. DOI:10.1016/j.jada.2006.09.007. PMID 17186637.
- ^ Brambilla, Francesca; Garcia, Cristina Segura; Fassino, Secondo; Daga, Giovanni Abbate; Favaro, Angela; Santonastaso, Paolo; Ramaciotti, Carla; Bondi, Emilia et al. (2007). "Olanzapine therapy in anorexia nervosa: psychobiological effects". International Clinical Psychopharmacology 22 (4): 197–204. DOI:10.1097/YIC.0b013e328080ca31. PMID 17519642.
- ^ Bissada H, Tasca GA, Barber AM, Bradwejn J (2008). "Olanzapine in the treatment of low body weight and obsessive thinking in women with anorexia nervosa: a randomized, double-blind, placebo-controlled trial". The American Journal of Psychiatry 165 (10): 1281–8. DOI:10.1176/appi.ajp.2008.07121900. PMID 18558642.
- ^ Pike KM, Walsh BT, Vitousek K, Wilson GT, Bauer J (2003). "Cognitive behavior therapy in the posthospitalization treatment of anorexia nervosa". The American Journal of Psychiatry 160 (11): 2046–9. DOI:10.1176/appi.ajp.160.11.2046. PMID 14594754.
- ^ Bowers WA, Ansher LS (2008). "The effectiveness of cognitive behavioral therapy on changing eating disorder symptoms and psychopathology of 32 anorexia nervosa patients at hospital discharge and one year follow-up". Annals of Clinical Psychiatry 20 (2): 79–86. DOI:10.1080/10401230802017068. PMID 18568579.
- ^ Ball J, Mitchell P (2004). "A randomized controlled study of cognitive behavior therapy and behavioral family therapy for anorexia nervosa patients". Eating Disorders 12 (4): 303–14. DOI:10.1080/10640260490521389. PMID 16864523.
- ^ a b c d e Robin, M., Gilroy, M., & Dennis, A. "Treatment of Eating Disorders in Children and Adolescents" Clinical Psychology Review, 1998, p.430
- ^ Berman MI, Boutelle KN, Crow SJ (2009). "A case series investigating acceptance and commitment therapy as a treatment for previously treated, unremitted patients with anorexia nervosa". European Eating Disorders Review 17 (6): 426–34. DOI:10.1002/erv.962. PMID 19760625.
- ^ a b Tchanturia K, Davies H, Campbell IC (2007). "Cognitive remediation therapy for patients with anorexia nervosa: preliminary findings". Annals of General Psychiatry 6 (1): 14. DOI:10.1186/1744-859X-6-14. PMC 1892017. PMID 17550611. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1892017.
- ^ NIMH · Eating Disorders. Nimh.nih.gov (2011-08-23). Retrieved on 2012-02-04.
- ^ Studies – Eating Disorders Program – Stanford University School of Medicine. Edresearch.stanford.edu (2008-06-20). Retrieved on 2012-02-04.
- ^ "Association for Behavioral and Cognitive Therapies – What is Family Therapy?". http://www.abct.org/sccap/?m=sPublic&fa=pub_WhatIsFT.
- ^ a b Eisler I, Dare C, Hodes M, Russell G, Dodge E, Le Grange D (2000). "Family therapy for adolescent anorexia nervosa: the results of a controlled comparison of two family interventions". Journal of Child Psychology and Psychiatry, and Allied Disciplines 41 (6): 727–36. DOI:10.1111/1469-7610.00660. PMID 11039685.
- ^ Lock J, le Grange D (2005). "Family-based treatment of eating disorders". The International Journal of Eating Disorders. 37 Suppl (S1): S64–7; discussion S87–9. DOI:10.1002/eat.20122. PMID 15852323.
- ^ Gore, S., Vander Wal, J., & Thelen, M. "Treatment of Eating Disorders in Children and Adolescents" p.297
- ^ a b c d e f Robin, M., Gilroy, M., & Dennis, A. "Treatment of Eating Disorders in Children and Adolescents" Clinical Psychology Review, 1998, p.434
- ^ le Grange D, Eisler I (2009). "Family interventions in adolescent anorexia nervosa". Child and Adolescent Psychiatric Clinics of North America 18 (1): 159–73. DOI:10.1016/j.chc.2008.07.004. PMID 19014864.
