Eating disorder: Difference between revisions
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* [[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]]) |
* [[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]]) |
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* [[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]] (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 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 | doi = 10.1111/j.1469-8749.1997.tb07373.x | last1 = Burke | first1 = CJ | last2 = Tannenberg | first2 = AE | last3 = Payton | first3 = DJ | title = Ischaemic cerebral injury, intrauterine growth retardation, and placental infarction | journal = Developmental medicine and child neurology | volume = 39 | issue = 11 | pages = 726–30 | year = 1997 | pmid = 9393885 }}</ref><ref>{{cite journal | doi=10.1001/archpsyc.56.7.634 | last1=Cnattingius | first1=S | last2=Hultman | first2=CM | last3=Dahl | first3=M | last4=Sparén | first4=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 | year=1999 |pmid= 10401509 }}</ref><ref>{{cite journal | last1 = Favaro | first1 = A | last2 = Tenconi | first2 = E | last3 = Santonastaso | first3 = P | 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 | year = 2006 | pmid = 16389201 | doi = 10.1001/archpsyc.63.1.82 }}</ref><ref>{{cite journal | last1 = Favaro | first1 = A | last2 = Tenconi | first2 = E | last3 = Santonastaso | first3 = 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 | year = 2008 | pmid = 18256341 | doi = 10.1097/PSY.0b013e318164604e }}</ref><ref>{{cite journal | doi = 10.1016/S0306-4522(02)00805-9 | last1 = Decker | first1 = MJ | last2 = Hue | first2 = GE | last3 = Caudle | first3 = WM | last4 = Miller | first4 = GW | last5 = Keating | first5 = GL | last6 = Rye | first6 = 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 }}</ref><ref>{{cite journal | last1 = Decker | first1 = MJ | last2 = Rye | first2 = DB | title = Neonatal intermittent hypoxia impairs dopamine signaling and executive functioning | journal = Sleep & breathing = Schlaf & Atmung | volume = 6 | issue = 4 | pages = 205–10 | year = 2002 | pmid = 12524574 | doi = 10.1007/s11325-002-0205-y }}</ref><ref>{{cite journal | doi = 10.1177/08830738030180020901 | last1 = Scher | first1 = 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 | year = 2003 | pmid = 12693773 }}</ref><ref>{{cite journal | doi = 10.1016/S0095-5108(02)00055-6 | last1 = Scher | first1 = MS | last2 = Wiznitzer | first2 = M | last3 = Bangert | first3 = 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 | year = 2002 | pmid = 12516742 }}</ref><ref>{{cite journal | doi = 10.1111/j.1469-8749.1995.tb12042.x | last1 = Burke | first1 = CJ | last2 = Tannenberg | first2 = AE | title = Prenatal brain damage and placental infarction--an autopsy study | journal = Developmental medicine and child neurology | volume = 37 | issue = 6 | pages = 555–62 | year = 1995 | pmid = 7789664 }}</ref><ref>{{cite journal | doi = 10.1111/j.1365-2990.1991.tb00691.x | last1 = Squier | first1 = M | last2 = Keeling | first2 = JW | title = The incidence of prenatal brain injury | journal = Neuropathology and applied neurobiology | volume = 17 | issue = 1 | pages = 29–38 | year = 1991 | pmid = 2057048 }}</ref><ref>{{cite journal | last1 = Al Mamun | first1 = A | last2 = Lawlor | first2 = DA | last3 = Alati | first3 = R | last4 = O'Callaghan | first4 = MJ | last5 = Williams | first5 = GM | last6 = Najman | first6 = 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 | year = 2006 | pmid = 16775040 | doi = 10.1093/aje/kwj209 }}</ref> |
* [[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]] (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 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 | doi = 10.1111/j.1469-8749.1997.tb07373.x | last1 = Burke | first1 = CJ | last2 = Tannenberg | first2 = AE | last3 = Payton | first3 = DJ | title = Ischaemic cerebral injury, intrauterine growth retardation, and placental infarction | journal = Developmental medicine and child neurology | volume = 39 | issue = 11 | pages = 726–30 | year = 1997 | pmid = 9393885 }}</ref><ref>{{cite journal | doi=10.1001/archpsyc.56.7.634 | last1=Cnattingius | first1=S | last2=Hultman | first2=CM | last3=Dahl | first3=M | last4=Sparén | first4=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 | year=1999 |pmid= 10401509 }}</ref><ref>{{cite journal | last1 = Favaro | first1 = A | last2 = Tenconi | first2 = E | last3 = Santonastaso | first3 = P | 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 | year = 2006 | pmid = 16389201 | doi = 10.1001/archpsyc.63.1.82 }}</ref><ref>{{cite journal | last1 = Favaro | first1 = A | last2 = Tenconi | first2 = E | last3 = Santonastaso | first3 = 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 | year = 2008 | pmid = 18256341 | doi = 10.1097/PSY.0b013e318164604e }}</ref><ref>{{cite journal | doi = 10.1016/S0306-4522(02)00805-9 | last1 = Decker | first1 = MJ | last2 = Hue | first2 = GE | last3 = Caudle | first3 = WM | last4 = Miller | first4 = GW | last5 = Keating | first5 = GL | last6 = Rye | first6 = 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 }}</ref><ref>{{cite journal | last1 = Decker | first1 = MJ | last2 = Rye | first2 = DB | title = Neonatal intermittent hypoxia impairs dopamine signaling and executive functioning | journal = Sleep & breathing = Schlaf & Atmung | volume = 6 | issue = 4 | pages = 205–10 | year = 2002 | pmid = 12524574 | doi = 10.1007/s11325-002-0205-y }}</ref><ref>{{cite journal | doi = 10.1177/08830738030180020901 | last1 = Scher | first1 = 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 | year = 2003 | pmid = 12693773 }}</ref><ref>{{cite journal | doi = 10.1016/S0095-5108(02)00055-6 | last1 = Scher | first1 = MS | last2 = Wiznitzer | first2 = M | last3 = Bangert | first3 = 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 | year = 2002 | pmid = 12516742 }}</ref><ref>{{cite journal | doi = 10.1111/j.1469-8749.1995.tb12042.x | last1 = Burke | first1 = CJ | last2 = Tannenberg | first2 = AE | title = Prenatal brain damage and placental infarction--an autopsy study | journal = Developmental medicine and child neurology | volume = 37 | issue = 6 | pages = 555–62 | year = 1995 | pmid = 7789664 }}</ref><ref>{{cite journal | doi = 10.1111/j.1365-2990.1991.tb00691.x | last1 = Squier | first1 = M | last2 = Keeling | first2 = JW | title = The incidence of prenatal brain injury | journal = Neuropathology and applied neurobiology | volume = 17 | issue = 1 | pages = 29–38 | year = 1991 | pmid = 2057048 }}</ref><ref>{{cite journal | last1 = Al Mamun | first1 = A | last2 = Lawlor | first2 = DA | last3 = Alati | first3 = R | last4 = O'Callaghan | first4 = MJ | last5 = Williams | first5 = GM | last6 = Najman | first6 = 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 | year = 2006 | pmid = 16775040 | doi = 10.1093/aje/kwj209 }}</ref> |
