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RobertBailey
"Whatever King Edmund II had to say is what I want to hear." -Robert Edgar David Bailey, Ph.D.
Status: Day 1 of Goth Craft, Wednesday, September 12th, 2012 starting at 5:05 PM
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Profile: My website: http://web.archive.org/web/20031218055028/http://robertbaileyphd.org/ I suffer from a variety of conditions: 1) PPD - Paranoid personality disorder is a mental disorder characterized by paranoia and a pervasive, long-standing suspiciousness and generalized mistrust of others. Individuals with this personality disorder may be hypersensitive, easily feel slighted, and habitually relate to the world by vigilant scanning of the environment for clues or suggestions that may validate their fears or biases. Paranoid individuals are eager observers. They think they are in danger and look for signs and threats of that danger, potentially not appreciating other evidence.[1] They tend to be guarded and suspicious and have quite constricted emotional lives. Their reduced capacity for meaningful emotional involvement and the general pattern of isolated withdrawal often lend a quality of schizoid isolation to their life experience.[2][verification needed] People with this particular disorder may or may not have a tendency to bear grudges, suspiciousness, tendency to interpret others' actions as hostile, persistent tendency to self-reference, or a tenacious sense of personal right.[3] A genetic contribution to paranoid traits and a possible genetic link between this personality disorder and schizophrenia exist. Psychosocial theories implicate projection of negative internal feelings and parental modeling.[4] [edit]Diagnosis [edit]WHO The World Health Organization's ICD-10 lists paranoid personality disorder as (F60.0) Paranoid personality disorder.[5] It is characterized by at least three of the following: excessive sensitivity to setbacks and rebuffs; tendency to bear grudges persistently, i.e. refusal to forgive insults and injuries or slights; suspiciousness and a pervasive tendency to distort experience by misconstruing the neutral or friendly actions of others as hostile or contemptuous; a combative and tenacious sense of personal rights out of keeping with the actual situation; recurrent suspicions, without justification, regarding sexual fidelity of spouse or sexual partner; tendency to experience excessive self-importance, manifest in a persistent self-referential attitude; preoccupation with unsubstantiated "conspiratorial" explanations of events both immediate to the patient and in the world at large. Includes: expansive paranoid, fanatic, querulant and sensitive paranoid personality (disorder) Excludes: delusional disorder schizophrenia It is a requirement of ICD-10 that a diagnosis of any specific personality disorder also satisfies a set of general personality disorder criteria. It is also pointed out that for different cultures it may be necessary to develop specific sets of criteria with regard to social norms, rules and obligations. [edit]APA The American Psychiatric Association's DSM-IV-TR has similar criteria. They require in general the presence of lasting distrust and suspicion of others, interpreting their motives as malevolent, from an early adult age, occurring in a range of situations. 4 of 7 specific issues must be present, which include different types of suspicions or doubt (such as of being exploited, or that remarks have a subtle threatening meaning), in some cases regarding others in general or specifically friends or partners, and in some cases referring to a response of holding grudges or reacting angrily.[6] [edit]Other Various researchers and clinicians may propose varieties and subsets or dimensions of personality related to the official diagnoses. Psychologist Theodore Millon has proposed five subtypes of paranoid personality:[7][8] fanatic paranoid — including narcissistic features malignant paranoid — including sadistic features obdurate paranoid — including compulsive features querulous paranoid — including negativistic (e.g. discontentment) features insular paranoid — including avoidant features [edit]Differential diagnosis Paranoid Personality Disorder can involve, in response to stress, very brief psychotic episodes (lasting minutes to hours). If long-lasting the disorder may develop into delusional disorder or schizophrenia. Individuals may also be at greater than average risk of experiencing major depressive disorder, agoraphobia, obsessive-compulsive disorder or alcohol and substance-related disorders. Criteria for other personality disorder diagnoses are commonly also met, such as:[9] schizoid personality disorder schizotypal personality disorder narcissistic personality disorder avoidant personality disorder borderline personality disorder [edit]Treatment Because of reduced levels of trust, there can be challenges in treating paranoid personality disorder. However, psychotherapy, antidepressants, antipsychotics and anti-anxiety medications can play a role when an individual is receptive to intervention.