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Anorexia nervosa From Wikipedia, the free encyclopedia For other uses, see Anorexia nervosa (disambiguation) and

Anorexia (disambiguati on). "Anorexic" redirects here. For the use of the term as an appetite suppressant, s ee Anorectic. Anorexia nervosa Classification and external resources "Miss A " pictured in 1866 and in 1870 after treatment. She was one of the earlies t anorexia nervosa case studies. From the published medical papers of Sir Willia m Gull ICD-10 F50.0-F50.1 ICD-9 307.1 OMIM 606788 DiseasesDB 749 MedlinePlus 000362 eMedicine emerg/34 med/144 MeSH D000856 Anorexia nervosa is an eating disorder characterized by immoderate food restrict ion and irrational fear of gaining weight, as well as a distorted body self-perc eption. It typically involves excessive weight loss and is usually found more in females than in males.[1] Because of the fear of gaining weight, people with th is disorder restrict the amount of food they consume. This restriction of food i ntake causes metabolic and hormonal disorders.[2] Outside of medical literature, the terms anorexia nervosa and anorexia are often used interchangeably; however , anorexia is simply a medical term for lack of appetite, and people with anorex ia nervosa do not in fact, lose their appetites.[3] Patients suffering from anor exia nervosa may experience dizziness, headaches, drowsiness and a lack of energ y. Anorexia nervosa is characterized by low body weight, inappropriate eating habit s, obsession with having a thin figure, and the fear of gaining weight. It is of ten coupled with a distorted self image[4][5] which may be maintained by various cognitive biases[6] that alter how the affected individual evaluates and thinks about her or his body, food and eating.[7] Those suffering from anorexia often view themselves as "too fat" even if they are already underweight.[8] They may p ractice repetitive weighing, measuring, and mirror gazing, alongside other obses sive actions to make sure they are still thin, a common practice known as "body checking".[9] Anorexia nervosa most often has its onset in adolescence and is more prevalent a mong adolescent females than adolescent males.[10] However, more recent studies show the onset age has decreased from an average of 13 to 17 years of age to 9 t o 12.[11] While it can affect men and women of any age, race, and socioeconomic and cultural background,[12] anorexia nervosa occurs in ten times more females t han males.[13] People with anorexia nervosa continue to feel hunger, but they deny themselves a ll but very small quantities of food.[7] The average caloric intake of a person with anorexia nervosa is 600 800 calories per day, but extreme cases of complete s elf-starvation are known. It is a serious mental illness with a high incidence o f comorbidity and similarly high mortality rates to serious psychiatric disorder s.[8] People suffering from anorexia have extremely high levels of ghrelin (the hunger hormone that signals a physiological desire for food) in their blood. The high levels of ghrelin suggests that their bodies are trying to desperately swi tch the hunger aspect on; however, that hunger call is being suppressed, ignored , or overridden. Nevertheless, one small single-blind study found that intraveno us administration of ghrelin to anorexia nervosa patients increased food intake by 12 36% over the trial period.[14] The term anorexia nervosa was established in 1873 by Sir William Gull, one of Qu een Victoria's personal physicians.[15] The term is of Greek origin: an- (??-, p refix denoting negation) and orexis (??e???, "appetite"), thus meaning a lack of

desire to eat.[16] However, while the term "anorexia nervosa" literally means " neurotic loss of appetite", the literal meaning of the term is somewhat misleadi ng. Many anorexics do enjoy eating and have certainly not lost their appetites a s the term "loss of appetite" is normally understood; it is better to regard ano rexia nervosa as a self-punitive addiction to fasting, rather than a literal los s of appetite. Contents [hide] 1 Signs and symptoms 2 Anorexia nervosa vs. bulimia nervosa 3 Medical complications 4 Causes 4.1 Biological 4.2 Environmental 4.2.1 Media effects 4.3 Relationship to autism 5 Diagnosis 5.1 Medical 5.2 Psychological 5.3 Differential diagnoses 6 Treatment 6.1 Dietary 6.2 Medication 6.3 Therapy 6.4 Alternative medicine 7 Prognosis 7.1 Relapse 8 Epidemiology 9 History 10 Research 11 Notable cases 12 See also 13 References 14 Bibliography 15 Further reading 16 External links Signs and symptoms [edit] Left: before three straight 40-day water fasts. Right: same woman after final da y of her third straight 40 day water fast.[17][18] Anorexia nervosa is an eating disorder characterized by attempts to lose weight, sometimes to the point of starvation. A person with anorexia nervosa may exhibi t a number of signs and symptoms, the type and severity of which may vary in eac h case and may be present but not readily apparent. Anorexia nervosa, and the as sociated malnutrition that results from self-imposed starvation, can cause sever e complications in every major organ system in the body.