Anorexia nervosa: Difference between revisions

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*[[weight loss]]: an obvious, rapid, dramatic weight loss
*[[weight loss]]: an obvious, rapid, dramatic weight loss
*[[Russell's sign]]<ref>{{cite journal |author=Strumìa R, Varotti E, Manzato E, Gualandi M |title=Skin signs in anorexia nervosa |journal=Dermatology |volume=203 |issue=4 |pages=314–7 |year=2001 |pmid=11752819 |doi=10.1159/000051779}}</ref> scarring of the [[knuckles]] from placing fingers down throat to induce vomiting.
*[[Russell's sign]]<ref>{{cite journal |author=Strumìa R, Varotti E, Manzato E, Gualandi M |title=Skin signs in anorexia nervosa |journal=Dermatology |volume=203 |issue=4 |pages=314–7 |year=2001 |pmid=11752819 |doi=10.1159/000051779}}</ref> scarring of the [[knuckles]] from placing fingers down throat to induce vomiting.
*[[lanugo]] soft fine hair grows on face and body <ref>Walsh JM ''et.al.'' The detection, evaluation and treatment of eating disorders the role of the primary care physician. J Gen Int Med.2000 Aug;15(8):577-90 PMID 10940151</ref>
*[[lanugo]] soft fine hair grows on face and body <ref>{{cite journal |author=Walsh JM, Wheat ME, Freund K |title=Detection, evaluation, and treatment of eating disorders the role of the primary care physician |journal=Journal of General Internal Medicine |volume=15 |issue=8 |pages=577–90 |year=2000 |month=August |pmid=10940151 |pmc=1495575}}</ref>
*[[fixation (psychology)|obsession]] with [[calories]], [[fat]] content
*[[fixation (psychology)|obsession]] with [[calories]], [[fat]] content
*preoccupation with [[food]], [[recipes]], [[cooking]], may cook elaborate dinners for others but not eat themselves<ref>Pietrowsky R. Food deprivation fails to affect preoccupation with thoughts of food in anorectic patients.Br J Clin Psychol. 2002 Sep;41(Pt 3):321-6.PMID 12396259</ref>
*preoccupation with [[food]], [[recipes]], [[cooking]], may cook elaborate dinners for others but not eat themselves<ref>{{cite journal |author=Pietrowsky R, Krug R, Fehm HL, Born J |title=Food deprivation fails to affect preoccupation with thoughts of food in anorectic patients |journal=The British Journal of Clinical Psychology |volume=41 |issue=Pt 3 |pages=321–6 |year=2002 |month=September |pmid=12396259}}</ref>
*[[dieting]] despite being thin or dangerously [[underweight]]
*[[dieting]] despite being thin or dangerously [[underweight]]
*[[fear]] of gaining weight or becoming overweight
*[[fear]] of gaining weight or becoming overweight
*rituals cuts food into tiny pieces, refuses to eat around others, hides or discards food
*rituals cuts food into tiny pieces, refuses to eat around others, hides or discards food
*purging uses: [[laxatives]], [[diet pills]], [[ipecac syrup]],[[water pills]] may engage in self induced [[vomiting]], may run to bathroom after eating, to vomit to quickly get rid of the [[calorie]]s<ref>Kovacs D, Palmer RL.The associations between laxative abuse and other symptoms among adults with anorexia nervosa. Int J Eat Disord. 2004 Sep;36(2):224-8.PMID 15282693</ref><ref>Friedman EJ. Death from ipecac intoxication in a patient with anorexia nervosa. Am J Psychiatry. 1984 May;141(5):702-3.PMID 6143508</ref>
*purging uses: [[laxatives]], [[diet pills]], [[ipecac syrup]],[[water pills]] may engage in self induced [[vomiting]], may run to bathroom after eating, to vomit to quickly get rid of the [[calorie]]s<ref>{{cite journal |author=Kovacs D, Palmer RL |title=The associations between laxative abuse and other symptoms among adults with anorexia nervosa |journal=The International Journal of Eating Disorders |volume=36 |issue=2 |pages=224–8 |year=2004 |month=September |pmid=15282693 |doi=10.1002/eat.20024}}</ref><ref>{{cite journal |author=Friedman EJ |title=Death from ipecac intoxication in a patient with anorexia nervosa |journal=The American Journal of Psychiatry |volume=141 |issue=5 |pages=702–3 |year=1984 |month=May |pmid=6143508 |url=http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=6143508}}</ref>
*[[exercise]]: may engage in frequent strenuous exercise<ref>Peñas-Lledó E''et al.'' Excessive exercise in anorexia nervosa and bulimia nervosa: relation to eating characteristics and general psychopathology.Int J Eat Disord. 2002 May;31(4):370-5.
*[[exercise]]: may engage in frequent strenuous exercise<ref>{{cite journal |author=Peñas-Lledó E, Vaz Leal FJ, Waller G |title=Excessive exercise in anorexia nervosa and bulimia nervosa: relation to eating characteristics and general psychopathology |journal=The International Journal of Eating Disorders |volume=31 |issue=4 |pages=370–5 |year=2002 |month=May |pmid=11948642 |doi=10.1002/eat.10042}}</ref>
PMID 11948642</ref>
*[[perception]]: perceives themselves to be overweight despite being told by others they are too thin
*[[perception]]: perceives themselves to be overweight despite being told by others they are too thin
*[[Hypothermia|cold]] becomes intolerant to cold , frequently complains of being cold due to loss of insulating body fat, body temperature lowers (hypothermia) in effort to conserve [[calories]].<ref>Haller E. Eating disorders. A review and update.
