|Classification and external resources|
File:Gull - Anorexia Miss A.jpg|
"Miss A" - pictured in 1866 and in 1870 after treatment. She was one of the earliest Anorexia nervosa case studies. From the published medical papers of Sir William Gull.
Anorexia nervosa is an eating disorder characterized by refusal to maintain a healthy body weight and an obsessive fear of gaining weight, often coupled with a distorted self image which may be maintained by various cognitive biases that alter how the affected individual evaluates and thinks about her or his body, food and eating. Persons with anorexia nervosa continue to feel hunger, but deny themselves all but very small quantities of food. The average calorific intake of a person with anorexia nervosa is 600-800 calories per day, but in extreme cases self-starvation is more extreme. It is a serious mental illness with a high incidence of comorbidity and the highest mortality rate of any psychiatric disorder.
The term anorexia nervosa was established in 1873 by Sir William Gull, one of Queen Victoria's personal physicians. The term is of Greek origin: a (α, prefix of negation), n (ν, link between two vowels) and orexis (ορεξις, appetite), thus meaning a lack of desire to eat.
Signs and symptomsEdit
A person with anorexia nervosa may exhibit a number of signs and symptoms, some of which are listed below. The type and severity 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.
It should be noted that some of the possible signs listed below (Russell's sign, scarring of knuckles, purging/self-induced vomiting and use/abuse of laxatives, diet pills, i.e., and swollen cheeks/enlargement of the salivary glands) are signs primarily of bulimia, which is a condition that often occurs simultaneously with anorexia.
Possible signs of anorexia nervosa
Dermatologic signs of anorexia nervosa
|seborrheic dermatitis||acrocyanosis||perniosis||petechiae||livedo reticularis|
|interdigital intertrigo||paronychia||generalized pruritus||acquired striae distensae||angular stomatitis|
|prurigo pigmentosa||edema||linear erythema craquele||acrodermatitis enteropathica||pellagra|
Possible medical complications of anorexia nervosa
|constipation||diarrhea||electrolyte imbalance||cavities||tooth loss|
|hyponatremia||hypokalemia||optic neuropathy||brain atrophy||leukopenia|
Studies have hypothesized that the continuance of disordered eating patterns may be epiphenomena of starvation. The results of the Minnesota Starvation Experiment showed that normal controls exhibit many of the behavioral patterns of anorexia nervosa when subjected to starvation. This may be due to the numerous changes in the neuroendocrine system, which results in a self perpetuating cycle. Studies have suggested that the initial weight loss such as dieting may be the triggering factor in developing AN in some cases, possibly due to an already inherent predisposition toward AN. One study reports 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.
- 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.
- Genetics: anorexia nervosa is believed to be highly heritable, with estimated inheritance rates ranging from 56% to 84%. Association studies have been performed, studying 128 different polymorphisms related to 43 genes including genes involved in regulation of eating behavior, motivation and reward mechanics, personality traits and emotion. Consistent associations have been identified for polymorphisms associated with agouti related peptide, brain derived neurotrophic factor, catechol-o-methyl transferase, SK3 and opioid receptor delta-1. In one study, variations in the norepinephrine transporter gene promoter were associated with restrictive anorexia nervosa, but not binge-purge anorexia. 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. 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.
- 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 due to epigenetic mechanisms, has been implicated in various eating disorders."We conclude that epigenetic mechanisms may contribute to the known alterations of ANP homeostasis in women with eating disorders."
- serotonin dysregulation; 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.
- Brain-derived neurotrophic factor (BDNF) is a protein that regulates neuronal development and neuroplasticity, it also plays a role in learning, memory and in the hypothalamic pathway that controls eating behavior and energy homeostasis. BDNF amplifies neurotransmitter responses and promotes synaptic communication in the enteric nervous system. Low levels of BDNF are found in patients with AN and some comorbid disorders such as major depression. Exercise increases levels of BDNF
- leptin and ghrelin; leptin is a hormone produced primarily by the fat cells in white adipose tissue of the body it has an inhibitory (anorexigenic) effect on appetite, by inducing a feeling of saiety. 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.