[19][20][21] Hypokalaemia, a drop in the level of potassium in the blood, is a sign of anorex ia nervosa. A significant drop in potassium can cause abnormal heart rhythms, co nstipation, fatigue, muscle damage and paralysis. Between 50% and 75% of individuals with an eating disorder experience depression . In addition, one in every four individuals who are diagnosed with anorexia ner vosa also exhibit obsessive-compulsive disorder.[22] Symptoms for a typical patient include: Refusal to maintain a normal body mass index for their age[23] Amenorrhea, the absence of three consecutive menstrual cycles[23] Fearful of even the slightest weight gain and takes all precautionary measures t o avoid weight gain and becoming overweight [23] Obvious, rapid, dramatic weight loss Lanugo: soft, fine hair growing on the face and body[24] One theory is that this is related to hypothyroidism as a similar hypertrichosis occurs in hypothyroidi

sm.[25] Obsession with calories and fat content of food Preoccupation with food, recipes, or cooking; may cook elaborate dinners for oth ers, but not eat the food themselves[26] Dieting despite being thin or dangerously underweight Rituals: cuts food into tiny pieces; refuses to eat around others; hides or disc ards food Purging: uses laxatives, diet pills, ipecac syrup, or water pills; may engage in self-induced vomiting; may run to the bathroom after eating in order to vomit a nd quickly get rid of the calories[27][28] (see also bulimia nervosa). May engage in frequent, strenuous exercise[29] Perception of self to be overweight despite being told by others they are too th in and, in most cases, underweight. Becomes intolerant to cold and frequently complains of being cold from loss of i nsulating body fat or poor circulation resulting from extremely low blood pressu re; body temperature lowers (hypothermia) in effort to conserve energy[30] Depression: may frequently be in a sad, lethargic state[31] Solitude: may avoid friends and family; becomes withdrawn and secretive Cheeks may become swollen because of enlargement of the salivary glands caused b y excessive vomiting[32] Swollen joints[33] Abdominal distension Bad breath (from vomiting or starvation-induced ketosis) Hair loss or thinning[34] Fatigue [35] Rapid mood swings Dermatologic signs of anorexia nervosa[36] xerosis cutis telogen effluvium carotenoderma acne vulgaris hyperpig mentation seborrhoeic dermatitis acrocyanosis chilblains petechiae livedo r eticularis interdigital intertrigo paronychia generalized pruritus acquired striae distensae angular stomatitis prurigo pigmentosa edema linear erythema craquele acrodermatitis e nteropathica pellagra Possible medical complications of anorexia nervosa constipation[37] diarrhea[38] electrolyte imbalance[39] cavities [40] tooth loss[41] cardiac arrest[42] amenorrhoea[43] edema[44] osteoporosis[45] osteopenia[46] hyponatremia[47] hypokalemia[48] optic neuropathy[49] brain atrophy[50 ][51] leukopenia[52][53] Recent findings suggest that the prevalent symptoms for anorexia nervosa (as dis cussed above) such as decreased body temperature, obsessive-compulsivity, and ch anges in psychological state, can actually be attributed to symptoms of starvati on. This theory can be supported by a past study involving rats who were only fe d a certain amount (at a certain time) each day; these rats showed dramatic incr eases in their activity on the wheel in their cage at times when not being fed. These findings could explain why those with anorexia nervosa are often seen exce ssively exercising; their overactivity is the result of fasting, and by increasi ng their activity they could raise their body temperature, increase their chance s of stumbling upon food, or could distract them from their desire for food (bec ause they do not, in fact, lose their appetite). While it is commonly believed t hat those with AN do not have a normal appetite, this is not the case. Those wit h AN are typically obsessive about food, cooking often for others, but not eatin g the food themselves. Despite the fact that the physiological cause behind each case of anorexia nervosa is different, the most common theme seen across the bo ard is the element of self-control. Therefore, when looking at the underlying ca use behind the disorder, one would see that it is rarely about the food itself;

