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Eating disorders - Biology of appetite and weight regulation

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  • Biochemical:Eating behavior is a complex process controlled by the neuroendocrine system of which the Hypothalamus-pituitary-adrenal-axis (HPA axis) is a major component. Dysregulation of the HPA-axis has been associated with eating disorders,[1][2] such as irregularities in the manufacture, amount or transmission of certain neurotransmitters, hormones[3] or neuropeptides[4].
  • 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 saiety. 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.[14]
  • 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.[15][16]
File:BrainLobesLabelled.jpg
  • infection:PANDAS, is an abbreviation for Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections. Children with PANDAS "have Obsessive Compulsive Disorder (OCD) and/or tic disorders such as Tourette's Syndrome, and in whom symptoms worsen following infections such as "Strep throat" and Scarlet Fever." (NIMH) There is a possibility that PANDAS may be a precipitating factor in the development of Anorexia nervosa in some cases, (PANDAS AN).[17]
  • lesions:studies have shown that lesions to the right frontal lobe or temporal lobe can cause the pathological symptoms of an eating disorder[18][19][20]
  • tumors:tumors in various regions of the brain have been implicated in the development of abnormal eating patterns.[21][22][23][24][25]
  • brain calcification: a study highlights a case in which prior calcification of the right thalumus may have contributed to development of anorexia nervosa.[26]
  • somatosensory homunculus; is the representation of the body located in the somatosensory cortex, first described by renowned neurosurgeon Wilder Penfield. The illustration was originally termed "Penfield's Homunculus", homunculus meaning little man. "In normal development this representation should adapt as the body goes through its pubertal growth spurt. However, in AN it is hypothesized that there is a lack of plasticity in this area, which may result in impairments of sensory processing and distortion of body image". (Bryan Lask, also proposed by VS Ramachandran)
  • Obstetric complications. There have been studies done which show maternal smoking, obstetric and perinatal complications such as maternal anemia, very pre-term birth (32<wks.), 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 this has been shown to contribute to executive dysfunction, ADHD, and may affect personality traits associated with both eating disorders and comorbid disorders such as impulsivity, mental rigidity and obsessionality. The problem of perinatal brain injury, in terms of the costs to society and to the affected individuals and their families, is extraordinary." (Yafeng Dong, PhD) [27][28][29][30][31][32][33][34][35][36][37]

See also=Edit

ReferencesEdit

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  2. Licinio J, Wong ML,The hypothalamic-pituitary-adrenal axis in anorexia nervosa. Gold PW.Psychiatry Res. 1996 Apr 16;62(1):75-83.PMID 8739117
  3. Chaudhri O, Small C, Bloom S. Gastrointestinal hormones regulating appetite. Philos Trans R Soc Lond B Biol Sci. 2006 Jul 29;361(1471):1187-209. PMID 16815798
  4. Gendall KA.Leptin, neuropeptide Y, and peptide YY in long-term recovered eating disorder patients. Biol Psychiatry. 1999 Jul 15;46(2):292-9. PMID 10418705
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  20. Trummer M et al.,Right hemispheric frontal lesions as a cause for anorexia nervosa report of three cases Acta Neurochir (Wien). 2002 Aug;144(8):797-801; discussion 801. PMID 12181689
  21. Winston AP Pineal germinoma presenting as anorexia nervosa: Case report and review of the literature. Int J Eat Disord. 2006 Nov;39(7):606-8. PMID 17041920
  22. Chipkevitch E, Fernandes AC. Hypothalamic tumor associated with atypical forms of anorexia nervosa and diencephalic syndrome. Arq Neuropsiquiatr. 1993 Jun;51(2):270-4. PMID 8274094
  23. Rohrer TR et al.Craniopharyngioma in a female adolescent presenting with symptoms of anorexia nervosa. Klin Padiatr. 2006 Mar-Apr;218(2):67-71. PMID 16506105
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