[10] [edit]Epidemiology Paranoid personality disorder occurs in about 0.5%–2.5% of the general population.[4][9] It is seen in 2%–10% of psychiatric outpatients. It occurs more commonly in males.[9] A large long-term Norwegian twin study found paranoid personality disorder to be modestly heritable and to share a portion of its genetic and environmental risk factors with schizoid and schizotypal personality disorder.[11] [edit]History See the history of paranoia. Some modern authorities, hostile to monotheism, have gone so far as to suggest that the Hebrew God Yahweh displayed a paranoid personality in the First Commandment injunction, "Thou shalt have no other Gods before me," which they interpret as reflecting psychotic jealousy, divine omnipotence and narcissistic injury[12]. Paranoid personality disorder is listed in DSM-III-R and was included in all previous versions of the DSM. One of the earliest descriptions of the paranoid personality comes from a French psychiatrist named Magnan who described a "fragile personality" that showed idiosyncratic thinking, hypochondria, undue sensitivity, referential thinking and suspiciousness[13]. Closely related to this description is Kraepelin's description from 1905 of a pseudo-querulous personality who is "always on the alert to find grievance, but without delusions", vain, self-absorbed, sensitive, irritable, litigious, obstinate, and living at strife with the world. In 1921, he renamed the condition paranoid personality and described these individuals as distrustful, feeling unjustly treated and feeling subjected to hostility, interference and oppression. He also observed a contradiction in these personalities: on the one hand, they stubbornly hold on to their unusual ideas, on the other hand, they often accept every piece of gossip as the truth[13]. Kraepelin also noted that paranoid personalities were often present in individuals who later developed paranoid psychoses. Subsequent writers also considered traits like suspiciousness and hostility to predispose people to developing delusional illnesses, particularly "late paraphrenias" of old age[14]. Following Kraepelin, Bleuler described "contentious psychopathy" or "paranoid constitution" as displaying the characteristic triad of suspiciousness, grandiosity and feelings of persecution. He also emphasized that the false assumptions of these individuals do not attain the form of real delusion[13]. Kretschmer emphasized the sensitive inner core of the paranoia-prone personality: they feel shy and inadequate but at the same time they have an attitude of entitlement. They attribute their failures to the machinations of others but secretly to their own inadequacy. They experience constant tension between feelings of self-importance and experiencing the environment as unappreciative and humiliating[13]. Jaspers, a German phenomenologist, described "self-insecure" personalities who resemble the paranoid personality. According to Jaspers, such individuals experience inner humiliation, brought about by outside experiences and their interpretations of them. They have an urge to get external confirmation to their self-deprecation and that makes them see insults in the behavior of other people. They suffer from every slight because they seek the real reason for them in themselves. This kind of insecurity leads to overcompensation: compulsive formality, strict social observances and exaggerated displays of assurance[13]. In 1950, Schneider described the "fanatic psychopaths" and divided them into two categories: the combative type that is very insistent about his false notions and actively quarrelsome, and the eccentric type that is passive, secretive, vulnerable to esoteric sects but nonetheless suspicious about others[13]. The descriptions of Leonhard and Sheperd from the sixties describe paranoid individuals as overvaluing their abilities and attributing their failure to the ill-will of others; they also mention that their interpersonal relations are disturbed and they are in constant conflict with others[13]. In 1975, Polatin described the paranoid personality as rigid, suspicious, watchful, self-centered and selfish, inwardly hypersensitive but emotionally undemonstrative. However, when there is a difference of opinion, the underlying mistrust, authoritarianism and rage burst through[13]. In the 1980s, paranoid personality disorder received little attention, and when it did receive it, the focus was on its potential relationship to paranoid schizophrenia. The most significant contribution of this decade comes from Millon who divided the features of paranoid personality disorder to four categories: 1) behavioral characteristics of