it is about the individual attempting to gain complete control over an aspect of their lives, in order to prove themselves, and distract them from another aspec t of their lives they wish they could control; they pride themselves on the abil ity to resist the temptation of food, even in the case of extreme hunger. For ex ample, a child who with a destructive family life restricting their food intake in order to compensate for the chaos occurring at home.[54] Anorexia nervosa vs. bulimia nervosa [edit] Although anorexia nervosa has many similarities with bulimia nervosa, a critical difference between the two is that anorexia nervosa is also partly caused by th e personality traits of perfectionism and obsessive compulsive tendencies.[citat ion needed] Whereas the main reason motivating people with bulimia nervosa tends to be self-perceived body image, people affected with anorexia nervosa are also driven to diet based on their desperate need to retain some control in their li ves. For many, monitoring their food intake is the only control they can have.[5 5] It is not uncommon for those diagnosed with anorexia nervosa to also exhibit symptoms of bulimia nervosa, such as binging and purging and vice-versa.[56] Medical complications [edit] Anorexia nervosa can have serious implications if its duration and severity are significant and if onset occurs before the completion of growth, pubertal matura tion or prior to attaining peak bone mass.[57] Complications specific to adolesc ents and children with anorexia nervosa can include the following: height gain may slow and can stop completely with severe weig Growth retardation ht loss or chronic malnutrition. In such cases, provided that growth potential i s preserved, height increase can resume and reach full potential after normal in take is resumed.[57] Height potential is normally preserved if the duration and severity of illness are not significant and/or if the illness is accompanied wit h delayed bone age (especially prior to a bone age of approximately 15 years), a s hypogonadism may negate the deleterious effects of undernutrition on stature b y allowing for a longer duration of growth compared to controls.[58] In such cas es, appropriate early treatment can preserve height potential and may even help to increase it in some post-anorexic subjects due to the aforementioned reasons in addition to factors such as long-term reduced estrogen-producing adipose tiss ue levels compared to premorbid levels.[59][60][61] Pubertal delay or arrest both height gain and pubertal development are dependent on the release of growth hormone and gonadotrophins (LH and FSH) from the pitui tary gland. Suppression of gonadotrophins in patients with anorexia nervosa has been frequently documented.[57] However, a study demonstrated that growth hormon e levels were not a predictor of height measures in anorexic patients, which is suggestive of a resistance to growth hormone effects at the growth plate, simila r to the resistance to growth hormone of bone-formation markers.[58] Instead, in sulin-like growth factor had a larger effect, with lower IGF-I levels and longer durations of illness tending to result in lower height measures than vice versa , although IGF-I levels in anorexic subjects may not necessarily be low enough t o affect height measures.[58] In some cases, especially where onset is pre-puber tal, physical consequences such as stunted growth and pubertal delay are usually fully reversible.[62] Reduction of Peak Bone Mass bone accretion is the highest during adolescence, an d if onset of anorexia nervosa occurs during this time and stalls puberty, bone mass may remain low.[57] Hepatic steatosis fatty infiltration of the liver, is an indicator of malnutriti on in children.[57] Heart disease and arrythmias Neurological disorders- seizures, tremors Death (Anorexia nervosa has the highest rate of mortality of any psychological d isorder)[63] Causes [edit] Studies have hypothesized the continuance of disordered eating patterns may be e

piphenomena of starvation. The results of the Minnesota Starvation Experiment sh owed normal controls exhibit many of the behavioral patterns of anorexia nervosa (AN) when subjected to starvation. This may be due to the numerous changes in t he neuroendocrine system, which results in a self-perpetuating cycle.[64][65][66 ][67] Studies have suggested the initial weight loss such as dieting may be the triggering factor in developing AN in some cases, possibly because of an already inherent predisposition toward AN. One study reported cases of AN resulting fro m unintended weight loss that resulted from varied causes, such as a parasitic i nfection, medication side effects, and surgery. The weight loss itself was the t riggering factor.[68][69] Even though anorexia does not affect males as often in comparison to females, studies have shown that males with a female twin have a higher chance of getting anorexia. Therefore anorexia may be linked to parental exposure to female hormones.[70] Biological [edit] Obstetric complications: various prenatal and perinatal complications may factor into the development of anorexia nervosa, such as maternal anemia, diabetes mel litus, preeclampsia, placental infarction, and neonatal cardiac abnormalities. N eonatal complications may also have an influence on harm avoidance, one of the p ersonality traits associated with the development of AN.