Editing Eating disorder (section)

== Mechanisms ==
* [[Biochemical]]: Eating behavior is a complex process controlled by the [[neuroendocrine]] system, of which the [[HPA axis|Hypothalamus-pituitary-adrenal-axis]] (HPA axis) is a major component. Dysregulation of the HPA axis has been associated with eating disorders,<ref>{{cite journal |vauthors=Gross MJ, Kahn JP, Laxenaire M, Nicolas JP, Burlet C |title=[Corticotropin-releasing factor and anorexia nervosa: reactions of the hypothalamus-pituitary-adrenal axis to neurotropic stress] |journal=Annales d'Endocrinologie |volume=55 |issue=6 |pages=221–8 |year=1994 |pmid=7864577}}</ref><ref>{{cite journal |vauthors=Licinio J, Wong ML, Gold PW |title=The hypothalamic-pituitary-adrenal axis in anorexia nervosa |journal=Psychiatry Research |volume=62 |issue=1 |pages=75–83 |date=April 1996 |pmid=8739117 |doi=10.1016/0165-1781(96)02991-5 |s2cid=10777927 |url=https://zenodo.org/record/1258351}}</ref> such as irregularities in the manufacture, amount or transmission of certain [[neurotransmitters]], [[hormones]]<ref>{{cite journal |vauthors=Chaudhri O, Small C, Bloom S |title=Gastrointestinal hormones regulating appetite |journal=Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences |volume=361 |issue=1471 |pages=1187–209 |date=July 2006 |pmid=16815798 |pmc=1642697 |doi=10.1098/rstb.2006.1856}}</ref> or [[neuropeptides]]<ref>{{cite journal |vauthors=Gendall KA, Kaye WH, Altemus M, McConaha CW, La Via MC |title=Leptin, neuropeptide Y, and peptide YY in long-term recovered eating disorder patients |journal=Biological Psychiatry |volume=46 |issue=2 |pages=292–9 |date=July 1999 |pmid=10418705 |doi=10.1016/S0006-3223(98)00292-3 |s2cid=6889214}}</ref> and [[amino acids]] such as [[homocysteine]], elevated levels of which are found in AN and BN as well as depression.<ref>{{cite journal |vauthors=Wilhelm J, Müller E, de Zwaan M, Fischer J, Hillemacher T, Kornhuber J, Bleich S, Frieling H |title=Elevation of homocysteine levels is only partially reversed after therapy in females with eating disorders |journal=Journal of Neural Transmission |volume=117 |issue=4 |pages=521–7 |date=April 2010 |pmid=20191295 |doi=10.1007/s00702-010-0379-6 |s2cid=7026873}}</ref>
** [[Serotonin]]: a neurotransmitter involved in depression also has an inhibitory effect on eating behavior.<ref>{{cite journal |vauthors=Jimerson DC, Lesem MD, Kaye WH, Hegg AP, Brewerton TD |title=Eating disorders and depression: is there a serotonin connection? |journal=Biological Psychiatry |volume=28 |issue=5 |pages=443–54 |date=September 1990 |pmid=2207221 |doi=10.1016/0006-3223(90)90412-U |s2cid=31058047}}</ref><ref>{{cite journal |vauthors=Leibowitz SF |title=The role of serotonin in eating disorders |journal=Drugs |volume=39 |issue=Suppl 3 |pages=33–48 |year=1990 |pmid=2197074 |doi=10.2165/00003495-199000393-00005 |s2cid=8612545}}</ref><ref>{{cite journal |vauthors=Blundell JE, Lawton CL, Halford JC |title=Serotonin, eating behavior, and fat intake |journal=Obesity Research |volume=3 |issue=Suppl 4 |pages=471S–476S |date=November 