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it makes you very sick and is horrible for health, please love your boby and LISTEN TO RASSHIL. |
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=== Psychological === |
=== Psychological === |
Revision as of 21:36, 7 December 2012
This article may require cleanup to meet Wikipedia's quality standards. The specific problem is: Invalid templates, bad wiki syntax. (May 2012) |
Eating disorder | |
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Specialty | Psychiatry, clinical psychology |
Eating disorders are conditions defined by abnormal eating habits that may involve either insufficient or excessive food intake to the detriment of an individual's physical and mental health. Bulimia nervosa, anorexia nervosa, and binge eating disorder are the most common specific forms in the United Kingdom.[1] Though primarily thought of as affecting females (an estimated 5–10 million being affected in the U.K.), eating disorders affect males as well. An estimated 10 – 15% of people with eating disorders are males (Gorgan, 1999). (an estimated 1 million U.K. males being affected).[2][3][4] Although eating disorders are increasing all over the world among both men and women, there is evidence to suggest that it is women in the Western world who are at the highest risk of developing them and the degree of westernization increases the risk.[5] Nearly half of all Americans personally know someone with an eating disorder. The skill to comprehend the central processes of appetite has increased tremendously since leptin was discovered, and the skill to observe the functions of the brain as well.[6]
The precise cause of eating disorders is not entirely understood, but there is evidence that it may be linked to other medical conditions and situations. Cultural idealization of thinness and youthfulness have contributed to eating disorders affecting diverse populations. One study showed that girls with ADHD have a greater chance of getting an eating disorder than those not affected by ADHD.[7][8] Another study suggested that women with PTSD, especially due to sexually related trauma, are more likely to develop anorexia nervosa.[9] One study showed that foster girls are more likely to develop bulimia nervosa.[10] Some think that peer pressure and idealized body-types seen in the media are also a significant factor. Some research show that for certain people there are genetic reasons why they may be prone to developing an eating disorder.[11]
While proper treatment can be highly effective for many suffering from specific types of eating disorders, the consequences of eating disorders can be severe, including death[12][12][13] (whether from direct medical effects of disturbed eating habits or from comorbid conditions such as suicidal thinking).[1][14]
Classification
- Anorexia nervosa (AN), characterized by refusal to maintain a healthy body weight, an obsessive fear of gaining weight, and an unrealistic perception of current body weight. However, some patients can suffer from Anorexia nervosa unconsciously. These patients are classified under "atypical eating disorders". Anorexia can cause menstruation to stop, and often leads to bone loss, loss of skin integrity, etc. It greatly stresses the heart, increasing the risk of heart attacks and related heart problems. The risk of death is greatly increased in individuals with this disease.[15]
- Bulimia nervosa (BN), characterized by recurrent binge eating followed by compensatory behaviors such as purging (self-induced vomiting, excessive use of laxatives/diuretics, or excessive exercise). Fasting and over exercise may also be used as a method of purging following a binge.
- Eating disorders not otherwise specified (EDNOS) is an eating disorder that does not meet the DSM-IV criteria for anorexia or bulimia.[16] Examples can be a female who suffers from anorexia but still has her period or someone who may be at a "healthy weight" but who has anorexic thought patterns and behaviors; it can mean the sufferer equally participates in some anorexic as well as bulimic behaviors (sometimes referred to as purge-type anorexia) or to any combination of eating disorder behaviors that do not directly put them in a separate category.[17]
- Binge eating disorder (BED) or 'compulsive overeating', characterized by binge eating, without compensatory behavior. This type of eating disorder is even more common than bulimia or anorexia. This disorder does not have a category of people in which it can develop. In fact, this disorder can develop in a range of ages and is unbiased to classes.[18][19]
- Compulsive overeating, (COE) characteristic of binge eating disorder, in which people tend to eat more than necessary resulting in more stress. This is mainly caused by 'binge eating disorder'.[20]
- Purging disorder, characterized by recurrent purging to control weight or shape in the absence of binge eating episodes.
- Rumination, characterized by involving the repeated painless regurgitation of food following a meal which is then either re-chewed and re-swallowed, or discarded.
- Diabulimia, characterized by the deliberate manipulation of insulin levels by diabetics in an effort to control their weight.
- Food maintenance, characterized by a set of aberrant eating behaviors of children in foster care.[21]
- Pica, characterized by a compulsive craving for eating, chewing or licking non-food items or foods containing no nutrition. These can include such things as chalk, paper, plaster, paint chips, baking soda, starch, glue, rust, ice, coffee grounds, and cigarette ashes. These individuals cannot distinguish a difference between food and non food items.
- Night eating syndrome, characterized by morning anorexia, evening polyphagia (abnormally increased appetite for consumption of food (frequently associated with insomnia, and injury to the hypothalamus).