[71][72] Genetics: anorexia nervosa is believed to be highly heritable, with estimated in heritance rates ranging from 56% to 84%.[73][74][75] Association studies have be en performed, studying 128 different polymorphisms related to 43 genes including genes involved in regulation of eating behavior, motivation and reward mechanic s, personality traits and emotion. Consistent associations have been identified for polymorphisms associated with agouti-related peptide, brain derived neurotro phic factor, catechol-o-methyl transferase, SK3 and opioid receptor delta-1.[76] In one study, variations in the norepinephrine transporter gene promoter were a ssociated with restrictive anorexia nervosa, but not binge-purge anorexia.[77] R ecent studies have advanced the theory that the sex difference in incidence and the common onset at the age of puberty may reflect an abnormal response of the b rain to anorexic (feeding suppressing) effects of the female sex hormone, estrog en.[78] This viewpoint has been recently supported by a report that abnormal for ms of the estrogen receptor are more common in women with anorexia nervosa of th e restricting type.[79] epigenetics: Epigenetic mechanisms: are means by which genetic mutations are cau sed by environmental effects that alter gene expression via methods such as DNA methylation, these are independent of and do not alter the underlying DNA sequen ce. They are heritable, as was shown in the verkalix study, but also may occur th roughout the lifespan, and are potentially reversible. Dysregulation of dopamine rgic neurotransmission and Atrial natriuretic peptide homeostasis resulting from epigenetic mechanisms has been implicated in various eating disorders.[80] "We conclude that epigenetic mechanisms may contribute to the known alterations of A NP homeostasis in women with eating disorders."[80][81] Dysregulation of the dopamine and serotonin pathways has been implicated in the etiology, pathogenesis and pathophysiology of anorexia nervosa.[82][83][84][85] serotonin dysregulation;[86] particularly high levels in those areas in the brai n with the 5HT1A receptor a system particularly linked to anxiety, mood and impu lse control. Starvation has been hypothesized to be a response to these effects, as it is known to lower tryptophan and steroid hormone metabolism, which might reduce serotonin levels at these critical sites and ward off anxiety. Other stud ies of the 5HT2A serotonin receptor (linked to regulation of feeding, mood, and anxiety), suggest that serotonin activity is decreased at these sites. There is evidence that both personality characteristics associated with AN, and disturban ces to the serotonin system are still apparent after patients have recovered fro m anorexia.[87] Brain-derived neurotrophic factor (BDNF) is a protein that regulates neuronal de velopment and neuroplasticity, it also plays a role in learning, memory and in t he hypothalamic pathway that controls eating behavior and energy homeostasis. BD

NF amplifies neurotransmitter responses and promotes synaptic communication in t he enteric nervous system. Low levels of BDNF are found in patients with AN and some comorbid disorders such as major depression.[88][89] Exercise increases lev els of BDNF[90] leptin and ghrelin; leptin is a hormone produced primarily by the fat cells in w hite adipose tissue of the body it has an inhibitory (anorexigenic) effect on ap petite, by inducing a feeling of satiety. Ghrelin is an appetite inducing (orexi genic) hormone produced in the stomach and the upper portion of the small intest ine. Circulating levels of both hormones are an important factor in weight contr ol. While often associated with obesity both have been implicated in the pathoph ysiology of anorexia nervosa and bulimia nervosa.[91] cerebral blood flow (CBF); neuroimaging studies have shown reduced CBF in the te mporal lobes of anorectic patients, which may be a predisposing factor in the on set of AN.[92] autoimmune system; Autoantibodies against neuropeptides such as melanocortin hav e been shown to affect personality traits associated with eating disorders such as those that influence appetite and stress responses.[93] Infections: Some people are hypothesized to have developed anorexia abruptly as a reaction to a streptococcus or mycoplasma infection. PANS is an acronym for Pe diatric acute-onset neuropsychiatric syndrome, a hypothesis describing children who have abrupt, dramatic onset of obsessive-compulsive disorder (OCD) or anorex ia nervosa coincident with the presence of two or more neuropsychiatric symptoms .[94] Nutritional deficiencies Zinc deficiency may play a role in anorexia. It is not thought responsible for c ausation of the initial illness but there is evidence that it may be an accelera ting factor that deepens the pathology of the anorexia. A 1994 randomized, doubl e-blind, placebo-controlled trial showed that zinc (14 mg per day) doubled the r ate of body mass increase compared to patients receiving the placebo.