1995 |pmid=8697045 |doi=10.1002/j.1550-8528.1995.tb00214.x |doi-access=free}}</ref><ref>{{cite journal |vauthors=Kaye WH |title=Anorexia nervosa, obsessional behavior, and serotonin |journal=Psychopharmacology Bulletin |volume=33 |issue=3 |pages=335–44 |year=1997 |pmid=9550876}}</ref><ref>{{cite journal |vauthors=Bailer UF, Price JC, Meltzer CC, Mathis CA, Frank GK, [[Lisa Weissfeld|Weissfeld L]], McConaha CW, Henry SE, Brooks-Achenbach S, Barbarich NC, Kaye WH |title=Altered 5-HT(2A) receptor binding after recovery from bulimia-type anorexia nervosa: relationships to harm avoidance and drive for thinness |journal=Neuropsychopharmacology |volume=29 |issue=6 |pages=1143–55 |date=June 2004 |pmid=15054474 |pmc=4301578 |doi=10.1038/sj.npp.1300430}}</ref>
** [[Norepinephrine]] is both a neurotransmitter and a [[hormone]]; abnormalities in either capacity may affect eating behavior.<ref>{{cite journal |vauthors=Hainer V, Kabrnova K, Aldhoon B, Kunesova M, Wagenknecht M |title=Serotonin and norepinephrine reuptake inhibition and eating behavior |journal=Annals of the New York Academy of Sciences |volume=1083 |issue=1 |pages=252–69 |date=November 2006 |pmid=17148744 |doi=10.1196/annals.1367.017 |bibcode=2006NYASA1083..252H |s2cid=21025584}}</ref><ref>{{cite journal |vauthors=George DT, Kaye WH, Goldstein DS, Brewerton TD, Jimerson DC |title=Altered norepinephrine regulation in bulimia: effects of pharmacological challenge with isoproterenol |journal=Psychiatry Research |volume=33 |issue=1 |pages=1–10 |date=July 1990 |pmid=2171006 |doi=10.1016/0165-1781(90)90143-S |s2cid=36244543}}</ref>
** [[Dopamine]]: which in addition to being a [[precursor (chemistry)|precursor]] of norepinephrine and [[epinephrine]] is also a neurotransmitter which regulates the rewarding property of food.<ref>{{cite journal |vauthors=Wang GJ, Volkow ND, Logan J, Pappas NR, Wong CT, Zhu W, Netusil N, Fowler JS |title=Brain dopamine and obesity |journal=Lancet |volume=357 |issue=9253 |pages=354–7 |date=February 2001 |pmid=11210998 |doi=10.1016/S0140-6736(00)03643-6 |s2cid=6413843 |url=https://zenodo.org/record/1259773}}</ref><ref>{{cite journal |vauthors=Zhulenko VN, Georgieva GN, Smirnova LA |title=[Mercury content in the organs and tissues of slaughter animals] |journal=Veterinariia |issue=4 |pages=96–8 |date=April 1975 |pmid=1216579}}</ref>
** [[Neuropeptide Y]] also known as NPY is a hormone that encourages eating and decreases metabolic rate.<ref name="CT7" /> Blood levels of NPY are elevated in patients with anorexia nervosa, and studies have shown that injection of this hormone into the brain of rats with restricted food intake increases their time spent running on a wheel. Normally the hormone stimulates eating in healthy patients, but under conditions of starvation it increases their activity rate, probably to increase the chance of finding food.<ref name="CT7" /> The increased levels of NPY in the blood of patients with eating disorders can in some ways explain the instances of extreme over-exercising found in most anorexia nervosa patients.