- Orthorexia nervosa, a term used by Steven Bratman to characterize an obsession with a "pure" diet, in which people develop an obsession with avoiding unhealthy foods to the point where it interferes with a person's life.
- Drunkorexia, commonly characterized by purposely restricting food intake in order to reserve food calories for alcoholic calories, exercising excessively in order to burn calories consumed from drinking, and over-drinking alcohols in order to purge previously consumed food.[22]
- Pregorexia, characterized by extreme dieting and over-exercising in order to control pregnancy weight gain. Undernutrition during pregnancy is associated with low birth weight, coronary heart disease, type 2 diabetes, stroke, hypertension, cardiovascular disease risk, and depression.[23]
Several of the above mentioned disorders, such as diabulimia, food maintenance syndrome and orthorexia nervosa, are not currently recognized as mental disorders in any of the medical manuals, such as the ICD-10[24] or the DSM-IV.[25]
Causes
The specific cause/ causes of eating disorders are unknown. However, it is believed to be due to a combination of biological, psychological and/or environmental abnormalities. A common belief is that "Genetics loads the gun, environment pulls the trigger."[citation needed] This would mean that some people are born with a predisposition to it, which can be brought to the surface pending on environment and reactions to it. Many people with eating disorders suffer also from body dysmorphic disorder, altering the way a person sees themselves.[citation needed] There are also many other possibilities such as environmental, social and interpersonal issues that could promote and sustain this illness.[26] Also, the media are oftentimes blamed for the rise in the incidence of eating disorders due to the fact that media images of idealized slim physical shape of people such as models and celebrities motivate or even force people to attempt to achieve slimness themselves. The media are accused of distorting reality, in the sense that people portrayed in the media are either naturally thin and thus unrepresentative of normality or unnaturally thin by forcing their bodies to look like the ideal image by putting excessive pressure on themselves to look a certain way.[27]
Biological
- Genetic: Numerous studies have been undertaken that show a possible genetic predisposition toward eating disorders as a result of Mendelian inheritance.[28][28][29]
- Epigenetics: Epigenetic mechanisms are means by which environmental effects alter gene expression via methods such as DNA methylation; these are independent of and do not alter the underlying DNA sequence. They are heritable, but also may occur throughout the lifespan, and are potentially reversible. Dysregulation of dopaminergic neurotransmission due to epigenetic mechanisms has been implicated in various eating disorders.[30]
"We conclude that epigenetic mechanisms may contribute to the known alterations of ANP homeostasis in women with eating disorders."[30][31]
- 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,[32][33] such as irregularities in the manufacture, amount or transmission of certain neurotransmitters, hormones[34] or neuropeptides[35] and amino acids such as homocysteine, elevated levels of which are found in AN and BN as well as depression.[36]
- serotonin: a neurotransmitter involved in depression also has an inhibitory effect on eating behavior.[37][38][39][40][41]
- norepinephrine is both a neurotransmitter and a hormone; abnormalities in either capacity may affect eating behavior.[42][43]
- dopamine: which in addition to being a precursor of norepinephrine and epinephrine is also a neurotransmitter which regulates the rewarding property of food.[44][45]
- 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.[46]
- 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.[47][48]
- 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 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).[49]
- lesions: studies have shown that lesions to the right frontal lobe or temporal lobe can cause the pathological symptoms of an eating disorder.[50][51][52]
- tumors: tumors in various regions of the brain have been implicated in the development of abnormal eating patterns.[53][54][55][56][57]
- brain calcification: a study highlights a case in which prior calcification of the right thalumus may have contributed to development of anorexia nervosa.[58]
- 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 which 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)[59][60][61][62][63][64][65][66][67][68][69]
it makes you very sick and is horrible for health, please love your boby and LISTEN TO RASSHIL.
Psychological
Eating disorders are classified as Axis I[70] disorders in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM-IV) published by the American Psychiatric Association. There are various other psychological issues that may factor into eating disorders, 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.[71] Some people have a previous disorder which may increase their vulnerability to developing an eating disorder.[72][73][74] Some develop them afterwards.[75] The severity and type of eating disorder symptoms have been shown to affect comorbidity.[76] The DSM-IV should not be used by laypersons to diagnose themselves, even when used by professionals there has been considerable controversy over the diagnostic criteria used for various diagnoses, including eating disorders. There has been controversy over various editions of the DSM including the latest edition, DSM-V, due in May 2013.[77][78][79][80][81]
Cognitive bias in eating disorders
Attentional bias is the inclination to believe that an emotionally dominant stimuli attracts and controls the attention of a person. This person will neglect information that does not comply with the emotionally dominant stimuli and it will affect them when making judgments in relation to the stimuli It is believed that attentional bias has an effect on eating disorders. Many studies have been performed to test this theory such as studies by Shafran, Lee, Cooper, Palmer & Fairburn (2007), Veenstra and de Jong (2012) and Smeets, Jansen, & Roefs (2005).
Evidence of the Effect of Attentional Bias on Eating Disorders
In each of these three studies the experimenters, found that attentional bias is present in eating disorders. Each study is explained in one of the following sections. The Shafran (2009) experiment is explained in the subsection Attentional Bias Compared to Control Groups. The Veenstra (2012) experiment is explained in the Attention Bias in Anorexia Nervosa subsection and the Jansen (2005) experiment is explained in the subsection Attentional Bias in body dissastifaction section. Finally all of these experiments’ relevance is explained in the Relevance of Studies on Attentional Biases on the Treatment of Eating Disorders subsection.