- cerebral blood flow (CBF); neuroimaging studies have shown reduced CBF in the temporal lobes of anorectic patients, which may be a predisposing factor in the onset of AN.
- autoimmune system; Autoantibodies against neuropeptides such as melanocortin have been shown to affect personality traits associated with eating disorders such as those that influence appetite and stress responses.
- 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.
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. 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. People in professions where there is a particular social pressure to be thin (such as models and dancers) were much more likely to develop anorexia during the course of their career, and further research has suggested that those with anorexia have much higher contact with cultural sources that promote weight-loss.
There is also evidence to suggest that patients who have anorexia nervosa can be characterised by Alexithymia and also a deficit in certain emotional functions. A research study showed that this was the case in both adult and adolescent anorexia nervosa patients.
There is a high rate of reported child sexual abuse experiences in clinical groups of who have been diagnosed with anorexia. Although prior sexual abuse is not thought to be a specific risk factor for anorexia, those who have experienced such abuse are more likely to have more serious and chronic symptoms.
Relationship to autismEdit
Since Gillberg's (1985) and others initial suggestion of relationship between anorexia nervosa and autism, a large scale longitudinal study into teenage onset anorexia nervosa conducted in Sweden confirmed that 23% of people with a long-standing eating disorder are on the autism spectrum. Those on autism spectrum tend to have a worse outcome, but may benefit from the combined use of behavioural and pharmacological therapies tailored to ameliorate autism rather than anorexia nervosa per se. Other studies, most notably research conducted at the Maudsley Hospital UK, furthermore suggest that autistic traits are common in people with anorexia nervosa, shared traits include e.g. executive function, autism quotient score, central coherence, theory of mind, cognitive-behavioural flexibility, emotion regulation and understanding facial expressions.
Zucker et al. (2007) proposed that conditions on the autism spectrum make up the cognitive endophenotype underlying anorexia nervosa and appealed for increased interdisciplinary collaboration (see figure to right). A pilot study into the effectiveness 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.
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.
- There are a variety of tests that may aid in the diagnosis of AN and the assessment of possible secondary effects caused by AN upon the patient.
|Medical Tests used in the Diagnosis and Assessment of Anorexia Nervosa|
- 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.
- "we therefore recommend performing a cranial MRI in all patients with suspected eating disorders"(Trummer M et al.2002)","intracranial pathology should also be considered however certain is the diagnosis of early-onset anorexia nervosa. Second, neuroimaging plays an important part in diagnosing early-onset anorexia nervosa,..".(O'Brien et al.2001).
Anorexia nervosa is classified as an Axis I disorder in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM-IV). Published by The American Psychiatric Association. The DSM-IV should not be used by laypersons to diagnose themselves.
- DSM-IV-TR: diagnostic criteria for AN includes intense fear of gaining weight, a refusal to maintain body weight above 85% of the expected weight for a given age and height, and three consecutive missed periods and either refusal to admit the seriousness of the weight loss, or undue influence of shape or weight on one's self image, or a disturbed experience in one's shape or weight. There are two types: the binge-eating/purging type is characterized by overeating or purging, and the restricting type is not.
- Criticism of DSM-IV There 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. Those who do not meet these criteria are usually classified as eating disorder not otherwise specified this may affect treatment options and insurance reimbursments. The validity of the AN subtype classification has also been questioned due to 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.
- 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".
Differential diagnosesEditThere are various medical and psychological conditions that have been misdiagnosed as anorexia nervosa, in some cases the correct diagnosis was not made for more than ten years. In a reported case of achalasia misdiagnosed as AN, the patient spent two months confined to a psychiatric hospital.
There are various other psychological issues that may factor into anorexia nervosa, some fulfill the criteria for a separate Axis I diagnosis or a personality disorder which is coded Axis II and thus are considered comorbid to the diagnosed eating disorder. Axis II disorders are subtyped into 3 "clusters", A, B and C.The causality between personality disorders and eating disorders has yet to be fully established. Some people have a previous disorder which may increase their vulnerability to developing an eating disorder. Some develop them afterwards. The severity and type of eating disorder symptoms have been shown to affect comorbidity.