[95] Environmental [edit] Sociocultural studies have highlighted the role of cultural factors, such as the promotion of thinness as the ideal female form in Western industrialized nation s, particularly through the media. There is a necessary connection between anore xia nervosa and culture and whether culture is a cause, a trigger, or merely a k ind of social address or envelope which determines in which segments of society or in which cultures anorexia nervosa will appear. The strong thesis of this con nection is that culture acts as a cause by providing a blueprint for anorexia ne rvosa. A moderate thesis is that a specific cultural factors trigger the illness which is determined by many factors including family interactions, individual p sychology, or biological predisposition. Culture change can trigger the emergenc e of anorexia in adolescent girls from immigrant families living in highly indus trialized Western Societies.[96] A recent epidemiological study of 989,871 Swedi sh residents indicated that gender, ethnicity and socio-economic status were lar ge influences on the chance of developing anorexia, with those with non-European parents among the least likely to be diagnosed with the condition, and those in wealthy, white families being most at risk.[97] People in professions where the re is a particular social pressure to be thin (such as models and dancers) were much more likely to develop anorexia during the course of their career,[98] and further research has suggested that those with anorexia have much higher contact with cultural sources that promote weight-loss.[99] Anorexia nervosa is more likely to occur in a person's pubertal years, especiall y for girls.[100] Female students are 10 times more likely to suffer from anorex ia nervosa than male students. According to a survey of 1799 Japanese female hig h school students, "85% who were a normal weight wanted to be thinner and 45% wh o were 10 20% underweight wanted to be thinner."[101] Teenage girls concerned abou t their weight and who believe that slimness is more attractive among peers tren d to weight-control behaviors. Teen girls are learning from each other to consum e low-caloric, low-fat foods and diet pills. This results in lack of nutrition a nd a greater chance of developing anorexia nervosa.[102] It has also been noted that anorexia nervosa is more likely to occur in populati

ons in which obesity is more prevalent. It has been suggested that anorexia nerv osa results from a sexually selected evolutionary drive to appear youthful in po pulations in which size becomes the primary indicator of age.[103] There is also evidence to suggest that patients who have anorexia nervosa can be characterised by alexithymia[104] and also a deficit in certain emotional funct ions. A research study showed that this was the case in both adult and adolescen t anorexia nervosa patients.[105] There is a high rate of reported child sexual abuse experiences in clinical grou ps of who have been diagnosed with anorexia. The connection between eating disor ders and abuse has been convincingly evidenced by a number of studies, including one published in Epidemiology (and strengthened by blind hypothesis survey), wh ich showed in a comparison of women with no history of eating disorders, women w ith a history of eating disorders were twice as likely to have reported childhoo d sexual abuse.[106] While the joint effect of both physical and sexual abuse re sulted in a nearly 4-fold risk of eating disorders that met DSM-IV criteria.[106 ] It is thought that links between childhood abuse and sexual abuse are complex, such as by influencing psychologic processes that increase a woman's susceptibi lity to the development of an eating disorder, or perhaps by producing changes i n psychobiologic process and neurotransmitting function, associated with eating behaviour.[106] Recent efforts have been made to dispel some of the myths around anorexia nervos a and eating disorders, such as the misconception that families, in particular m others, are responsible for their daughter developing an eating disorder.[107] Media effects [edit] Media are among the principal social agents in many societies around the world. Television, magazines, newspapers, radio, cinema, advertising, the Internet, and other so-called "new media" or "new technologies" are the principal factors beh ind body dissatisfaction, concerns about weight, and disordered eating behaviour . Mass media interventions frequently offer a distorted vision of the world, and it may be difficult for children and adolescents to distinguish whether what th ey see is real or not, so that they are more vulnerable to the messages transmit ted. Field, Cheung, et al.'s survey of 548 preadolescent and adolescent girls fo und that 69% acknowledged that images in magazines had influenced their concepti on of the ideal body, while 47% reported that they wanted to lose weight after s eeing such images.