Attentional Bias compared to Control Groups
One of the studies that concentrated on testing if attentional bias has an effect on eating disorders is one performed by Shafran, Lee, Cooper, Palmer and Fairburn (2007). The hypothesis for this experiment was that attentional biases will be more prevalent for eating weight and shape in patients who suffered from an eating disorder than in the control groups. The participants were five groups of volunteers. The first group consisted of 23 females with eating disorders (anorexia, bulimia, and eating disorders not otherwise specified.) The control groups consisted of volunteers with low, moderate, and high levels of interest in their size and one group of females who had a high level of anxiety. These participants were instructed to rate each picture by their emotional response to the picture as either “good” “bad” or “neutral.” Their emotional response to the picture was operationalized by how the picture made them feel. If the person in the picture seemed to be portraying bad eating habits, such as eating high calorie food or binge eating or a thicker body picture, they would consider it “bad”. If the person in the picture was portraying healthy eating tips and slim bodies the picture was considered “good” and if the person did not feel either way about the picture, or it consisted of body parts not associated with weight it was considered “neutral. In this study the experimenters showed participants four different groups of pictures. The first three groups were pictures portraying good, bad and neutral pictures in relation to eating, weight and shape. The fourth group was the control group, showing pictures of animals. There were four separate measures for this experiment. They involved the Eating Disorder Examination, The Beck Depression Inventory II, BAI and their Body Mass Index. The Eating Disorder Examination rated the behavioral functions of eating disorders. Some of these functions are episodes of binge eating, restriction of food, and vomiting. It also creates subscales that measure concern for the weight, shape and eating habits. The Beck Depression Inventory II assess if the participant suffers from depression or symptoms of depression. The BAI helps rate the person’s anxiety levels, and the person’s Body Mass Index indicates how much body fat a person has based on their height and weight. For statistical purposes experimenters performed an ANOVA for compare the five different variables and ANCOVA to account for the BMI and the Depression scores. The results indicate that there was a significant bias for the “good” body image pictures shown by patients with an eating disorder. The participants with an eating disorder took longer to decide if the positive pictures were “good” than it took them to decide if the negative pictures were “bad”. The results show that there was no differences for the neutral and shapes groups across the three different conditions. The hypothesis for this experiment was supported and shows that although females in the different level of anxiety control group all share the same attentional biases, females with eating disorders suffer from different attentional baises. The data show that participants with eating disorders responded quicker to the probe when it showed a negative eating picture, than when it showed a positive eating picture. This study tested attentional bias in several different types of eating disorders. Future studies could expand upon this and concentrate on one specific type of eating disorder and how attentional bias affects that disorder.
Attentional Bias in Anorexia Nervosa
A study that studies a more specific section of eating disorders is one performed by Veenstra and de Jong (2012.) The experimenters looked at restrictive type of anorexia nervosa and how attentional bias affects how they select what they eat. Anorexic participants are very good at restricting their food intake. The experimenters tested to determine if patients that were diagnosed with anorexia showed attentional biased against pictures of food. The researchers found that both the control and the eating disorder patients showed attentional bias against high fat foods and negative eating pictures. The eating disorder patients showed a larger attentional bias against the foods that are considered “bad.” They also found that this could facilitate the restricted food intake of the eating disorder patients.
Attentional Bias in body dissatisfaction
Smeets, Jansen, & Roefs (2005) studied body dissatisfaction and its relation to attentional bias. Another aspect to attentional blindness is selective attention. This study tested to determine if selective attention has an impact on eating disorders and body dissatisfaction. The experimenters hypothesized that the eating disorder patients would concentrate and pay more attention to the parts of their bodies that they find unattractive, and the healthy control groups would pay more attention to the parts of their body that they find attractive. The experimenters tested to determine if an experimentally created bias for body parts that are attractive, will help induce body satisfaction in participants who are not happy or satisfied with their bodies. For this experiment the experimenters had the participants use an eye tracker which tracked the parts of their bodies that they defined unattractive or attractive. The results show that the induced bias for unattractive body parts made the participants feel worse about themselves and their body satisfaction decreased and the opposite happened when they showed the participants a positive bias. When the experimenters showed the body-dissatisfied participants the positive body their body satisfaction increased.
Relevance of Studies on Attentional Biases on the Treatment of Eating Disorders
In conclusion, there are many different studies that have been performed to try to determine if attentional bias has an effect on eating disorders. According to the studies previously discussed it seems that the hypothesis is supported and that attentional bias has an effect on eating disorders, on how a person restricts their diet and body dissatisfaction. These studies are important to the field because they can lead to better intervention strategies when it comes to counseling individuals with eating disorders. Jansen’s (2005) experiment can lead counselors and other therapists to build a program in order to help eating disorder patients to feel better about their bodies by creating a positive bias.
Personality traits
There are various childhood personality traits associated with the development of eating disorders.[95] During adolescence these traits may become intensified due to a variety of physiological and cultural influences such as the hormonal changes associated with puberty, stress related to the approaching demands of maturity and socio-cultural influences and perceived expectations, especially in areas that concern body image. Many personality traits have a genetic component and are highly heritable. Maladaptive levels of certain traits may be acquired as a result of anoxic or traumatic brain injury, neurodegenerative diseases such as Parkinson's disease, neurotoxicity such as lead exposure, bacterial infection such as Lyme disease or viral infection such as Toxoplasma gondii as well as hormonal influences. While studies are still continuing via the use of various imaging techniques such as fMRI; these traits have been shown to originate in various regions of the brain[96] such as the amygdala[97][98] and the prefrontal cortex[99] Disorders in the prefrontal cortex and the executive functioning system have been shown to affect eating behavior.[100][101]
Environmental
Child maltreatment
Child abuse which encompasses physical, psychological and sexual abuse, as well as neglect has been shown by innumerable studies to be a precipitating factor in a wide variety of psychiatric disorders, including eating disorders. Children who are subjected to abuse may develop eating disorders in an effort to gain some sense of control or for a sense of comfort, or they may be in an environment where the diet is unhealthy or insufficient. Child abuse and neglect can cause profound changes in both the physiological structure and the neurochemistry of the developing brain. Children who, as wards of the state, were placed in orphanages or foster homes are especially susceptible to developing a disordered eating pattern. In a study done in New Zealand 25% of the study subjects in foster care exhibited an eating disorder (Tarren-Sweeney M. 2006). An unstable home environment is detrimental to the emotional well-being of children, even in the absence of blatant abuse or neglect the stress of an unstable home can contribute to the development of an eating disorder.[102][103][104][105][106][107][108][109][110]
Social isolation
Social isolation has been shown to have a deleterious effect on an individual's physical and emotional well-being. Those that are socially isolated have a higher mortality rate in general as compared to individuals that have established social relationships. This effect on mortality is markedly increased in those with pre-existing medical or psychiatric conditions, and has been especially noted in cases of coronary heart disease. "The magnitude of risk associated with social isolation is comparable with that of cigarette smoking and other major biomedical and psychosocial risk factors." (Brummett et al.)