- ^ Carei TR, Fyfe-Johnson AL, Breuner CC, Brown MA (2010). "Randomized Controlled Clinical Trial of Yoga in the Treatment of Eating Disorders". The Journal of Adolescent Health 46 (4): 346–51. DOI:10.1016/j.jadohealth.2009.08.007. PMC 2844876. PMID 20307823. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2844876.
- ^ Hudson JI, Hiripi E, Pope HG, Kessler RC (2007). "The Prevalence and Correlates of Eating Disorders in the National Comorbidity Survey Replication". Biological Psychiatry 61 (3): 348–58. DOI:10.1016/j.biopsych.2006.03.040. PMC 1892232. PMID 16815322. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1892232.
- ^ Eisler I, Le Grange D, Asen KE (2003). "Family interventions". In Treasure J, Schmidt U, van Furth E. Handbook of eating disorders (2nd ed.). Chichester: Wiley. pp. 291–310.
- ^ Strober M, Freeman R, Morrell W (1997). "The long-term course of severe anorexia nervosa in adolescents: survival analysis of recovery, relapse, and outcome predictors over 10–15 years in a prospective study". The International Journal of Eating Disorders 22 (4): 339–60. DOI:10.1002/(SICI)1098-108X(199712)22:4<339::AID-EAT1>3.0.CO;2-N. PMID 9356884.
- ^ Treasure J, Claudino AM, Zucker N (2010). "Eating disorders". Lancet 375 (9714): 583–93. DOI:10.1016/S0140-6736(09)61748-7. PMID 19931176.
- ^ Gowers S, Bryant-Waugh R (2004). "Management of child and adolescent eating disorders: the current evidence base and future directions". Journal of Child Psychology and Psychiatry, and Allied Disciplines 45 (1): 63–83. DOI:10.1046/j.0021-9630.2003.00309.x. PMID 14959803.
- ^ Attia, Evelyn , and Timothy Walsh. "Anorexia Nervosa Evelyn Attia; B. Timothy Walsh." The American Journal of Psychiatry 164 (2007): 1805-1810.Print.
- ^ a b Richard Morton: Origins of Anorexia nervosa. Content.karger.com. Retrieved on 2012-02-04.
- ^ a b Hepworth, Julie. 1999. The Social Construction of Anorexia Nervosa. Thousand Oaks, CA: Sage Publications ISBN 0-7619-5309-4
- ^ McSherry, JA (1985). "Was Mary, Queen of Scots, anorexic?". Scottish medical journal 30 (4): 243–5. PMID 3912990.
- ^ Cannabinoid Receptor (CB1) Agonist Treatment in Severe Chronic Anorexia Nervosa. clinicaltrials.gov. September 25, 2008
- ^ Hotta M, Ohwada R, Akamizu T, Shibasaki T, Takano K, Kangawa K (2009). "Ghrelin increases hunger and food intake in patients with restricting-type anorexia nervosa: a pilot study". Endocrine Journal 56 (9): 1119–28. DOI:10.1507/endocrj.K09E-168. PMID 19755753.
- Anorexia Nervosa and Related Eating Disorders in Childhood and Adolescence By Bryan Lask, Rachel Bryant-Waugh Publisher: Psychology Press; 2 edition (October 12, 2000) ISBN 0-86377-804-6 ISBN 978-0863778049
- Help Your Teenager Beat an Eating Disorder. James Lock MD PhD, Daniel le Grange PhD. Publisher: The Guilford Press; 1 edition (January 1, 2005) Language: English ISBN 1-57230-908-3 ISBN 978-1572309081
- Too Fat or Too Thin?: A Reference Guide to Eating Disorders; Cynthia R. Kalodner. Publisher: Greenwood Press; 1 edition (August 30, 2003) Language: English ISBN 0-313-31581-7 ISBN 978-0313315817
- Wasted: A Memoir of Anorexia and Bulimia Marya Hornbacher. Publisher: Harper Perennial; 1 edition (January 15, 1999) Language: English ISBN 0-06-093093-4 ISBN 978-0060930936
- Cardboard: A woman left for dead. 1st ed Local Consumption Publications (1989). Winner of the National Book Council's Award for New Writers. 2nd ed January 2010 ISBN 978-1-4505-0202-3
- Eating with Your Anorexic: How My Child Recovered Through Family-based Treatment and Yours Can Too by Laura Collins Publisher: McGraw-Hill; 1 edition (December 15, 2004) Language: English ISBN 0-07-144558-7 ISBN 978-0071445580
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