*[[Hypothermia|cold]] becomes intolerant to cold , frequently complains of being cold due to loss of insulating body fat, body temperature lowers (hypothermia) in effort to conserve [[calories]].<ref>{{cite journal |author=Haller E |title=Eating disorders. A review and update |journal=The Western Journal of Medicine |volume=157 |issue=6 |pages=658–62 |year=1992 |month=December |pmid=1475950 |pmc=1022101}}</ref>
*[[Depression (mood)|depression]] may frequently be in a sad [[lethargic]] state<ref>{{cite journal |author=Lucka I |title=[Depression syndromes in patients suffering from anorexia nervosa] |language=Polish |journal=Psychiatria Polska |volume=38 |issue=4 |pages=621–9 |year=2004 |pmid=15518310}}</ref>
West J Med. 1992 Dec;157(6):658-62.PMID 1475950</ref>
*[[Depression (mood)|depression]] may frequently be in a sad [[lethargic]] state<ref>Lucka I.[Depression syndromes in patients suffering from anorexia nervosa][Abstrat: English/Article in Polish]
Psychiatr Pol. 2004 Jul-Aug;38(4):621-9.PMID 15518310</ref>
*[[solitude]]: may avoid friends and family, become withdrawn and secretive
*[[solitude]]: may avoid friends and family, become withdrawn and secretive
*clothing:may wear baggy, loose fitting clothes to cover weight loss
*clothing:may wear baggy, loose fitting clothes to cover weight loss
*[[cheeks]] may become swollen due to enlargement of the [[salivary gland]]s caused by excessive vomiting<ref>Bozzato A. ''et al.''Salivary gland biometry in female patients with eating disorders. Eur Arch Otorhinolaryngol. 2008 Sep;265(9):1095-102. Epub 2008 Feb 6.PMID 18253742</ref>
*[[cheeks]] may become swollen due to enlargement of the [[salivary gland]]s caused by excessive vomiting<ref>{{cite journal |author=Bozzato A, Burger P, Zenk J, Uter W, Iro H |title=Salivary gland biometry in female patients with eating disorders |journal=European Archives of Oto-rhino-laryngology |volume=265 |issue=9 |pages=1095–102 |year=2008 |month=September |pmid=18253742 |doi=10.1007/s00405-008-0598-8}}</ref>
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|bgcolor="B0CBE5" colspan="5"|<div align="center">'''Dermatologic Signs of Anorexia Nervosa'''<ref>Strumia R. Dermatologic signs in patients with eating disorders. Am J Clin Dermatol. 2005;6(3):165-73.
|bgcolor="B0CBE5" colspan="5"|<div align="center">'''Dermatologic Signs of Anorexia Nervosa'''<ref>{{cite journal |author=Strumia R |title=Dermatologic signs in patients with eating disorders |journal=American Journal of Clinical Dermatology |volume=6 |issue=3 |pages=165–73 |year=2005 |pmid=15943493}}</ref></div>
PMID 15943493</ref></div>
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|bgcolor="FBF4CE"|[[Xerosis]]||bgcolor="FBF4CE"|[[telogen effluvium]]||bgcolor="FBF4CE"|[[carotenoderma]]||bgcolor="FBF4CE"|[[acne]]||bgcolor="FBF4CE"|[[hyperpigmentation]]
|bgcolor="FBF4CE"|[[Xerosis]]||bgcolor="FBF4CE"|[[telogen effluvium]]||bgcolor="FBF4CE"|[[carotenoderma]]||bgcolor="FBF4CE"|[[acne]]||bgcolor="FBF4CE"|[[hyperpigmentation]]
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|bgcolor="B0CBE5" colspan="5"|<div align="center">'''Possible Medical Complications of Anorexia Nervosa</div>
|bgcolor="B0CBE5" colspan="5"|<div align="center">'''Possible Medical Complications of Anorexia Nervosa</div>
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|bgcolor="FBF4CE"|[[constipation]]<ref>Chiarioni G. ''et al.''Anorectal dysfunction in constipated women with anorexia nervosa. Mayo Clin Proc. 2000 Oct;75(10):1015-9.PMID 11040849</ref> ||bgcolor="FBF4CE"|[[diarrhea]]<ref>Waldholtz BD, Andersen AE. Gastrointestinal symptoms in anorexia nervosa. A prospective study. Gastroenterology. 1990 Jun;98(6):1415-9.PMID 2338185</ref>||bgcolor="FBF4CE"|[[Electrolyte|electrolyte imbalance]]<ref>Olson AF. Outpatient management of electrolyte imbalances associated with anorexia nervosa and bulimia nervosa. J Infus Nurs. 2005 Mar-Apr;28(2):118-22.PMID 15785332</ref>||bgcolor="FBF4CE"|[[Dental caries|cavities]]<ref>van Nieuw Amerongen A, Vissink A.Ned Oral complications of anorexia nervosa, bulimia nervosa and other metabolic disorders.[Article in Dutch] Tijdschr Tandheelkd. 2001 Jun;108(6):242-7.PMID 11441717</ref>||bgcolor="FBF4CE"|[[tooth|tooth loss]]<ref>de Moor RJ. Eating disorder-induced dental complications: a case report.J Oral Rehabil. 2004 Jul;31(7):725-32.PMID 15210036</ref>