Social isolation can be inherently stressful, depressing and anxiety provoking. In an attempt to ameliorate these distressful feelings an individual may engage in emotional eating in which food serves as a source of comfort. The loneliness of social isolation and the inherent stressors thus associated have been implicated as triggering factors in binge eating as well.[111][112][113][114]
Waller, Kennerley and Ohanian (2007) argued that both bingeing–vomiting and restriction are emotion suppression strategies, but they are just utilized at different times. For example, restriction is used to pre-empt any emotion activation, while bingeing– vomiting is used after an emotion has been activated[115]
Parental influence
Parental influence has been shown to be an intrinsic component in the development of eating behaviors of children. This influence is manifested and shaped by a variety of diverse factors such as familial genetic predisposition, dietary choices as dictated by cultural or ethnic preferences, the parents' own body shape and eating patterns, the degree of involvement and expectations of their children's eating behavior as well as the interpersonal relationship of parent and child. This is in addition to the general psychosocial climate of the home and the presence or absence of a nurturing stable environment. It has been shown that maladaptive parental behavior has an important role in the development of eating disorders. As to the more subtle aspects of parental influence it has been shown that eating patterns are established in early childhood and that children should be allowed to decide when their appetite is satisfied as early as the age of two. A direct link has been shown between obesity and parental pressure to eat more.
Coercive tactics in regard to diet have not been proven to be efficacious in controlling a child's eating behavior. Affection and attention have been shown to affect the degree of a childs' finickiness and their acceptance of a more varied diet.[116][117][118][119][120][121]
Peer pressure
In various studies such as one conducted by The McKnight Investigators, peer pressure was shown to be a significant contributor to body image concerns and attitudes toward eating among subjects in their teens and early twenties.
Eleanor Mackey and co-author, Annette M. La Greca of the University of Miami, studied 236 teen girls from public high schools in southeast Florida. "Teen girls' concerns about their own weight, about how they appear to others and their perceptions that their peers want them to be thin are significantly related to weight-control behavior," says psychologist Eleanor Mackey of the Children's National Medical Center in Washington and lead author of the study. "Those are really important."
According to one study, 40% of 9- and 10-year-old girls are already trying to lose weight.[122] Such dieting is reported to being influenced by peer behavior, with many of those individuals on a diet reporting that their friends also were dieting. The number of friends dieting and the number of friends who pressured them to diet also played a significant role in their own choices.[123][124][125][126]
Elite athletes have a significantly higher rate in eating disorders. Female athletes in sports such as gymnastics, ballet, diving, etc. are found to be at the highest risk among all athletes. Women are more likely than men to acquire an eating disorder between the ages of 13-30. !0-15% of those with Bulimia and Anorexia are men.[citation needed]
Cultural pressure
There is a cultural emphasis on thinness which is especially pervasive in western society. There is an unrealistic stereotype of what constitutes beauty and the ideal body type as portrayed by the media, fashion and entertainment industries. "The cultural pressure on men and women to be "[perfect]" is an important predisposing factor for the development of eating disorders" (Prof. Bryan Lask).[127][128] Further, when women of all races base their evaluation of their self upon what is considered the culturally ideal body, the incidence of eating disorders increases.[129] Eating disorders are becoming more prevalent in non Western countries where thinness is not seen as the ideal, showing that social and cultural pressures are not the only causes of eating disorders.[130] For example, observations of anorexia in all of the non-Western regions of the world point to the disorder not being “culture-bound” as once thought.[131] However, studies on rates of bulimia suggest that it might be culturally bound. In non-Western countries, bulimia is less prevalent than anorexia, but these non-Western countries where it is observed can be said to have probably or definitely been influenced or exposed to Western culture and ideology.[132]
Socioeconomic status has been viewed as a risk factor for eating disorders, presuming that possessing more resources allows for an individual to actively choose to diet and reduce body weight.[133] Some studies have also shown a relationship between increasing body dissatisfaction with increasing socioeconomic status.[134] However, once high SES has been achieved, this relationship weakens and, in some cases, no longer exists.[135]
It is important to realize some of the limitations and challenges of many studies that try to examine the roles of culture, ethnicity, and SES. For starters, most of the cross-cultural studies use definitions from the DSM-IV-TR, which has been criticized as reflecting a Western cultural bias. Thus, assessments and questionnaires may not be constructed to detect some of the cultural differences associated with different disorders. Also, when looking at individuals in areas potentially influenced by Western culture, few studies have attempted to measure how much an individual has adopted the mainstream culture or retained the traditional cultural values of the area. Lastly, the majority of the cross-cultural studies on eating disorders and body image disturbances occurred in Western nations and not in the countries or regions being examined.[136]
While there are many influences to how an individual processes their body image, the media does play a major role. Along with the media, parental influence, peer influence, and self-efficacy beliefs also play a large role in an individual’s view of themselves.The way the media presents images can have a lasting effect on an individual’s perception of their body image. Eating disorders are a worldwide issue and while women are more likely to be affected by an eating disorder it still affects both genders (Schwitzer 2012). The media has an impact on eating disorders whether shown in a positive or negative light, it then has a responsibility to use caution when promoting images that projects an ideal that many turn to eating disorders to attain. [137]
Pro-Ana Subculture
Pro-anorexic websites are a trend that allow individuals to communicate in order to maintain eating disorders. Members of these websites typically feel that their eating disorder is the only aspect of a chaotic life that they can control.[138] These pro-anorexic websites are interactive and have discussion boards where individuals can share ideas on diet and exercise plans that have allowed them to achieve dangerously low weights.[139]
In men
To date, the evidence suggests that the gender bias of clinicians means that diagnosing either bulimia or anorexia in men is less likely despite identical behavior. Men are more likely to be diagnosed as suffering depression with associated appetite changes than receive a primary diagnosis of an eating disorder. Using examples from a Canadian context below, it is possible to engage with some of the more nuanced issues facing men suffering from disordered eating.