[108] There was also the survey by Utter et al. who studied 4, 746 adolescent boys and girls demonstrating the tendency of magazine articles an d advertisements to activate weight concerns and weight management behaviour. He discovered that girls who frequently read fashion and glamour magazines and gir ls who frequently read articles about diets and issues related to weight loss we re seven times more likely to practice a range of unhealthy weight control behav iours and six times more likely to engage in extremely unhealthy weight control behaviours (e.g., taking diet pills, vomiting, using laxatives, and using diuret ics) [108] from magazines, websites that stress the message of thinness as the i deal have surfaced the internet and has managed to embed itself as an increasing source of influence. The possibility that pro-anorexia websites may reinforce r estrictive eating and exercise behaviours is an area of concern. Pro-anorexia we bsites contain images and writing that support the pursuit of an ideal thin body image. Research has shown that these websites stress thinness as the ideal choi ce for women and in some websites ideal images of muscularity and thinness for m en [109] It has also been shown that women who had viewed these websites at leas t once had a decrease in self-esteem and reports also show an increased likeliho od of future engagement in many negative behaviours related to food, exercise, a nd weight.[109] Evidence of the value of thinness in majority U.S culture is fou nd in Hollywood's elite and the media promotion of waif models in fashion and ce lebrity circles (e.g. Nicole Richie, Mary Kate Olsen, Kate Moss, and Lady Gaga[1 10]). Relationship to autism [edit] A summary of the strategy Zucker et al. (2007) used to assess the relationship b

etween anorexia nervosa and the autism spectrum.[111] Since Gillberg's (1983 & 1985)[112][113] and others' initial suggestion of relat ionship between anorexia nervosa and autism,[114][115] a large-scale longitudina l study into teenage-onset anorexia nervosa conducted in Sweden confirmed that 2 3% of people with a long-standing eating disorder are on the autism spectrum.[11 6][117][118][119][120][121][122] Those on the autism spectrum tend to have a wor se outcome,[123] but may benefit from the combined use of behavioural and pharma cological therapies tailored to ameliorate autism rather than anorexia nervosa p er se.[124][125] Other studies, most notably research conducted at the Maudsley Hospital, UK, furthermore suggest that autistic traits are common in people with anorexia nervosa; shared traits include, e.g., poor executive function, autism quotient score, central coherence, theory of mind, cognitive-behavioural flexibi lity, emotion regulation and understanding facial expressions.[126][127][128][12 9][130][131] Zucker et al. (2007) proposed that conditions on the autism spectrum make up the cognitive endophenotype underlying anorexia nervosa and appealed for increased interdisciplinary collaboration (see figure to right).[111] A pilot study into t he effectiveness cognitive behaviour therapy, which based its treatment protocol on the hypothesised relationship between anorexia nervosa and an underlying aut istic like condition, reduced perfectionism and rigidity in 17 out of 19 partici pants.[132] Autistic traits are more prominent during the acute phase of AN.[133] Diagnosis [edit] Medical [edit] The initial diagnosis should be made by a competent medical professional. There are multiple medical conditions, such as viral or bacterial infections, hormonal imbalances, neurodegenerative diseases and brain tumors which may mimic psychia tric disorders including anorexia nervosa. According to an in depth study conduc ted by psychiatrist Richard Hall as published in the Archives of General Psychia try: Medical illness often presents with psychiatric symptoms. It is difficult to distinguish physical disorders from functional psychiatric di sorders on the basis of psychiatric symptoms alone. Detailed physical examination and laboratory screening are indicated as a routin e procedure in the initial evaluation of psychiatric patients. Most patients are unaware of the medical illness that is causative of their psyc hiatric symptoms. The conditions of patients with medically induced symptoms are often initially m isdiagnosed as a functional psychosis.[134][135] Complete Blood Count (CBC): a test of the white blood cells. red blood cells and platelets used to assess the presence of various disorders such as leukocytosis , leukopenia, thrombocytosis and anemia which may result from malnutrition.[136] urinalysis: a variety of tests performed on the urine used in the diagnosis of m edical disorders, to test for substance abuse, and as an indicator of overall he alth[137] ELISA: Various subtypes of ELISA used to test for antibodies to various viruses and bacteria such as Borrelia burgdoferi (Lyme Disease)[138] Western Blot Analysis: Used to confirm the preliminary results of the ELISA[139] Chem-20: Chem-20 also known as SMA-20 a group of twenty separate chemical tests performed on blood serum. Tests include cholesterol, protein and electrolytes su ch as potassium, chlorine and sodium and tests specific to liver and kidney func tion.[140] glucose tolerance test: Oral glucose tolerance test (OGTT) used to assess the bo dy's ability to metabolize glucose. Can be useful in detecting various disorders such as diabetes, an insulinoma, Cushing's Syndrome, hypoglycemia and polycysti c ovary syndrome[141][142] Secritin-CCK Test: Used to assess function of pancreas and gall bladder[143][144 ] Serum cholinesterase test: a test of liver enzymes (acetylcholinesterase and pse