|bgcolor="FBF4CE"|[[constipation]]<ref>{{cite journal |author=Chiarioni G, Bassotti G, Monsignori A, ''et al.'' |title=Anorectal dysfunction in constipated women with anorexia nervosa |journal=Mayo Clinic Proceedings |volume=75 |issue=10 |pages=1015–9 |year=2000 |month=October |pmid=11040849}}</ref> ||bgcolor="FBF4CE"|[[diarrhea]]<ref>{{cite journal |author=Waldholtz BD, Andersen AE |title=Gastrointestinal symptoms in anorexia nervosa. A prospective study |journal=Gastroenterology |volume=98 |issue=6 |pages=1415–9 |year=1990 |month=June |pmid=2338185}}</ref>||bgcolor="FBF4CE"|[[Electrolyte|electrolyte imbalance]]<ref>{{cite journal |author=Olson AF |title=Outpatient management of electrolyte imbalances associated with anorexia nervosa and bulimia nervosa |journal=Journal of Infusion Nursing |volume=28 |issue=2 |pages=118–22 |year=2005 |pmid=15785332}}</ref>||bgcolor="FBF4CE"|[[Dental caries|cavities]]<ref>{{cite journal |author=van Nieuw Amerongen A, Vissink A |title=[Oral complications of anorexia nervosa, bulimia nervosa and other metabolic disorders] |language=Dutch |journal=Nederlands Tijdschrift Voor Tandheelkunde |volume=108 |issue=6 |pages=242–7 |year=2001 |month=June |pmid=11441717}}</ref>||bgcolor="FBF4CE"|[[tooth|tooth loss]]<ref>{{cite journal |author=de Moor RJ |title=Eating disorder-induced dental complications: a case report |journal=Journal of Oral Rehabilitation |volume=31 |issue=7 |pages=725–32 |year=2004 |month=July |pmid=15210036 |doi=10.1111/j.1365-2842.2004.01282.x}}</ref>
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|bgcolor="FBF4CE"|[[cardiac arrest]]<ref>{{cite journal |author=García-Rubira JC, Hidalgo R, Gómez-Barrado JJ, Romero D, Cruz Fernández JM |title=Anorexia nervosa and myocardial infarction |journal=International Journal of Cardiology |volume=45 |issue=2 |pages=138–40 |year=1994 |month=June |pmid=7960253}}</ref>||bgcolor="FBF4CE"|[[amenorrhoea]]<ref>{{cite journal |author=Golden NH, Shenker IR |title=Amenorrhea in anorexia nervosa. Neuroendocrine control of hypothalamic dysfunction |journal=The International Journal of Eating Disorders |volume=16 |issue=1 |pages=53–60 |year=1994 |month=July |pmid=7920581}}</ref>||bgcolor="FBF4CE"|[[edema]]<ref>{{cite journal |author=Demaerel P, Daele MC, De Vuysere S, Wilms G, Baert AL |title=Orbital fat edema in anorexia nervosa: a reversible finding |journal=American Journal of Neuroradiology |volume=17 |issue=9 |pages=1782–4 |year=1996 |month=October |pmid=8896638 |url=http://www.ajnr.org/cgi/pmidlookup?view=long&pmid=8896638}}</ref> ||bgcolor="FBF4CE"|[[osteoporosis]]<ref>{{cite journal |author=Joyce JM, Warren DL, Humphries LL, Smith AJ, Coon JS |title=Osteoporosis in women with eating disorders: comparison of physical parameters, exercise, and menstrual status with SPA and DPA evaluation |journal=Journal of Nuclear Medicine |volume=31 |issue=3 |pages=325–31 |year=1990 |month=March |pmid=2308003 |url=http://jnm.snmjournals.org/cgi/pmidlookup?view=long&pmid=2308003}}</ref>||bgcolor="FBF4CE"|[[Osteopenia]]<ref>{{cite journal |author=Golden NH |title=Osteopenia and osteoporosis in anorexia nervosa |journal=Adolescent Medicine |volume=14 |issue=1 |pages=97–108 |year=2003 |month=February |pmid=12529194}}</ref>
|bgcolor="FBF4CE"|[[cardiac arrest]]<ref>García-Rubira JC. ''et al.''Anorexia nervosa and myocardial infarction.Int J Cardiol. 1994 Jun 15;45(2):138-40.PMID 7960253</ref>||bgcolor="FBF4CE"|[[amenorrhoea]]<ref>Golden NH, Shenker IR.Amenorrhea in anorexia nervosa. Neuroendocrine control of hypothalamic dysfunction.
Int J Eat Disord. 1994 Jul;16(1):53-60.PMID 7920581</ref>||bgcolor="FBF4CE"|[[edema]]<ref>Demaerel P. ''et al.''Orbital fat edema in anorexia nervosa: a reversible finding. AJNR Am J Neuroradiol. 1996 Oct;17(9):1782-4.PMID 8896638</ref> ||bgcolor="FBF4CE"|[[osteoporosis]]<ref>Joyce JM ''et.al.'' Osteoporosis in women with eating disorders... J Nucl Med 2003 Mar;31(3):325-31 PMID 2308003</ref>||bgcolor="FBF4CE"|[[Osteopenia]]<ref>Golden NH. Osteopenia and osteoporosis in anorexia nervosa.Adolesc Med. 2003 Feb;14(1):97-108.PMID 12529194</ref>
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|bgcolor="FBF4CE"|[[hyponatremia]]<ref>Bahia A, Chu ES, Mehler PS. Polydipsia and hyponatremia in a woman with anorexia nervosa.Int J Eat Disord. 2010 Feb 2. [Epub ahead of print]PMID 20127934</ref>||bgcolor="FBF4CE"|[[hypokalemia]]<ref>Bonne OB, Bloch M, Berry EM.Int J Eat Disord. 1993 Jan;13(1):125-8.PMID 8477271</ref>||bgcolor="FBF4CE"|[[Optic neuropathy]]<ref>Mroczkowski MM.Reversible vision loss secondary to malnutrition in a woman with severe anorexia nervosa, purging type, and alcohol abuse. Int J Eat Disord. 2010 Feb 22. [Epub ahead of print]PMID 20186722</ref> ||bgcolor="FBF4CE"|[[cerebral atrophy|brain atrophy]]<ref>Drevelengas A ''Et. Al.'' Reversible brain atrophy and subcortical high signal on MRI in a patient with anorexia nervosa. Neuroradiology. 2001 Oct;43(10):838-40. PMID 11688699</ref><ref>Addolorato G ''et. al'' A case of marked cerebellar atrophy in a woman with anorexia nervosa and cerebral atrophy and a review of the literature Int J Eat Disord. 1998 Dec;24(4):443-7. PMID 9813771</ref>||bgcolor="FBF4CE"|[[leukopenia]]<ref>Hütter G, Ganepola S, Hofmann WK. The hematology of anorexia nervosa.Int J Eat Disord. 2009 May;42(4):293-300.PMID 19040272</ref><ref>Allende LM. ''et al.''Immunodeficiency associated with anorexia nervosa is secondary and improves after refeeding.Immunology. 1998 Aug;94(4):543-51.PMID 9767443</ref>