There are many societal, familial and individual factors that can influence the development of an eating disorder. Individuals who are struggling with their identity and self-image can be at risk, as well as those who have experienced a traumatic event (A Report on Mental Illness in Canada, 2002). In addition, many sufferers of eating disorders report feeling powerless about their socioeconomic environment, and view dieting, exercise and purging as empowering means of controlling their lives. The conventional approach (Trebay, 2008 and Derenne & Beresin, 2006) to understanding the root causes of disordered eating focuses on the role of media and sociocultural pressures; an emphasis on thinness (for women) and muscularity (for men) often goes beyond simple body image. There is an implicit media message that not only are those with ‘ideal’ bodies can be more confident, successful, healthy and happy but that slimness is associated with positive character qualities, such as reliability, trustworthiness and honesty (Harvey & Robinson, 2003).The traditional understanding of eating disorders reflects a media construct where thin and attractive people are not only the most successful and desirable members of the community, but rather they are the only members of the community who can be attractive and desirable.
In such a view, society is focused on appearance; body image becomes central to young people’s feelings of self-esteem and self-worth — overshadowing qualities and achievements in other aspects of their lives (Maine & Bunnell, 2008). Teenagers may associate success or acceptance by their peers with achieving the ‘perfect’ physical standard portrayed by the media. As a result, during the period where children and teenagers become increasingly more exposed to prevailing cultural norms, both males and females are at risk of developing skewed conceptions of self and their bodies (Andersen & Homan, 1997). When the desired goals are not met of achieving the ideal body image, they might experience feelings of failure that contribute to further drop in self-esteem, confidence, and an increase in body image dissatisfaction. Some also suffer psychological and physical costs such as feelings of shame, failure, deprivation, and yo-yo dieting (Maine & Bunnell, 2008). Eating disorders may cause individuals to feel tired and depressed, decreased mental functioning and concentration, and can lead to malnutrition with risk to bone health, physical growth, and brain development. There are also increased risks of osteoporosis and fertility problems, weakened immune system, heart rate, blood pressure and metabolic rate is also decreased (NEDIC, 2006). Additionally, sufferers from eating disorders show the third highest susceptibility for self-abuse and suicide, with rates 13.6 and 9.8 times higher than the Canadian average, respectively (Löwe et al., 2001).
Until recently, eating disorders have been characterized as an almost exclusively female problem (Maine and Bunnell 2008). The majority of early academic scholarship during the early 1990s tended to dismiss the prevalence in men as largely, if not entirely, irrelevant when compared to that in women (Weltzin et al. 2005.). Only recently have sociologists and feminist thinkers expanded the scope of eating disorders to identify with the unique challenges facing male sufferers.
Eating disorders are the third most common chronic illness in adolescent boys (NEDIC, 2006). Using currently available data, it is estimated that 3% of men will be affected by eating disorders in their lifetime (Public Health Agency of Canada, 2002). Eating disorder rates are not only increasing among females but also males are more concerned with their body image than ever before. The Public Health Agency of Canada (2002) found that almost one in every two girls and almost one in every five boys of grade 10 either were on a diet or wanted to lose weight. Since 1987, hospitalizations for eating disorders in general hospitals have increased by 34% among young men under the age of 15 and by 29% among men between 15–24 years old (Public Health Agency of Canada, 2002). Across Canada, age-standardized hospital separation rates for eating disorders were highest among men in British Columbia (15.9 per 100,000) and New Brunswick (15.1 per 100,000) and lowest in Saskatchewan (8.6) and Alberta (8.6 per 100,000) (Public Health Agency of Canada, 2002).
Part of the challenge with addressing the prevalence of eating disorders in men is a lack of research and statistics that are both current and appropriate. Recent work, such as that by Schoen and Greenberg (Greenberg & Schoen, 2008) suggests that the same prevailing social factors which led to a rise in eating disorders amongst women in the late 1980s may have also clouded public perceptions of similar male vulnerabilities. As a result, male eating disorders and prevalence have been underreported and misdiagnosed. Specifically, attention has recently been drawn to the gendered nature of diagnosis and dissimilar methods of presentation in men; diagnostic criteria focusing on weight loss, fear of fat and physical symptoms such as amenorrhea are cannot be applied to male sufferers, many of whom exercise excessively, are concerned with muscularity and definition rather than absolute weight loss and rebel against terms such as ‘fear of fat’, which they view as disempowering and effeminising (Derenne & Beresin, 2006). As a result of these earlier attempts to express eating disorders amongst men using the language and concepts of non-comparable disorders amongst women, there is a substantial lack of data on prevalence, incidence and burden of disease for men, with much of what is available difficult to evaluate, poorly reported or simple incorrect.
The message that there is no ideal size, shape or weight that every individual should strive to achieve is still largely targeted at women, and those campaigns which include men still prominently feature gendered iconography (such as the ribbon), further raising the barrier to access for male sufferers (Maine & Bunnell, 2008). Male body image is not as homogenous in the media (that is, there range for ‘acceptable’ male physiques is wider), but instead focuses on perceived or projected masculinity (Gaughen, 2004, 7 and Maine & Bunnell, 2008). More pressingly, there is no consensus in the literature regarding unique risk factors as they relate to gay or bisexual men; the US center for Population Research in LGBT health estimates prevalence in the LGBT community to be about twice the national average for women and approximately 3.5 times higher for men. At the same time, a similar research study (Feldman & Meyer, 2007) fails to establish an explanatory framework to address these findings, and a subsequent study (Hatzenbuehler et al., 2009) suggests that membership in the LGBT community offers some protection against psychiatric morbidity, including that from eating disorders. As mentioned above, a distinct lack of research is continues to present a barrier to drawing a broad conclusion on this topic.