* [[Leptin]] and [[ghrelin]]: leptin is a hormone produced primarily by the fat cells in the body; it has an inhibitory effect on appetite by inducing a feeling of satiety. Ghrelin is an appetite inducing hormone produced in the stomach and the upper portion of the small intestine. Circulating levels of both hormones are an important factor in weight control. While often associated with obesity, both hormones and their respective effects have been implicated in the pathophysiology of anorexia nervosa and bulimia nervosa.<ref>{{cite journal |vauthors=Frederich R, Hu S, Raymond N, Pomeroy C |title=Leptin in anorexia nervosa and bulimia nervosa: importance of assay technique and method of interpretation |journal=The Journal of Laboratory and Clinical Medicine |volume=139 |issue=2 |pages=72–9 |date=February 2002 |pmid=11919545 |doi=10.1067/mlc.2002.121014}}</ref> Leptin can also be used to distinguish between constitutional thinness found in a healthy person with a low BMI and an individual with anorexia nervosa.<ref name="CT2" /><ref name="CT8">{{cite journal |vauthors=Ferron F, Considine RV, Peino R, Lado IG, Dieguez C, Casanueva FF |title=Serum leptin concentrations in patients with anorexia nervosa, bulimia nervosa and non-specific eating disorders correlate with the body mass index but are independent of the respective disease |journal=Clinical Endocrinology |volume=46 |issue=3 |pages=289–93 |date=March 1997 |pmid=9156037 |doi=10.1046/j.1365-2265.1997.1260938.x |s2cid=25268127}}</ref>
* Gut bacteria and [[immune system]]: studies have shown that a majority of patients with anorexia and bulimia nervosa have elevated levels of [[autoantibodies]] that affect hormones and neuropeptides that regulate appetite control and the stress response. There may be a direct correlation between autoantibody levels and associated psychological traits.<ref>{{cite journal |vauthors=Fetissov SO, Harro J, Jaanisk M, Järv A, Podar I, Allik J, Nilsson I, Sakthivel P, Lefvert AK, Hökfelt T |title=Autoantibodies against neuropeptides are associated with psychological traits in eating disorders |journal=Proceedings of the National Academy of Sciences of the United States of America |volume=102 |issue=41 |pages=14865–70 |date=October 2005 |pmid=16195379 |pmc=1253594 |doi=10.1073/pnas.0507204102 |bibcode=2005PNAS..10214865F |doi-access=free}}</ref><ref>{{cite journal |vauthors=Sinno MH, Do Rego JC, Coëffier M, Bole-Feysot C, Ducrotté P, Gilbert D, Tron F, Costentin J, Hökfelt T, Déchelotte P, Fetissov SO |title=Regulation of feeding and anxiety by alpha-MSH reactive autoantibodies |journal=Psychoneuroendocrinology |volume=34 |issue=1 |pages=140–9 |date=January 2009 |pmid=18842346 |doi=10.1016/j.psyneuen.2008.08.021 |s2cid=8860223}}</ref> Later study revealed that autoantibodies reactive with alpha-MSH are, in fact, generated against ClpB, a protein produced by certain gut bacteria e.g. Escherichia coli. ClpB protein was identified as a conformational antigen-mimetic of alpha-MSH. In patients with eating disorders plasma levels of anti-ClpB IgG and IgM correalated with patients' psychological traits<ref>{{cite journal |vauthors=Tennoune N, Chan P, Breton J, Legrand R, Chabane YN, Akkermann K, Järv A, Ouelaa W, Takagi K, Ghouzali I, Francois M, Lucas N, Bole-Feysot C, Pestel-Caron M, do Rego JC, Vaudry D, Harro J, Dé E, Déchelotte P, Fetissov SO |title=Bacterial ClpB heat-shock protein, an antigen-mimetic of the anorexigenic peptide α-MSH, at the origin of eating disorders |journal=Translational Psychiatry |volume=4 |issue=10 |page=e458 |date=October 2014 |pmid=25290265 |pmc=4350527 |doi=10.1038/tp.2014.98}}</ref>