|bgcolor="FBF4CE"|[[hyponatremia]]<ref>{{cite journal |author=Bahia A, Chu ES, Mehler PS |title=Polydipsia and hyponatremia in a woman with anorexia nervosa |journal=The International Journal of Eating Disorders |volume= |issue= |pages= |year=2010 |month=February |pmid=20127934 |doi=10.1002/eat.20792}}</ref>||bgcolor="FBF4CE"|[[hypokalemia]]<ref>{{cite journal |author=Bonne OB, Bloch M, Berry EM |title=Adaptation to severe chronic hypokalemia in anorexia nervosa: a plea for conservative management |journal=The International Journal of Eating Disorders |volume=13 |issue=1 |pages=125–8 |year=1993 |month=January |pmid=8477271}}</ref>||bgcolor="FBF4CE"|[[Optic neuropathy]]<ref>{{cite journal |author=Mroczkowski MM, Redgrave GW, Miller NR, McCoy AN, Guarda AS |title=Reversible vision loss secondary to malnutrition in a woman with severe anorexia nervosa, purging type, and alcohol abuse |journal=The International Journal of Eating Disorders |volume= |issue= |pages= |year=2010 |month=February |pmid=20186722 |doi=10.1002/eat.20806}}</ref> ||bgcolor="FBF4CE"|[[cerebral atrophy|brain atrophy]]<ref>{{cite journal |author=Drevelengas A, Chourmouzi D, Pitsavas G, Charitandi A, Boulogianni G |title=Reversible brain atrophy and subcortical high signal on MRI in a patient with anorexia nervosa |journal=Neuroradiology |volume=43 |issue=10 |pages=838–40 |year=2001 |month=October |pmid=11688699}}</ref><ref>{{cite journal |author=Addolorato G, Taranto C, Capristo E, Gasbarrini G |title=A case of marked cerebellar atrophy in a woman with anorexia nervosa and cerebral atrophy and a review of the literature |journal=The International Journal of Eating Disorders |volume=24 |issue=4 |pages=443–7 |year=1998 |month=December |pmid=9813771 |doi=10.1002/(SICI)1098-108X(199812)24:4<443::AID-EAT13>3.0.CO;2-4}}</ref>||bgcolor="FBF4CE"|[[leukopenia]]<ref>{{cite journal |author=Hütter G, Ganepola S, Hofmann WK |title=The hematology of anorexia nervosa |journal=The International Journal of Eating Disorders |volume=42 |issue=4 |pages=293–300 |year=2009 |month=May |pmid=19040272 |doi=10.1002/eat.20610}}</ref><ref>{{cite journal |author=Allende LM, Corell A, Manzanares J, ''et al.'' |title=Immunodeficiency associated with anorexia nervosa is secondary and improves after refeeding |journal=Immunology |volume=94 |issue=4 |pages=543–51 |year=1998 |month=August |pmid=9767443 |pmc=1364233}}</ref>
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==Causes==
==Causes==
Studies have [[hypothesis|hypothesized]] that the continuance of disorded eating patterns may be [[Epiphenomenon|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.<ref>Zandian M, Ioakimidis I, Bergh C, Södersten P. Cause and treatment of anorexia nervosa.Physiol Behav. 2007 Sep 10;92(1-2):283-90. Epub 2007 May 25.
Studies have [[hypothesis|hypothesized]] that the continuance of disorded eating patterns may be [[Epiphenomenon|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.<ref>{{cite journal |author=Zandian M, Ioakimidis I, Bergh C, Södersten P |title=Cause and treatment of anorexia nervosa |journal=Physiology & Behavior |volume=92 |issue=1-2 |pages=283–90 |year=2007 |month=September |pmid=17585973 |doi=10.1016/j.physbeh.2007.05.052}}</ref><ref>{{cite book |first=M. S. |last=Thambirajah |title=Case Studies in Child and Adolescent Mental Health |publisher=Radcliffe Publishing |location= |year=2007 |page=145 |isbn=978-1-85775-698-2 |oclc=84150452}}</ref><ref>{{cite journal |author=Kaye W |title=Neurobiology of anorexia and bulimia nervosa |journal=Physiology & Behavior |volume=94 |issue=1 |pages=121–35 |year=2008 |month=April |pmid=18164737 |pmc=2601682 |doi=10.1016/j.physbeh.2007.11.037}}</ref><ref>{{cite journal |author=Støving RK, Hansen-Nord M, Hangaard J, Hagen C |title=[Neuroendocrine disorders in anorexia nervosa--primary or secondary?] |language=Danish |journal=Ugeskrift for Laeger |volume=158 |issue=49 |pages=7052–6 |year=1996 |month=December |pmid=8999610}}</ref>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.<ref>{{cite journal |author=Brandenburg BM, Andersen AE |title=Unintentional onset of anorexia nervosa |journal=Eating and Weight Disorders |volume=12 |issue=2 |pages=97–100 |year=2007 |month=June |pmid=17615494 |url=http://www.kurtis.it/abs/index.cfm?id_articolo_numero=3749}}</ref><ref>{{cite journal |author=Nygaard JA |title=Anorexia nervosa. Treatment and triggering factors |journal=Acta Psychiatrica Scandinavica. Supplementum |volume=361 |issue= |pages=44–9 |year=1990 |pmid=2291425}}</ref>
PMID 17585973</ref><ref> Case Studies in Child and Adolescent Mental Health - Page 145 by M. S. Thambirajah Publisher: Radcliffe Publishing Ltd; 1 edition (Nov 2006) Language English ISBN 1857756983 ISBN 978-1857756982 </ref><ref>Kaye W.Neurobiology of anorexia and bulimia nervosa.Physiol Behav. 2008 Apr 22;94(1):121-35. Epub 2007 Nov 29.PMID 18164737</ref><ref>Støving RK, Hansen-Nord M, Hangaard J, Hagen C.Ugeskr Laeger. Neuroendocrine disorders in anorexia nervosa--primary or secondary 1996 Dec 2;158(49):7052-6.
PMID 8999610</ref>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.<ref>Brandenburg BM, Andersen AE.Unintentional onset of anorexia nervosa. Eat Weight Disord. 2007 Jun;12(2):97-100.PMID 17615494</ref><ref>Nygaard JA. Anorexia nervosa. Treatment and triggering factors.Acta Psychiatr Scand Suppl. 1990;361:44-9.PMID 2291425</ref>