udocholinesterase) useful as a test of liver function and to assess the effects of malnutrition[145] Liver Function Test: A series of tests used to assess liver function some of the tests are also used in the assessment of malnutrition, protein deficiency, kidn ey function, bleeding disorders, Crohn's Disease[146] Lh response to GnRH: Luteinizing hormone (Lh) response to gonadotropin-releasing hormone (GnRH): Tests the pituitary glands' response to GnRh a hormone produced in the hypothalumus. Central hypogonadism is often seen in anorexia nervosa cas es.[147] Creatine Kinase Test (CK-Test): measures the circulating blood levels of creatin e kinase an enzyme found in the heart (CK-MB), brain (CK-BB) and skeletal muscle (CK-MM).[148][149] Blood urea nitrogen (BUN) test: urea nitrogen is the byproduct of protein metabo lism first formed in the liver then removed from the body by the kidneys. The BU N test is used primarily to test kidney function. A low BUN level may indicate t he effects of malnutrition.[150] BUN-to-creatinine ratio: A BUN to creatinine ratio is used to predict various co nditions. High BUN/creatinine ratio can occur in severe hydration, acute kidney failure, congestive heart failure, intestinal bleeding. A low BUN/creatinine can indicate a low protein diet, celiac disease rhabdomyolysis, cirrhosis of the li ver.[151][152][153] electrocardiogram (EKG or ECG): measures electrical activity of heart can be use d to detect various disorders such as hyperkalemia[154] electroencephalogram (EEG): measures the electrical activity of the brain. Can b e used to detect abnormalities such as those associated with pituitary tumors[15 5][156] Upper GI Series: test used to assess gastrointestinal problems of the middle and upper intestinal tract[157] Thyroid Screen TSH, t4, t3 :test used to assess thyroid functioning by checking levels of thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronin e (T3)[158] Parathyroid hormone (PTH) test: tests the functioning of the parathyroid by meas uring the amount of (PTH) in the blood. Test is used to diagnose parahypothyroid ism. PTH also controls the levels of calcium and phosphorus in the blood (homeos tasis).[159] barium enema: an x-ray examination of the lower gastrointestinal tract[160] neuroimaging; via the use of various techniques such as PET scan, fMRI, MRI and SPECT imaging should be included in the diagnostic procedure for any eating diso rder to detect cases in which a lesion, tumor or other organic condition has bee n either the sole causative or contributory factor in an eating disorder.[citati on needed] Psychological [edit] Not only does starvation result in physical complications, but mental complicati ons as well.[161] It has been shown that eating disorders such as anorexia nervo sa are reinforced by reward and attention. P. Sodersten and colleagues suggest t hat effective treatment of this disorder depends on re-establishing reinforcemen t for normal eating behaviours instead of unhealthy weight loss.[3] Anorexia nervosa is classified as an Axis I[162] disorder in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM-IV), published by the America n Psychiatric Association. The DSM-IV should not be used by laypersons to diagno se themselves. DSM-IV-TR: diagnostic criteria for AN includes intense fear of gaining weight, a refusal to maintain body weight above 85% of the expected weight for a given ag e and height, and three consecutive missed periods and either refusal to admit t he seriousness of the weight loss, or undue influence of shape or weight on one' s self-image, or a disturbed experience in one's shape or weight. There are two types: the binge-eating/purging type is characterized by overeating or purging, and the restricting type is not.[163] Criticism of DSM-IV There has been criticisms over various aspects of the diagno stic criteria utilized for anorexia nervosa in the DSM-IV. Including the require