Existing treatment for men with eating disorders occurs in a similar environment as that for women. Men living in isolated, rural or small communities who are experiencing violence that sometimes lead to eating disorders face barriers accessing the treatment, as well as additional stigma due to suffering from a ‘feminine’ disease (Public Health Agency of Canada, 2002). The Public Health Agency of Canada (2011 report) also states that integrated treatment approaches to family violence and eating disorders are likely to become increasingly scarce as the resources required to ensure accessibility to services, appropriate medical care, sufficient staffing, shelters and transition houses and counseling for underlying abuse issues are no longer available. Many cases in Canada are referred to USA for the treatments due to the lack of appropriate services offered (Vitiello & Lederhendler 2000). For example, in one case, a patient suffering from anorexia nervosa, originally admitted to The Hospital For Sick Children in Toronto was later recommended for a transfer to a facility in Arizona (Jones, 2007). In 2006, the province of Ontario alone sent 45 patients (36 of them male) to the US for eating disorder treatment at a gross cost of $ 3,719,440 (Jones, 2007), a decision motivated by the lack of specialized facilities domestically.
Speaking from the feminist relational position, Maine and Bunnell (2008) suggest a unique approach towards managing eating disorders in men. They advocate for counseling that focuses on how patients respond to pressures and expectations rather than on addressing the individual pathology of disordered eating. Current treatments in this vein show some success (Public Health Agency of Canada, 2011), but lack patient-based review and feedback. Monitoring of physical symptoms, behavioral therapy, cognitive therapy, body image therapy, nutritional counseling, education and medication if necessary are currently available in some form, yet all of these programs are delivered regardless of patient gender (Public Health Agency, 2002 and Maine & Bunnell, 2008). Up to twenty percent of patients with eating disorders eventually die of their illness, and another fifteen percent resort to suicide. With access to treatment, 75 to 80% of female adolescents recover, yet less than half of males do (Macleans, 2005). Moreover, there are several limitations in the collection of data, as most studies are based on clinical samples, which make it hard to tell about the findings to general population. People with eating disorders require a broad range of treatment for both physical complications and psychological issues, at a cost of about $ 1 600 per day (Timothy & Cameron, 2005, 100). Treatment for patients who were diagnosed following a hospitalization resulting from their condition is both more expensive (approximately three times more), and also less successful, with a corresponding drop of over twenty percent in women and forty percent in men (Macleans, 2005).
Symptoms-complications
Symptoms and complications vary according to the nature and severity of the eating disorder:[140]
acne | xerosis | amenorrhoea | tooth loss, cavities |
constipation | diarrhea | water retention and/or edema | lanugo |
telogen effluvium | cardiac arrest | hypokalemia | death |
osteoporosis[141] | electrolyte imbalance | hyponatremia | brain atrophy[142][143] |
pellagra[144] | scurvy | kidney failure | suicide[145][146][147] |
Some physical symptoms of eating disorders are weakness, fatigue, sensitivity to cold, reduced beard growth in men, reduction in waking erections, reduced libido, weight loss and failure of growth.[148] Polycystic ovary syndrome (PCOS) is the most common endocrine disorder to affect women. Though often associated with obesity it can occur in normal weight individuals. PCOS has been associated with binge eating and bulimic behavior.[149][150][151][152][153][154]
Psychopathology
The psychopathology of eating disorders centers around body image disturbance, such as concerns with weight and shape; self-worth being too dependent on weight and shape; fear of gaining weight even if when underweight; denial of how severe the symptoms are and a distortion in the way the body is experienced [148]
Diagnosis
The initial diagnosis should be made by a competent medical professional. "The medical history is the most powerful tool for diagnosing eating disorders"(American Family Physician).[155] There are many medical disorders that mimic eating disorders and comorbid psychiatric disorders. All organic causes should be ruled out prior to a diagnosis of an eating disorder or any other psychiatric disorder is made. In the past 30 years eating disorders have become increasingly conspicuous and it is uncertain whether the changes in presentation reflect a true increase.[citation needed] Anorexia nervosa and Bulimia nervosa are the most clearly defined subgroups of a wider range of eating disorders. Many patients present with subthreshold expressions of the two main diagnoses: others with different patterns and symptoms.[156]
Medical
The diagnostic workup typically includes complete medical and psychosocial history and follows a rational and formulaic approach to the diagnosis. Neuroimaging using fMRI, MRI, PET and SPECT scans have been used 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. "Right frontal intracerebral lesions with their close relationship to the limbic system could be causative for eating disorders, 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, both from a clinical and a research prospective".(O'Brien et al. 2001).[52][157]
Psychological
Eating Attitudes Test[158] | SCOFF questionnaire[159] |
Body Attitudes Test[160] | Body Attitudes Questionnaire[161] |
Eating Disorder Inventory[162] | Eating Disorder Examination Interview[163] |
After ruling out organic causes and the initial diagnosis of an eating disorder being made by a medical professional, a trained mental health professional aids in the assessment and treatment of the underlying psychological components of the eating disorder and any comorbid psychological conditions. The clinician conducts a clinical interview and may employ various psychometric tests. Some are general in nature while others were devised specifically for use in the assessment of eating disorders. Some of the general tests that may be used are the Hamilton Depression Rating Scale[164] and the Beck Depression Inventory.[165][166] longitudinal research showed that there is an increase in chance that a young adult female would develop bulimia due to their current psychological pressure and as the person ages and matures, their emotional problems change or are resolved and then the symptoms decline.[167]
Differential diagnoses
There are a variety of medical conditions which may be misdiagnosed as an eating disorder such as Lyme disease which is known as the "great imitator", as it may present as a variety of psychiatric or neurologic disorders including anorexia nervosa.[168][169]
- 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.[170]
- gastric adenocarcinoma is one of the most common forms of cancer in the world. Complications due to this condition have been misdiagnosed as an eating disorder.[171]
- helicobacter pylori is a bacterium which causes stomach ulcers and gastritis and has been shown to be a precipitating factor in the development of gastric carcinomas. It also has an effect on circulating levels of leptin and ghrelin, two hormones which help regulate appetite. Upon successful treatment of helicobacter pylori associated gastritis in pre-pubertal children they showed "significant increase in BMI, lean and fat mass along with a significant decrease in circulating ghrelin levels and an increase in leptin levels" (Pacifico, L)."SUMMARY: H. pylori has an influence on the release of gastric hormones and therefore plays a role in the regulation of body weight, hunger and satiety,"(Weigt J, Malfertheiner P).[172][173]
- hypothyroidism, hyperthyroidism, hypoparathyroidism and hyperparathyroidism may mimic some of the symptoms of, can occur concurrently with, be masked by or exacerbate an eating disorder.[174][175][176][177][178][179][180][181]
There are multiple medical conditions which may be misdiagnosed as a primary psychiatric disorder. These may have a synergistic effect on conditions which mimic an eating disorder or on a properly diagnosed ED. They also may make it more difficult to diagnose and treat an ED.