===Biological===
===Biological===

Revision as of 06:31, 20 April 2010

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Anorexia nervosa
SpecialtyPsychiatry, clinical psychology Edit this on Wikidata

Anorexia nervosa (AN) is an eating disorder characterized by refusal to maintain a healthy body weight, and an obsessive fear of gaining weight due to a distorted self image[1][2] which may be maintained by various cognitive biases that alter how the affected individual evaluates and thinks about their body, food and eating. AN is a serious mental illness with morbidity and mortality rates as high as those seen in any psychiatric illness.[3]

While the stereotype is that AN affects young white women, it can affect men and women of all ages, races, socioeconomic and cultural backgrounds.[4][5][6][7][8]

The term anorexia nervosa was established in 1873 by Sir William Gull, one of Queen Victoria's personal physicians.[9] 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.[10]

Signs and symptoms

There are various characteristic behavioral and physical signs associated with Anorexia Nervosa, not every sign is manifested in every individual. In addition to the visibly obvious dermatolgical signs like growing body and facial hair called lanugo, it causes dental cavities and tooth loss, the abdomen may become distended, and the joints may become swollen. The type and severity of the signs and symptoms vary in each case, and may be present, but not readily apparent. Anorexia nervosa and the associated malnutrition that results from self imposed starvation causes severe complications in every major organ system in the body.[11][12][13]