* Infection: [[PANDAS]] is an abbreviation for the controversial Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections hypothesis. Children with PANDAS are postulated to "have obsessive-compulsive disorder (OCD) and/or [[tic disorder]]s such as [[Tourette syndrome]], and in whom symptoms worsen following infections such as [[strep throat]]". ([[National Institute of Mental Health|NIMH]]) PANDAS and the broader PANS are hypothesized to be a precipitating factor in the development of anorexia nervosa in some cases, (PANDAS AN).<ref name= Wilbur2019>{{cite journal |vauthors=Wilbur C, Bitnun A, Kronenberg S, Laxer RM, Levy DM, Logan WJ, Shouldice M, Yeh EA |title=PANDAS/PANS in childhood: Controversies and evidence |journal=Paediatr Child Health |volume=24 |issue=2 |pages=85–91 |date=May 2019 |pmid=30996598 |pmc=6462125 |doi=10.1093/pch/pxy145}}</ref><ref name=Sigra2018>{{cite journal |vauthors=Sigra S, Hesselmark E, Bejerot S |title=Treatment of PANDAS and PANS: a systematic review |journal=Neurosci Biobehav Rev |volume=86 |pages=51–65 |date=March 2018 |pmid=29309797 |s2cid=40827012 |doi=10.1016/j.neubiorev.2018.01.001 |doi-access=free}}</ref><ref>{{cite journal |vauthors=Sokol MS |title=Infection-triggered anorexia nervosa in children: clinical description of four cases |journal=Journal of Child and Adolescent Psychopharmacology |volume=10 |issue=2 |pages=133–45 |year=2000 |pmid=10933123 |doi=10.1089/cap.2000.10.133}}</ref>
* [[Lesions]]: studies have shown that lesions to the right [[frontal lobe]] or [[temporal lobe]] can cause the pathological symptoms of an eating disorder.<ref>{{cite journal |vauthors=Uher R, Treasure J |title=Brain lesions and eating disorders |journal=Journal of Neurology, Neurosurgery, and Psychiatry |volume=76 |issue=6 |pages=852–7 |date=June 2005 |pmid=15897510 |pmc=1739667 |doi=10.1136/jnnp.2004.048819}}</ref><ref>{{cite journal |vauthors=Houy E, Debono B, Dechelotte P, Thibaut F |title=Anorexia nervosa associated with right frontal brain lesion |journal=The International Journal of Eating Disorders |volume=40 |issue=8 |pages=758–61 |date=December 2007 |pmid=17683096 |doi=10.1002/eat.20439 |doi-access=free}}</ref><ref name="Trummer2002">{{cite journal |vauthors=Trummer M, Eustacchio S, Unger F, Tillich M, Flaschka G |title=Right hemispheric frontal lesions as a cause for anorexia nervosa report of three cases |journal=Acta Neurochirurgica |volume=144 |issue=8 |pages=797–801; discussion 801 |date=August 2002 |pmid=12181689 |doi=10.1007/s00701-002-0934-5 |s2cid=549924}}</ref>
* [[Tumors]]: tumors in various regions of the brain have been implicated in the development of abnormal eating patterns.<ref>{{cite journal |vauthors=Winston AP, Barnard D, D'Souza G, Shad A, Sherlala K, Sidhu J, Singh SP |title=Pineal germinoma presenting as anorexia nervosa: Case report and review of the literature |journal=The International Journal of Eating Disorders |volume=39 |issue=7 |pages=606–8 |date=November 2006 |pmid=17041920 |doi=10.1002/eat.20322}}</ref><ref>{{cite journal |vauthors=Chipkevitch E, Fernandes AC |title=Hypothalamic tumor associated with atypical forms of anorexia nervosa and diencephalic syndrome |journal=Arquivos de Neuro-Psiquiatria |volume=51 |issue=2 |pages=270–4 |date=June 1993 |pmid=8274094 |doi=10.1590/S0004-282X1993000200022 |doi-access=free}}</ref><ref>{{cite journal |vauthors=Rohrer TR, Fahlbusch R, Buchfelder M, Dörr HG |title=Craniopharyngioma in a female adolescent presenting with symptoms of anorexia nervosa |journal=Klinische Padiatrie |volume=218 |issue=2 |pages=67–71 |year=2006 |pmid=16506105 |doi=10.1055/s-2006-921506 |s2cid=37147413}}</ref><ref>{{cite journal |vauthors=Chipkevitch E |title=Brain tumors and anorexia nervosa syndrome |journal=Brain & Development |volume=16 |issue=3 |pages=175–9, discussion 180–2 |year=1994 |pmid=7943600 |doi=10.1016/0387-7604(94)90064-7 |s2cid=4766012}}</ref><ref>{{cite journal |vauthors=Lin L, Liao SC, Lee YJ, Tseng MC, Lee MB |title=Brain tumor presenting as anorexia nervosa in a 19-year-old man |journal=Journal of the Formosan Medical Association = Taiwan Yi Zhi |volume=102 |issue=10 |pages=737–40 |date=October 2003 |pmid=14691602}}</ref>