ment of maintaining a body weight below 85% of the expected weight and the requi rement of amenorrhea for diagnosis; some women have all the symptoms of AN and c ontinue to menstruate.[164] Those who do not meet these criteria are usually cla ssified as eating disorder not otherwise specified; this may affect treatment op tions and insurance reimbursments.[165] The validity of the AN subtype classific ation has also been questioned because of the considerable diagnostic overlap be tween the binge-eating/purging type and the restricting type and the propensity of the patient to switch between the two.[166][167] Criticisms of DSM-IV and Diagnosing Adolescents with Anorexia Nervosa There have been criticisms over the diagnostic criteria utilized for anorexia nervosa in t he DSM- IV and its applicability in diagnosing adolescents with anorexia nervosa . Several criticisms of the DSM-IV in diagnosing adolescents with anorexia nervo sa are: Fulfillment of DSM- IV criteria B and C for anorexia nervosa are dependent on co mplex abstract reasoning, the capacity to describe internal experiences, and the ability to perceive risk.[168] While formal thought emerges between ages 11 13, c omplex abstract reasoning continues to develop late into adolescence. The abilit y to perceive risk also continues to develop through adolescence, as some preado lescents have difficult perceiving the relative risk of alternative outcomes.[16 8] Adolescents and children must first develop these internal thought processes in order to then endorse fear of weight gain or distortion of body image, and de ny the seriousness of low body weight despite their behaviors that contribute to harmful weight loss, which are necessary to fulfill criteria B and C.[169] Thes e developmental factors may impede an adolescent or child from receiving a diagn osis of anorexia nervosa. It is the hope of certain professionals that the DSM-V will take the unique developmental stages of children and adolescents into acco unt when revising the current criteria. One proposed amendment would be to allow behavioral indicators as a means of substituting internally referenced cognitiv e criteria.[168] Another criticism focuses on the current weight criteria specified to receive a diagnosis of anorexia nervosa. Critics state that there is wide variability in t he rate, timing and magnitude of both height and weight gain during normal puber ty.[170] Physical development varies greatly during puberty, making it a challen ge to define an optimal weight range for a growing child or adolescents.[169] ICD-10: The criteria are similar, but in addition, specifically mention: The ways that individuals might induce weight-loss or maintain low body weight ( avoiding fattening foods, self-induced vomiting, self-induced purging, excessive exercise, excessive use of appetite suppressants or diuretics). If onset is before puberty, that development is delayed or arrested. Certain physiological features, including "widespread endocrine disorder involvi ng hypothalamic-pituitary-gonadal axis is manifest in women as amenorrhoea and i n men as loss of sexual interest and potency. There may also be elevated levels of growth hormones, raised cortisol levels, changes in the peripheral metabolism of thyroid hormone and abnormalities of insulin secretion". Dr. Hilde Bruch, in her 1973 book, Eating Disorders: Obesity, Anorexia Nervosa, and the Person Within, explains that Anorexia Nervosa is "not a static condition ," but one that continually provokes new problems with its various stages. She w rites, "The state of starvation is associated by marked psychological changes .. . camouflaged by rationalizations." She identifies the family interaction become s difficult, marked by rising anxiety, annoyance and resentment. It also brings about social isolation. (Bruch 215). Dr. Bruch believed that anorexia, which is simply not eating enough, as a result from schizophrenia, depression, or esophageal problems often were misdiagnosed as anorexia nervosa. In her assessment, this blurred the definition of anorexia nervosa. For this reason, she distinguished between, what she calls "atypical" a nd "primary" cases of anorexia nervosa. The atypical cases of anorexia were brou ght about by a range of stimuli (from schizophrenia to depression, as noted abov e). (Bruch 227). In contrast to the atypical group, Bruch observed primary, or genuine anorexia n ervosa, "amazingly uniform". The first outstanding symptom is "disturbance of de

lusional proportions in the body image". The second outstanding characteristic i s "disturbance in the accuracy of their perception or cognitive interpretation o f stimuli arising from the body ... failure to recognize hunger and denial of fa tigue". The third outstanding characteristic is a "paralyzing sense of ineffecti veness". "Anorexics struggle against a feeling of enslaved, exploited, and not b eing permitted to lead a life of their own. They would rather starve than contin ue a life of accommodation. In this blind search for a sense of identity and sel fhood they will not accept anything that their parents, or the world around them , has to offer." It is a "desperate struggle for a self respecting identity". Sh e understood that the personality disorder (struggle for control, for a sense of identity, competence, and effectiveness) precedes the somatic disorders (such a s emaciation, amenorrhea, constipation, etc.) (Bruch 250 255).