vigilance, abrasive irritability and counterattack, 2) complaints indicating oversensitivity, social isolation and mistrust, 3) the dynamics of denying personal insecurities, attributing these to others and self-inflation through grandiose fantasies and 4) coping style of detesting dependence and hostile distancing of oneself from others[13]. The DSM-IV-TR[15] describes the paranoid personality disorder as a pattern of pervasive distrust and suspiciousness of others such that their motives are interpreted as malevolent.To qualify for a diagnoses, the patient must meet at least 4 out of the following criteria: (1) suspects, without sufficient basis, that others are exploiting, harming, or deceiving him or her (2) is preoccupied with unjustified doubts about the loyalty or trustworthiness of friends or associates (3) is reluctant to confide in others because of unwarranted fear that the information will be used maliciously against him or her (4) reads hidden demeaning or threatening meanings into benign remarks or events (5) persistently bears grudges, i.e., is unforgiving of insults, injuries, or slights (6) perceives attacks on his or her character or reputation that are not apparent to others and is quick to react angrily or to counterattack (7) has recurrent suspicions, without justification, regarding fidelity of spouse or sexual partner. The DSM-5[16] does not list paranoid personality disorder as a specific type but still enlists traits that allow to describe it: suspiciousness, intimacy avoidance, hostility and unusual beliefs/experiences. 2) Bulimia - Bulimia nervosa is an eating disorder characterized by binge eating and purging, or consuming a large amount of food in a short amount of time followed by an attempt to rid oneself of the food consumed (purging), typically by vomiting, taking a laxative or diuretic, and/or excessive exercise. These acts are also commonly accompanied with fasting over an extended period of time.[1][2] Bulimia nervosa is considered to be less life threatening than anorexia; however, the occurrence of bulimia nervosa is higher.[3] Bulimia nervosa is nine times more likely to occur in women than men (Barker 2003). The vast majority of those with bulimia nervosa are at normal weight.[4] Antidepressants, especially SSRIs, are widely used in the treatment of bulimia nervosa (Newell and Gournay 2000). Patients who have bulimia nervosa are often linked with having impulsive behaviors involving overspending and sexual behaviors as well as having family histories of alcohol and substance abuse, mood and eating disorders.[5] The term bulimia comes from Greek βουλιμία (boulīmia; ravenous hunger), a compound of βους (bous), ox + λιμός (līmos), hunger.[6] Bulimia nervosa was named and first described by the British psychiatrist Gerald Russell in 1979.[7][8] Bulimia is strongly familial. Twin studies estimate the heritability of syndromic bulimia to be 54-83%.[9][10] Contents [hide] 1 Symptoms 2 Signs 2.1 Related disorders 3 Diagnosis 4 Causes 4.1 Biological 4.2 Social 5 Epidemiology 6 Treatment 6.1 Psychotherapy 6.2 Pharmacological treatment 7 Further reading 8 See also 9 Notes [edit]Symptoms These cycles often involve rapid and out-of-control eating, which may stop when the bulimic is interrupted by another person or the stomach hurts from over-extension, followed by self-induced vomiting or other forms of purging. This cycle may be repeated several times a week or, in more serious cases, several times a day [11] and may directly cause: Chronic gastric reflux after eating Dehydration and hypokalemia caused by frequent vomiting Electrolyte imbalance, which can lead to cardiac arrhythmia, cardiac arrest, and even death Esophagitis, or inflammation of the esophagus Boerhaave syndrome, a rupture in the esophageal wall due to vomiting Oral trauma, in which repetitive insertion of fingers or other objects causes lacerations to the lining of the mouth or throat Gastroparesis or delayed emptying Constipation Infertility Enlarged glands in the neck, under the jaw line Peptic ulcers Calluses or scars on back of hands due to repeated trauma from incisors[12][13] Constant weight fluctuations are common The erosion on the lower teeth was caused by Bulimia. For comparison, the upper teeth were restored with porcelain veneers.[14] The frequent contact between teeth and gastric acid, in particular, may cause: Severe dental erosion Perimolysis, or the erosion of tooth enamel[15] Swollen salivary glands[15][16] Constant vomiting can lead to gastroesophageal reflux[17] [edit]Signs These are some of the many signs that may indicate whether someone has bulimia nervosa: fixation on amount of calories consumed fixated and extremely conscious of weight low self-esteem low blood pressure irregular menstrual cycle constant trips to the bathroom depression [18] As with many psychiatric illnesses, delusions can occur with other signs and symptoms leaving the person with a false belief that is not ordinarily accepted by others.