- Body dysmorphic disorder (BDD) is listed as a somatoform disorder that affects up to 2% of the population. BDD is characterized by excessive rumination over an actual or perceived physical flaw. BDD has been diagnosed equally among men and women. While BDD has been misdiagnosed as anorexia nervosa, it also occurs comorbidly in 25% to 39% of AN cases.
BDD is a chronic and debilitating condition which may lead to social isolation, major depression, suicidal ideation and attempts. Neuroimaging studies to measure response to facial recognition have shown activity predominately in the left hemisphere in the left lateral prefrontal cortex, lateral temporal lobe and left parietal lobe showing hemispheric imbalance in information processing. There is a reported case of the development of BDD in a 21 year old male following an inflammatory brain process. Neuroimaging showed the presence of new atrophy in the frontotemporal region.
The distinction between the diagnoses of anorexia nervosa, bulimia nervosa and eating disorder not otherwise specified (EDNOS) is often difficult to make as there is considerable overlap between patients diagnosed with these conditions. Seemingly minor changes in a patient's overall behavior or attitude can change a diagnosis from "anorexia: binge-eating type" to bulimia nervosa. It is not unusual for a person with an eating disorder to "move through" various diagnoses as his or her behavior and beliefs change over time.
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.
- Diet and Nutrition
- Essential fatty acids:The omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) have been shown to benefit various neuropsychiatric disorders. There was reported rapid improvement in a case of severe AN treated with ethyl-eicosapentaenoic acid (E-EPA) and micronutrients. DHA and EPA supplementation has been shown to be a benefit in many of the comorbid disorders of AN including: attention deficit/hyperactivity disorder (ADHD), autism, major depressive disorder (MDD), bipolar disorder, and borderline personality disorder. Accelerated cognitive decline and mild cognitive impairment (MCI) correlate with lowered tissue levels of DHA/EPA, and supplementation has improved cognitive function.
- Nutrition counseling
- Psychotherapy/Cognitive remediation
- Cognitive behavioral therapy (CBT) – "The term 'cognitive-behavioral therapy (CBT); is a very general term for a classification of therapies with similarities. There are several approaches to cognitive-behavioral therapy". CBT is an evidence based approach which in studies to date has shown to be useful in adolescents and adults with anorexia nervosa.
| Cognitive Behavioral Therapies
|Rational Emotive Behavior Therapy||Dialectical behavior therapy||Rational Living Therapy||Rational Behavior Therapy||Cognitive Therapy|
- Cognitive Remediation Therapy (CRT): is a cognitive rehabilitation therapy developed at King's College in London designed to improve neurocognitive abilities such as attention, working memory, cognitive flexibility and planning, and executive functioning which leads to improved social functioning. Neuropsychological studies have shown that patients with AN have difficulties in cognitive flexibility. In studies conducted at Kings College and in Poland with adolescents CRT was proven to be beneficial in treating anorexia nervosa, in the United States clinical trials are still being conducted by the National Institute of Mental Health on adolescents age 10-17 and Stanford University in subjects over 16 as a conjunctive therapy with Cognitive behavioral therapy.
- Family therapy: various forms of family therapy 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... ".
- Maudsley Family Therapy: A 4 to 5 year follow up study of the Maudsley approach, shows full recovery at rates up to 90%.
- Adjunctive/Alternate Therapies
- 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.
- Acupuncture/Tui na: According to a study in China positive results were obtained in treating AN with a combination treatment utilizing acupuncture and Tui na, a form of manipulation therapy.
- Marinol (dronabinol): a synthetic form of delta-9-THC a psychoactive compound extracted from the resin of the cannabis sativa plant is currently the subject of a clinical trial for use in the treatment of AN, the study is slated to end in 2011.