Possible Signs of Anorexia Nervosa
Russell's sign is the scarring that occurs on the dorsum of the hand, primarily the knuckles due to sticking fingers down throat to induce vomiting. The scars occur due to the skins repeated contact with the teeth.
Russell's sign scarring on knuckles due to sticking fingers down throat to force vomiting[14]
Chilblains are ulcers that affect such areas as the toes, they may occur when a predisposed individual is exposed to cold and humidity
Chilblains, also known as Perniosis.
Possible cutaneous complication of anorexia nervosa.[15]
Dermatologic Signs of Anorexia Nervosa[25]
Xerosis telogen effluvium carotenoderma acne hyperpigmentation
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[26] diarrhea[27] electrolyte imbalance[28] cavities[29] tooth loss[30]
cardiac arrest[31] amenorrhoea[32] edema[33] osteoporosis[34] Osteopenia[35]
hyponatremia[36] hypokalemia[37] Optic neuropathy[38] brain atrophy[39][40] leukopenia[41][42]

Causes

Studies have hypothesized that the continuance of disorded 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.[43][44][45][46]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.[47][48]

Biological

Dysregulation of the neurogenic pathways of serotonin and dopamine, two important neurotransmitters have been implicated in the etiology, pathogenesis and pathophsiology of various neuropsychiatric disorders, including anorexia nervosa.
Dysregulation of the dopamine and serotonin pathways has been implicated in the etiology, pathogenesis and pathophysiology of anorexia nervosa.[59][60][61][62]
  • serotonin dysregulation;[63] 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 and disturbances to the serotonin system are still apparent after patients have recovered from anorexia.[64]
  • Brain-derived neurotrophic factor (BDNF) is a protein that regulates neuronal development and neuroplasticity, 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.[65][66]Exercise increases levels of BDNF[67]
  • 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.[68]
  • 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.[69]
  • Nutritional deficiencies
    • Zinc deficiency may be an accelerating factor that deepens the pathology of anorexia[71]

Environmental

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.[72][73] 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.[74] 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,[75] and further research has suggested that those with anorexia have much higher contact with cultural sources that promote weight-loss.[76]

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.[77]

Relationship to autism

Since Christopher Gillberg's (1985) and others initial suggestion of relationship between anorexia nervosa and autism,[78][79][80] 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.[81][82][83][84][85][86][87]

Those on the autism spectrum tend to have a worse outcome,[88] but may benefit from the combined use of behavioural and pharmacological therapies tailored to ameliorate autism rather than anorexia nervosa per se.[89][90]

Other studies, most notably research conducted at the Maudsley Hospital UK, suggest that autistic traits are common in people with anorexia nervosa, shared traits include; executive function, autism quotient score, central coherence, theory of mind, cognitive-behavioural flexibility, emotion regulation and understanding facial expressions.[91][92][93][94][95][96]

Zucker et al. (2007) proposed that conditions on the autism spectrum make up the cognitive endophenotype underlying anorexia nervosa.[97]

In men

Dennis Quad was one of the estimated 1 million men to suffer from manorexia, or male anorexia, in a given year.
Dennis Quaid suffered from "Manorexia".[98]

There has been an increasing rate of males suffering from anorexia nervosa. There is a perceived stigma attached, as AN is generally viewed as primarily affecting young white women. Among men the rates of eating disorders are higher in the gay and bi-sexual communities (Feldman & Meyer, 2007)[99], yet it also affects heterosexual men.

Despite the perceived stigma, some high profile male celebrities have publicised their struggles with eating disorders such as actor Dennis Quaid. Quaid said his problems began when he went on a diet to lose forty pounds to play Doc Holliday in the movie "Wyatt Earp" in 1994.[citation needed]

Thomas Holbrook, M.D., is Clinical Director of the Eating Disorders Program at Rogers Memorial Hospital in Oconomowoc, Wisconsin despite being a psychiatrist specializing in eating disorders, he suffered from anorexia nervosa with compulsive exercising. At one time the 6-ft.-tall psychiatrist weighed just 135 lbs. "I was terrified," he says, "of being fat." His story has been chronicled in various publications including USA Today and People Magazine.

Diagnosis

Medical

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.[100][101]
  • medical tests:There are a variety of tests that may be performed to diagnose AN and to assess the secondary effects caused by AN upon the patient.
  • 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).[128][129]

Differential diagnoses

There are various medical and conditions which have been misdiagnosed as anorexia nervosa, in some cases the correct diagnosis wasn't made for over 10 years. In a reported case of achalasia misdiagnosed as AN, the patient spent two months confined to a psychiatric hospital,[130]Some of the differential diagnoses may include:

  • Lupus: various neuropsychiatric symptoms are associated with systemic lupus erythematosus (SLE), including depression.Anorexia and weight loss also may occur with SLE and while rare it may be misdiagnosed as AN.[131][132]
  • acute pandysautonomia is one form of an autonomic neuropathy, which are a collection of various syndromes and diseases which affect the autonomic neurons of the autonomic nervous system (ANS). Autonomic neuropathies may be the result of an inherited condition or they may be acquired due to various premorbid conditions such as diabetes and alcoholism, bacterial infection such as Lyme disease or a viral illness. Some of the symptoms of ANS which may be associated with an ED include nausea, dysphagia, constipation, pain in the salivary glands early saiety. It also affects peristalsis in the stomach. Acute pandysautonomia may cause emotional instability and has been misdiagnosed as various psychiatric disorders including hysterical neurosis and anorexia nervosa.[133]
Disorders of the gastrointestinal tract such as achalasia which affects peristalsis (muscular contractions) of the esophagus, may mimic the signs of an eating disorder such as anorexia nervosa.