[19] The person may also suffer physical complications such as tetany, epileptic seizures, cardiac arrhythmias and muscle weakness.(ICD-10)[citation needed]. People with bulimia nervosa may also exercise to a point that excludes other activities.[19] [edit]Related disorders Bulimics are much more likely than non-bulimics to have an affective disorder, such as depression or general anxiety disorder: A 1985 Columbia University study on female bulimics at New York State Psychiatric Institute found 70% had suffered depression some time in their lives (as opposed to 25.8% for adult females in a control sample from the general population), rising to 88% for all affective disorders combined.[20] Another study by the Royal Children's Hospital in Melbourne on a cohort of 2000 adolescents similarly found that those meeting at least two of the DSM-IV criteria for bulimia nervosa or anorexia nervosa had a sixfold increase in risk of anxiety and a doubling of risk for substance dependency.[21] Some sufferers of anorexia nervosa exhibit episodes of bulimic tendencies through purging (either through self-induced vomiting or laxatives) as a way to quickly remove food in their system.[22] Bulimia also has negative effects on the sufferer's dental health due to the acid passed through the mouth from frequent vomiting causing acid erosion, mainly on the posterior dental surface. [edit]Diagnosis The onset of bulimia nervosa is often during adolescence, between 13 and 20 years of age, and many cases have previously suffered obesity, with many sufferers relapsing in adulthood into episodic binging and purging even after initially successful treatment and remission.[23] Bulimia nervosa may affect up to 1% of young woman and after 10 years of diagnosis, half will recover fully, a third will recover partially, and 10-20% will still have symptoms.[24] Adolescents with bulimia nervosa are more likely to have self-imposed perfectionism and compulsivity issues in eating compared to their peers. This means that the high expectations and unrealistic goals that these individuals set for themselves are internally motivated rather than by social views or expectations.[25] According to Barker, "persons with bulimia are more able to live and interact in everyday chores and tasks such as work and having relationships without the condition overly affecting their abilities".[26] Bulimia nervosa can be difficult to detect, compared to anorexia nervosa, because bulimics tend to be of average or slightly above or below average weight. Many bulimics may also engage in significantly disordered eating and exercising patterns without meeting the full diagnostic criteria for bulimia nervosa.[27] The diagnostic criteria utilized by the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) published by the American Psychiatric Association includes repetitive episodes of binge eating (a discrete episode of overeating during which the individual feels out of control of consumption) compensated for by excessive or inappropriate measures taken to avoid gaining weight.[28] The diagnosis is made only when the behavior is not a part of the symptom complex of anorexia nervosa and when the behavior reflects an overemphasis on physical mass or appearance. There are two sub-types of bulimia nervosa: Purging type bulimics self-induce vomiting (usually by triggering the gag reflex or ingesting emetics such as syrup of ipecac) to rapidly remove food from the body before it can be digested, or use laxatives, diuretics, or enemas. Non-purging type bulimics (approximately 6%–8% of cases) exercise or fast excessively after a binge to offset the caloric intake after eating. Purging-type bulimics may also exercise or fast, but as a secondary form of weight control.[29] [edit]Causes [edit]Biological Like with anorexia nervosa, there is evidence of genetic predispositions contributing to the onset of this eating disorder.[30] Abnormal levels of many hormones, notably serotonin, have been shown to be responsible for some disordered eating behaviours. Brain-derived neurotrophic factor (BDNF) is under investigation as a possible mechanism.[31][32] There is evidence that sex hormones may influence appetite and eating in women, and the onset of bulimia nervosa. Studies have shown that women with Hyperandrogenism and Polycystic ovary syndrome have a dysregulation of appetite, along with carbohydrates and fats. This dysregulation of appetite is also seen in women with bulimia nervosa. In addition, gene knockout studies in mice have shown that mice that have the gene encoding estrogen receptors have decreased fertility due to ovarian dysfunction and dysregulation of androgen receptors. In humans, there is evidence that there is an association between polymorphisms in the ERβ (estrogen receptor β) and bulimia, suggesting there is a correlation between sex hormones and bulimia nervosa.