- Ghrelin treatment: pilot studies have been concluded in the use of ghrelin infusion for the inhospital treatment of patients with AN. The results showed positive effect in the reduction of the associated gastrointestinal symptoms, an increase in appetite and energy intake without adverse effects.
The long term prognosis of anorexia is more on 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..."
In cases of adolescent anorexia nervosa that utilize Family treatment 75% of patients have a good outcome and an additional 15% show an intermediate yet more positive outcome. In a five year post treatment follow-up of Maudsley Family Therapy the full recovery rate was between 75% and 90%. Even in severe cases of AN, despite a noted 30% relapse rate after hospitalization, and a lengthy time to recovery ranging from 57–79 months, the full recovery rate was still 76%. There were minimal cases of relapse even at the long term follow-up conducted between 10–15 years. The long-term prognosis of anorexia nervosa is changeable: one-fifth of patients stay severely ill. one-fifth of patients recover fully and three-fifth's 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. The condition largely affects young adolescent women, with between 15 and 19 years old making up 40% of all cases. Approximately 90% of people with anorexia are female. 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).
The history of anorexia nervosa begins with early descriptions dating from the 16th and 17th centuries and the first recognition and description of anorexia nervosa as a disease in the late 19th century.
In the late 19th century, the public attention drawn to "fasting girls" provoked conflict between religion and science. Such cases as Sarah Jacob (the "Welsh Fasting Girl") and Mollie Fancher (the "Brooklyn Enigma") stimulated controversy as experts weighed the claims of complete abstinence from food. Believers referenced the duality of mind and body, while skeptics insisted on the laws of science and material facts of life. Critics accused the fasting girls of hysteria, superstition, and deceit. The progress of secularization and medicalization passed cultural authority from clergy to physicians, transforming anorexia nervosa from revered to reviled.
- Anti-fat bias
- Binge eating disorder
- Bulimia nervosa
- Cigarette smoking for weight loss
- Hungry: A Mother and Daughter Fight Anorexia (book)
- Karen Carpenter
- Depression (differential diagnoses)
- Marya Hornbacher
- National Association of Anorexia Nervosa and Associated Disorders
- Orthorexia nervosa
- ↑ Rosen JC, Reiter J, Orosan P (January 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 (June 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. doi:10.1016/j.cpr.2010.09.006.
- ↑ Frude, N. 1998. Understanding Abnormal Psychology. Oxford: Blackwell Publishing.
- ↑ Attia E (February 2010). "Anorexia Nervosa: Current Status and Future Directions". Annual Review of Medicine 61: 425–35. doi:10.1146/annurev.med.050208.200745. PMID 19719398.
- ↑ Hill R, Haslett C, Kumar S (April 2001). "Anorexia nervosa in an elderly woman". The Australian and New Zealand Journal of Psychiatry 35 (2): 246–8. doi:10.1046/j.1440-1614.2001.00871.x. PMID 11284909.
- ↑ Dally P (1984). "Anorexia tardive--late onset marital anorexia nervosa". Journal of Psychosomatic Research 28 (5): 423–8. doi:10.1016/0022-3999(84)90074-6. PMID 6512734.
- ↑ Striegel-Moore RH, Schreiber GB, Pike KM, Wilfley DE, Rodin J (July 1995). "Drive for thinness in black and white preadolescent girls". The International Journal of Eating Disorders 18 (1): 59–69. doi:10.1002/1098-108X(199507)18:1<59::AID-EAT2260180107>3.0.CO;2-6. PMID 7670444.
- ↑ Bennett J (September 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.
- ↑ Fassino S, Abbate-Daga G, Leombruni P, Amianto F, Rovera G, Rovera GG (November 2001). "Temperament and character in italian men with anorexia nervosa: a controlled study with the temperament and character inventory". The Journal of Nervous and Mental Disease 189 (11): 788–94. doi:10.1097/00005053-200111000-00009. PMID 11758663.
- ↑ Woodside et al Comparisons of Men With Full or Partial Eating Disorders, Men Without Eating Disorders, and Women With Eating Disorders in the Community. American journal of pyschiatry 2001 ;158 pp 570-574
- ↑ Gull WW (September 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 0585189226.