Achalasia:disorder of the esophagus which affects peristalsis has been misdiagnosed as anorexia nervosa.[134]
  • Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is a rare genetic disorder characterized by gastrointestinal dysmotility, severe cachexia progressive external ophthalmoplegia, post-prandial emesis (vomiting after eating), peripheral neuropathy, and diffuse leukoencephalopathy. Onset is prior to age 20 in 60% of cases. ""Miss A" was a 21-year-old Indian woman diagnosed as having treatment-resistant anorexia nervosa." It was subsequently proven to be MNGIE[135][136][137]
  • achalasia; There have been cases where achalasia, a disorder of the esophagus which affects peristalsis, has been misdiagnosed as AN. It has been reported in cases where there is sub-clinical manifestation of anorexia nervosa and also in cases where the full diagnostic criteria AN has been met.[138]
  • superior mesenteric artery syndrome: (SMA) syndrome; "is a gastrointestinal disorder characterized by the compression of the third or transverse portion of the duodenum against the aorta by the superior mesenteric artery resulting in chronic partial, incomplete, acute or intermittent duodenal obstruction". It may occur as a complication of AN or as a differential diagnosis. There have been reported cases of a tentative diagnosis of AN, where upon treatment for SMA syndrome the patient is asymptomatic.[139][140]
  • Lyme Disease is known as the "great imitator", as it may present as a variety of psychiatric or neurologic disorders including anorexia nervosa. "A 12 year old boy with confirmed Lyme arthritis treated with oral antibiotics subsequently became depressed and anorectic. After being admitted to a psychiatric hospital with the diagnosis of anorexia nervosa, he was noted to have positive serologic tests for Borrelia burgdorferi. Treatment with a 14 day course of intravenous antibiotics led to a resolution of his depression and anorexia; this improvement was sustained on 3 year follow-up."[141][142] Serologic testing can be helpful but should not be the sole basis for diagnosis. The Centers for Disease Control (CDC) issued a cautionary statement (MMWR 54;125) regarding the use of several commercial tests. Clinical diagnostic criteria has been issued by the CDC (CDC, MMWR 1997; 46: 531-535).
  • Addison's Disease; is a disorder of the adrenal cortex which results in decreased hormonal production. Addison's disease, even in subclinical form may mimic many of the symptoms of anorexia nervosa.[143]
  • Brain tumors: There are multiple cases were the neuropsychiatric symptoms of a brain tumor were attributed to AN resulting in misdiagnosis. The tumors in these cases were noted in various regions of the brain including the medulla oblongata, hypothalamus, pituitary gland, pineal gland and the obex. [144][145][146][147]
  • Celiac Disease is an inflammatory disorder triggered by peptides from wheat and similar grains which cause an immune reaction in the small intestine."information on the role of the gastrointestinal system in causing or mimicking eating disorders is scarce."(Leffler DA et al.)[153]
  • Gall bladder disease which may be caused by inflammation, infection, gallstones, obstruction of the gallbladder or torsion of the gall bladder. Many of the symptoms of gall bladder disease may mimic anorexia nervosa (AN). Laura Daly, a woman from Missouri, suffered from an inherited disorder in which the gall bladder was not properly attached; the resultant complications led to multiple erroneous diagnoses of AN. Upon performance of a CCK test, standard imaging techniques are done with the patient lying prone, in this instance it was done with the patient in an upright position. The gall bladder was shown to be in an abnormal position having flipped over the liver. The gallbladder was removed and the patient has since recovered. The treatment was performed by William P. Smedley, M.D., F.A.C.S. in Pennsylvania.
  • colonic tuberculosis misdiagnosed as anorexia nervosa in a physician at the hospital where she worked. "This patient, who had severe wasting, was misdiagnosed as having anorexia nervosa despite the presence of other symptoms suggestive of an organic disease, namely, fever and diarrhea"(Madani, A 2002).[154]
  • Crohn's Disease: "We report three cases of young 18 to 25 year-old girls, initially treated for anorexia nervosa in a psychiatric department. Diagnosis of Crohn's disease was made within 5 to 13 years."(Blanchet C, Luton JP. 2002)"This disease should be diagnostically excluded before accepting anorexia nervosa as final diagnosis". (Wellmann W et al.)[155][156][157][158]
  • Insulinomas, are (pancreatic tumors) that cause an overproduction of insulin, causing hypoglycemia. Various neurological deficits have been ascribed to this condition including misdiagnosis as an eating disorder.[159][160][161][162][163]
  • hypothyroidism, hyperthyroidism, hypoparathyroidism and hyperparathyroidism may mimic some of the symptoms of, can occur concurrently with, be masked by or exacerbate an eating disorder and/or various comorbid disorders such as anxiety and depression. [164][165][166][167][168][169][170][171]
  • Multiple sclerosis (Encephalomyelitis disseminata) is a progressive autoimmune disorder in which the protective covering (myelin sheath) of nerve cells is damaged as a result of inflammation and resultant attack by the bodies own immune system. In its initial presentation MS has been misdiagnosed as an eating disorder.[172]

Psychological

Anorexia nervosa is classified as Axis I[173] disorders 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 types eat too much or purge themselves, and the restricting types do not.[174]
    • 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 above 85% of the expected weight and the requirement of amenorrhea for diagnosis; some women have all the symptoms of AN and continue to menstrate.[175] Those who do not meet these criteria are usually classified as eating disorder not otherwise specified this may affect treatment options and insurance reimbursments.[176] 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.[177][178]
  • ICD-10: The criteria are similar, but in addition, specifically mention
  1. 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).
  2. If onset is before puberty, that development is delayed or arrested.
  3. 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 diagnoses

File:Body dysmorphiic disorder.jpg
Constant mirror checking is one of the hallmarks of body dysmorphic disorder.