* Brain [[calcification]]: a study highlights a case in which prior calcification of the right thalumus may have contributed to development of anorexia nervosa.<ref>{{cite journal |vauthors=Conrad R, Wegener I, Geiser F, Imbierowicz K, Liedtke R |title=Nature against nurture: calcification in the right thalamus in a young man with anorexia nervosa and obsessive-compulsive personality disorder |journal=CNS Spectrums |volume=13 |issue=10 |pages=906–10 |date=October 2008 |pmid=18955946 |doi=10.1017/S1092852900017016 |s2cid=13013352}}</ref>
* [[Cortical homunculus|Somatosensory homunculus]]: is the representation of the body located in the [[post central gyrus|somatosensory cortex]], first described by renowned [[neurosurgery|neurosurgeon]] [[Wilder Penfield]]. The illustration was originally termed "Penfield's Homunculus", homunculus meaning little man. "In normal development this representation should adapt as the body goes through its pubertal growth spurt. However, in AN it is hypothesized that there is a lack of plasticity in this area, which may result in impairments of sensory processing and distortion of body image". (Bryan Lask, also proposed by [[VS Ramachandran]])
* [[Obstetrics|Obstetric]] complications: There have been studies done which show [[Smoking and pregnancy|maternal smoking]], obstetric and [[perinatal]] complications such as maternal [[anemia]], very [[Preterm birth|pre-term birth]] (less than 32 weeks), being born [[small for gestational age]], neonatal cardiac problems, [[preeclampsia]], placental infarction and sustaining a [[cephalhematoma]] at birth increase the risk factor for developing either anorexia nervosa or bulimia nervosa. Some of this developmental risk as in the case of placental infarction, maternal anemia and cardiac problems may cause [[intrauterine hypoxia]], umbilical cord occlusion or cord prolapse may cause [[ischemia]], resulting in cerebral injury, the [[prefrontal cortex]] in the [[fetus]] and [[neonate]] is highly susceptible to damage as a result of oxygen deprivation which has been shown to contribute to [[Frontal lobe disorder|executive dysfunction]], [[ADHD]], and may affect personality traits associated with both eating disorders and comorbid disorders such as impulsivity, mental rigidity and obsessionality. The problem of perinatal brain injury, in terms of the costs to society and to the affected individuals and their families, is extraordinary. (Yafeng Dong, PhD)<ref>{{cite journal |vauthors=Burke CJ, Tannenberg AE, Payton DJ |title=Ischaemic cerebral injury, intrauterine growth retardation, and placental infarction |journal=Developmental Medicine and Child Neurology |volume=39 |issue=11 |pages=726–30 |date=November 1997 |pmid=9393885 |doi=10.1111/j.1469-8749.1997.tb07373.x |doi-access=free}}</ref><ref>{{cite journal |vauthors=Cnattingius S, Hultman CM, Dahl M, Sparén P |title=Very preterm birth, birth trauma, and the risk of anorexia nervosa among girls |journal=Archives of General Psychiatry |volume=56 |issue=7 |pages=634–8 |date=July 1999 |pmid=10401509 |doi=10.1001/archpsyc.56.7.634 |doi-access=free}}</ref><ref>{{cite journal |vauthors=Favaro A, Tenconi E, Santonastaso P |s2cid=45181444 |title=Perinatal factors and the risk of developing anorexia nervosa and bulimia nervosa |journal=Archives of General Psychiatry |volume=63 |issue=1 |pages=82–8 |date=January 2006 |pmid=16389201 |doi=10.1001/archpsyc.63.1.82}}</ref><ref>{{cite journal |vauthors=Favaro A, Tenconi E, Santonastaso P |title=The relationship between obstetric complications and temperament in eating disorders: a mediation hypothesis |journal=Psychosomatic Medicine |volume=70 |issue=3 |pages=372–7 |date=April 2008 |pmid=18256341 |doi=10.1097/PSY.0b013e318164604e |s2cid=347034}}</ref><ref>{{cite journal |vauthors=Decker MJ, Hue GE, Caudle WM, Miller GW, Keating GL, Rye DB |title=Episodic neonatal hypoxia evokes executive dysfunction and regionally specific alterations in markers of dopamine signaling |journal=Neuroscience |volume=117 |issue=2 |pages=417–25 |year=2003 |pmid=12614682 |doi=10.1016/S0306-4522(02)00805-9 |s2cid=3104915}}</ref><ref>{{cite journal |vauthors=Decker MJ, Rye DB |title=Neonatal intermittent hypoxia impairs dopamine signaling and executive functioning |journal=Sleep & Breathing = Schlaf & Atmung |volume=6 |issue=4 |pages=205–10 |date=December 2002 |pmid=12524574 |doi=10.1007/s11325-002-0205-y |s2cid=25243556}}</ref><ref>{{cite journal |vauthors=Scher MS |title=Fetal and neonatal neurologic case histories: assessment of brain disorders in the context of fetal-maternal-placental disease. Part 1: Fetal neurologic consultations in the context of antepartum events and prenatal brain development |journal=Journal of Child Neurology |volume=18 |issue=2 |pages=85–92 |date=February 2003 |pmid=12693773 |doi=10.1177/08830738030180020901 |s2cid=643779}}</ref><ref>{{cite journal |vauthors=Scher MS, Wiznitzer M, Bangert BA |title=Cerebral infarctions in the fetus and neonate: maternal-placental-fetal considerations |journal=Clinics in Perinatology |volume=29 |issue=4 |pages=693–724, vi-vii |date=December 2002 |pmid=12516742 |doi=10.1016/S0095-5108(02)00055-6}}</ref><ref>{{cite journal |vauthors=Burke CJ, Tannenberg AE |title=Prenatal brain damage and placental infarction--an autopsy study |journal=Developmental Medicine and Child Neurology |volume=37 |issue=6 |pages=555–62 |date=June 1995 |pmid=7789664 |doi=10.1111/j.1469-8749.1995.tb12042.x |s2cid=32597000}}</ref><ref>{{cite journal |vauthors=Squier M, Keeling JW |title=The incidence of prenatal brain injury |journal=Neuropathology and Applied Neurobiology |volume=17 |issue=1 |pages=29–38 |date=February 1991 |pmid=2057048 |doi=10.1111/j.1365-2990.1991.tb00691.x |s2cid=32778004}}</ref><ref>{{cite journal |vauthors=Al Mamun A, Lawlor DA, Alati R, O'Callaghan MJ, Williams GM, Najman JM |title=Does maternal smoking during pregnancy have a direct effect on future offspring obesity? Evidence from a prospective birth cohort study |journal=American Journal of Epidemiology |volume=164 |issue=4 |pages=317–25 |date=August 2006 |pmid=16775040 |doi=10.1093/aje/kwj209 |doi-access=free}}</ref>
* Symptom of [[starvation]]: Evidence suggests that the symptoms of eating disorders are actually symptoms of the starvation itself, not of a mental disorder. In a study involving thirty-six healthy young men that were subjected to semi-starvation, the men soon began displaying symptoms commonly found in patients with eating disorders.<ref name="CT7">{{cite book |vauthors=Carlson N |year=2013 |chapter=Ingestive Behavior |title=Physiology of Behavior |pages=428–432 |location=University of Massachusetts, Amherst |publisher=Pearson |isbn=978-0-205-23939-9}}</ref><ref name="CT6">{{cite book |vauthors=Keys A, Brozek J, Henschel A, Mickelsen O, Taylor H |title=The Biology of Human Starvation |publisher=University of Minnesota Press |year=1950}}</ref> In this study, the healthy men ate approximately half of what they had become accustomed to eating and soon began developing symptoms and thought patterns (preoccupation with food and eating, ritualistic eating, impaired cognitive ability, other physiological changes such as decreased body temperature) that are characteristic symptoms of anorexia nervosa.<ref name="CT7" /> The men used in the study also developed hoarding and obsessive collecting behaviors, even though they had no use for the items, which revealed a possible connection between eating disorders and [[obsessive–compulsive disorder]].<ref name="CT7" />