- ↑ Abell TL, Malagelada JR, Lucas AR, et al. (November 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 (February 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 (May 2001). "Update on endocrine disturbances in anorexia nervosa". Journal of Pediatric Endocrinology & Metabolism 14 (5): 459–80. PMID 11393567.
- ↑ Rustin MH, Foreman JC, Dowd PM (August 1990). "Anorexia nervosa associated with acromegaloid features, onset of acrocyanosis and Raynaud's phenomenon and worsening of chilblains". Journal of the Royal Society of Medicine 83 (8): 495–6. PMC 1292774. PMID 2231576.
- ↑ White KP, Rothe MJ, Milanese A, Grant-Kels JM (March 1994). "Perniosis in association with anorexia nervosa". Pediatric Dermatology 11 (1): 1–5. doi:10.1111/j.1525-1470.1994.tb00063.x. PMID 8170840.
- ↑ Strumìa R, Varotti E, Manzato E, Gualandi M (2001). "Skin signs in anorexia nervosa". Dermatology 203 (4): 314–7. doi:10.1159/000051779. PMID 11752819.
- ↑ Walsh JM, Wheat ME, Freund K (August 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.
- ↑ Pietrowsky R, Krug R, Fehm HL, Born J (September 2002). "Food deprivation fails to affect preoccupation with thoughts of food in anorectic patients". The British Journal of Clinical Psychology 41 (Pt 3): 321–6. doi:10.1348/014466502760379172. PMID 12396259.
- ↑ Kovacs D, Palmer RL (September 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 (May 1984). "Death from ipecac intoxication in a patient with anorexia nervosa". The American Journal of Psychiatry 141 (5): 702–3. PMID 6143508. http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=6143508.
- ↑ Peñas-Lledó E, Vaz Leal FJ, Waller G (May 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 (December 1992). "Eating disorders. A review and update". The Western Journal of Medicine 157 (6): 658–62. PMC 1022101. PMID 1475950.
- ↑ Lucka I (2004). "[Depression syndromes in patients suffering from anorexia nervosa]" (in Polish). Psychiatria Polska 38 (4): 621–9. PMID 15518310.
- ↑ Bozzato A, Burger P, Zenk J, Uter W, Iro H (September 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.
- ↑ Strumia R (2005). "Dermatologic signs in patients with eating disorders". American Journal of Clinical Dermatology 6 (3): 165–73. doi:10.2165/00128071-200506030-00003. PMID 15943493.
- ↑ Chiarioni G, Bassotti G, Monsignori A, et al. (October 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 (June 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 (June 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 (July 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 (June 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 (July 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 (October 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 (March 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 (February 2003). "Osteopenia and osteoporosis in anorexia nervosa". Adolescent Medicine 14 (1): 97–108. PMID 12529194.
- ↑ Bahia A, Chu ES, Mehler PS (February 2010). "Polydipsia and hyponatremia in a woman with anorexia nervosa". The International Journal of Eating Disorders: NA. doi:10.1002/eat.20792. PMID 20127934.
- ↑ Bonne OB, Bloch M, Berry EM (January 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.
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- ↑ Cannabinoid Receptor (CB1) Agonist Treatment in Severe Chronic Anorexia Nervosa...Sep 25, 2008 
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- 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 0863778046 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 1572309083 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 0313315817 ISBN 978-0313315817
- Wasted: A Memoir of Anorexia and Bulimia Marya Hornbacher. Publisher: Harper Perennial; 1 edition (January 15, 1999) Language: English ISBN 0060930934 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 9781450502023
- 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 0071445587 ISBN 978-0071445580
- National Eating Disorders Association
- Eating Disorders Glossary
- American Psychiatric Association Guidelines
- National Association of Anorexia Nervosa and Associated Disorders
- MayoClinic eating disorders information
- BBC Mental Health on eating disorders
- Anorexia nervosa NHS Direct
- Anorexia nervosa eMedicine
- Dying to Be Thin on PBS
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