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.[179] Some people have a previous disorder which may increase their vulnerability to developing an eating disorder.[180][181][182] Some develop them afterwards.[183] The severity and type of eating disorder symptoms have been shown to affect comorbidity.[184]These comorbid disorders themselves have multiple differential diagnoses, such as depression which may be caused by such disparate causes such as Lyme disease or hypothyroidism.

  • Emetophobia is an anxiety disorder characterized by an intense fear of vomiting. A person so afflicted may develop rigorous standards of food hygiene, such as not touching food with their hands. They may become socially withdrawn to avoid situations which in their perception may make them vomit. Many who suffer from emetophobia are diagnosed with anorexia or self-starvation. In severe cases of emetophobia they may drastically reduce their food intake.[185][186]
  • phagophobia is an anxiety disorder characterized by a fear of eating, it is usually initiated by an adverse experience while eating such as choking or vomiting. Individuals with this disorder may present with complaints of pain while swallowing. There have been cases of it being misdiagnosed as AN.[187][188] A similar phobic anxiety disorder, swallowing phobia may also lead to a misdiagnosis of anorexia nervosa; such individuals do not want to lose weight but typically want to put weight back on that they have lost due to their phobia.[189]
  • 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.[190]

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.[191][192][193][194][195]

Comorbid Disorders
Axis I Axis II
depression[196] obsessive compulsive personality disorder[197]
substance abuse, alcoholism[198] borderline personality disorder[199]
anxiety disorders[200] narcissistic personality disorder[201]
obsessive compulsive disorder[202][203] histrionic personality disorder[204]
Attention-Deficit-Hyperactivity-Disorder[205][206][207][208] avoidant personality disorder[209]

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.[97]

Treatment

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.[210]

  • Diet and Nutrition
    • Zinc supplementation has been shown in various studies to beneficial in the treatment of AN even in patients not suffering from zinc deficiency, by helping to increase weight gain.[211]

"On the basis of these findings and the low toxicity of zinc, zinc supplementation should be included in the treatment protocol for anorexia nervosa".

[212]

CONCLUSIONS: Oral administration of 14 mg of elemental zinc daily for 2 months in all patients with AN should be routine.[213]

    • 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[214]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)[215], 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.[216][217]
    • Nutrition counseling[218][219]
      • 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.[220][221][222]
  • Medication
    • 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.[223][224]
  • Psycotherapy/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.[225][226][227]
Cognitive Behavioral Therapies

Rational Emotive Behavior Therapy Dialectical behavior therapy[228] Rational Living Therapy Rational Behavior Therapy Cognitive Therapy
    • 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.[229]

Green Red Blue
Purple Blue Purple


Blue Purple Red
Green Purple Green


Used in Cognitive Remediation Therapy. Naming the color of the first set of words is easier and quicker than the second set.
    • 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[230] and in Poland with adolescents CRT was proven to be beneficial in treating anorexia nervosa[231], in the United States clinical trials are still being conducted by the National Institute of Mental Health[232] on adolescents age 10-17 and Stanford University in subjects over 16 as a conjuctive therapy with Cognitive behavioral therapy.[233]
    • 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... ".[234][235]
    • Maudsley Family Therapy:A 4 to 5 year follow up study of the Maudsley approach, shows full recovery at rates up to 90%.[236]
  • 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.[237]
    • 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.[238]
  • Experimental Therapy

Prognosis

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..."[241]

In cases of adoloscent anorexia nervosa that utilize Family treatment 75% of patients have a good outcome and an additional 15% show an intermediate yet more positive outcome[242]In a five year post treatment follow-up of Maudsley Family Therapy the full recovery rate was between 75% and 90%.[243] 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.[244]

Epidemiology

Anorexia has an incidence of between 8 and 13 cases per 100,000 persons per year and an average prevalence of 0.3% using strict criteria for diagnosis.[245][246] 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.[247]

History

The history of anorexia nervosa begins with early descriptions dating from the 16th century and 17th century 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.[248]

See also

References

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Bibliography

  • 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
  • Anorexia Misdiagnosed Publisher:Laura A. Daly; 1st edition (December 15, 2006) Language:English ISBN 0938279076 ISBN 978-0938279075
  • Wasted: A Memoir of Anorexia and Bulimia Marya Hornbacher. Publisher: Harper Perennial; 1 edition (January 15, 1999) Language: English ISBN 0060930934 ISBN 978-0060930936
  • 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
  • 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
  • Overcoming Binge Eating; Christopher Fairburn. Publisher: The Guilford Press; Reissue edition (March 10, 1995) Language:English ISBN 0898621798 ISBN 978-0898621792

External links

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