- Lupus: 19 psychiatric conditions have been associated with systemic lupus erythematosus (SLE), including depression and bipolar disorder.[182]
- Toxoplasma seropositivity: even in the absence of symptomatic toxoplasmosis, toxoplasma gondii exposure has been linked to changes in human behavior and psychiatric disorders including those comorbid with eating disorders such as depression. In reported case studies the response to antidepressant treatment improved only after adequate treatment for toxoplasma.[183]
- neurosyphilis: It is estimated that there may be up to one million cases of untreated syphyilis in the US alone. "The disease can present with psychiatric symptoms alone, psychiatric symptoms that can mimic any other psychiatric illness". Many of the manifestations may appear atypical. Up to 1.3% of short term psychiatric admissions may be attributable to neurosyphilis, with a much higher rate in the general psychiatric population. Neurosyphilis like Lyme disease has been given the appellation the "great imitator" for it may present in various ways such as depression and chronic alcoholism. (Ritchie, M Perdigao J,)[184]
- dysautonomia: a wide variety of autonomic nervous system (ANS) disorders may cause a wide variety of psychiatric symptoms including anxiety, panic attacks and depression. Dysautonomia usually involves failure of sympathetic or parasympathetic components of the ANS system but may also include excessive ANS activity. Dysautonomia can occur in conditions such as diabetes and alcoholism.
There are separate psychological disorders which may be misdiagnosed as an eating disorder.
- 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. Persons with this disorder may present with complaints of pain while swallowing.[187]
- 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 39% of eating disorder cases. BDD is a chronic and debilitating condition which may lead to social isolation, major depression and 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 a new atrophy in the frontotemporal region.[188][189][190][190][191]
Prevention of Eating Disorders
Prevention aims to promote a healthy development before the occurrence of eating disorders. It also intends early identification of an eating disorder before it is too late to treat.
Internet and modern technologies provide new opportunities for prevention. On-line programs have the potential to increase the use of prevention programs. The development and practice of prevention programs via on-line sources makes it possible to reach a wide range of people at minimal cost.[192] Such an approach can also make prevention programs to be sustainable. Those kind of programs can be examined under the category eHealth.
Treatment
Treatment varies according to type and severity of eating disorder, and usually more than one treatment option is utilized.[193] However, there is lack of good evidence about treatment and management, which means that current views about treatment are based mainly on clinical experience. Therefore, before treatment takes place, family doctors will play an important role in early treatment as patients suffering from eating disorders will be reluctant to see a psychiatrist and a lot will depend on trying to establish a good relationship with the patient and family in primary care.[194] That said, some of the treatment methods are:
- Cognitive behavioral therapy (CBT),[195][196][197] which postulates that an individual's feelings and behaviors are caused by their own thoughts instead of external stimuli such as other people, situations or events; the idea is to change how a person thinks and reacts to a situation even if the situation itself does not change. See Cognitive behavioral treatment of eating disorders.
- Acceptance and commitment therapy: a type of CBT[198]
- Cognitive Remediation Therapy (CRT), a set of cognitive drills or compensatory interventions designed to enhance cognitive functioning.[199][200][201][202]
- Dialectical behavior therapy[203]* Family therapy[204] including "conjoint family therapy" (CFT), "separated family therapy" (SFT) and Maudsley Family Therapy.[205][206]
- Behavioral therapy: focuses on gaining control and changing unwanted behaviors.[207]
- Interpersonal psychotherapy (IPT)[208]
- Music Therapy
- Recreation Therapy
- Art therapy[209]
- Nutrition counseling[210] and Medical nutrition therapy[211][212][213]
- Medication: Orlistat is used in obesity treatment. Olanzapine seems to promote weight gain as well as the ability to ameliorate obsessional behaviors concerning weight gain. zinc supplements have been shown to be helpful, and cortisol is also being investigated.[214][215][216][217][218][219]
- Self-help and guided self-help have been shown to be helpful in AN, BN and BED;[197][220][221][222] this includes support groups and self-help groups such as Eating Disorders Anonymous and Overeaters Anonymous.[223][224]
- Psychoanalysis
- Inpatient care
There are few studies on the cost-effectiveness of the various treatments.[225] Treatment can be expensive;[226][227] due to limitations in health care coverage, patients hospitalized with anorexia nervosa may be discharged while still underweight, resulting in relapse and rehospitalization.[228]
Prognosis estimates are complicated by non-uniform criteria used by various studies, but for AN, BN, and BED, there seems to be general agreement that full recovery rates are in the 50% to 85% range, with larger proportions of patients experiencing at least partial remission.[223][229][230][231]
See also
References
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