[33] [edit]Social Media portrayals of an 'ideal' body shape are widely considered to be a contributing factor to bulimia[1] (Barker 2003). In a 1991 study by Weltzin, Hsu, Pollicle, and Kaye, it was stated that 19% of bulimics undereat, 37% of bulimics eat an amount of food that is normal for an average human being, and 44% of bulimics overeat.[34] A survey of 15–18 year-old high school girls in Nadroga, Fiji found the self-reported incidence of purging rose from 0% in 1995 (a few weeks after the introduction of television in the province) to 11.3% in 1998.[35] Through the cognitive and socio-cultural perspectives, indications towards the origin of bulimia nervosa can be established. Fairburn et al.’s cognitive behavioral model of bulimia nervosa provides a chief indication of the cause of bulimia through a cognitive perspective, while the “thin ideal” is particularly responsible for the etiology of bulimia nervosa through a socio-cultural context. When attempting to decipher the origin of bulimia nervosa in a cognitive context, Fairburn and et al.’s cognitive behavioral model is often considered the golden standard. Fairburn et al.’s model discusses the process in which an individual falls into the binge-purge cycle and thus develops bulimia. Fairburn et al. argue that extreme concern with weight and shape coupled with low self esteem will result in strict, rigid, and inflexible dietary rules. Accordingly, this would lead to unrealistic restricted eating, which may consequently induce an eventual “slip” where the individual commits a minor infraction of the strict and inflexible dietary rules. Moreover, the cognitive distortion due to dichotomous thinking leads the individual to binge. The binge subsequently should trigger a perceived loss of control, promoting the individual to purge in hope of counteracting the binge. However, Fairburn et al. assert the cycle repeats itself, and thus consider the binge-purge cycle to be self-perpetuating. In contrast, Byrne and Mclean’s findings differed slightly from Fairburn et al.’s cognitive behavioral model of bulimia nervosa in that the drive for thinness was the major cause of purging as a way of controlling weight. In turn, Byrne and Mclean argued that this makes the individual vulnerable to binging, indicating that it is not a binge-purge cycle but rather a purge-binge cycle in that purging comes before binging. Similarly, Fairburn et al.’s cognitive behavioral model of bulimia nervosa is not necessarily applicable to every individual and is certainly reductionist. Everyone differs from another, and taking such a complex behavior like bulimia and applying the same one theory to everyone would certainly be invalid. In addition, the cognitive behavioral model of bulimia nervosa is very cultural bound in that it may not be necessarily applicable to cultures outside of the Western society. To evaluate, Fairburn et al.’s model and more generally the cognitive explanation of bulimia nervosa is more descriptive than explanatory, as it does not necessarily explain how bulimia arises. Furthermore, it is difficult to ascertain cause and effect, because it may be that distorted eating leads to distorted cognition rather than vice versa.[36][37] When exploring the etiology of bulimia through a socio-cultural perspective, the “thin ideal internalization” is significantly responsible. The thin ideal internalization is the extent to which individuals adapt to the societal ideals of attractiveness. Individuals first accept and “buy into” the ideals, and then attempt to transform themselves in order to reflect the societal ideals of attractiveness. J. Kevin Thompson and Eric Stice claim that family, peers, and most evidently media reinforce the thin ideal, which may lead to an individual accepting and “buying into” the thin ideal. In turn, Thompson and Stice assert that if the thin ideal is accepted, one could begin to feel uncomfortable with their body shape or size since it may not necessarily reflect the thin ideal set out by society. Thus, people feeling uncomfortable with their bodies may result in suffering from body dissatisfaction, and may develop a certain drive for thinness. Consequently, body dissatisfaction coupled with drive for thinness is thought to promote dieting and negative affects, which could eventually lead to bulimic symptoms such as purging or binging. Binges lead to self-disgust which causes purging to prevent weight gain.[38] A study dedicated to investigating the thin ideal internalization as a factor of bulimia nervosa is Thompson’s and Stice’s research. The aim of their study was to investigate how and to what degree does media effect the thin ideal internalization. Thompson and Stice used randomized experiments (more specifically programs) dedicated to teaching young women how to be more critical when it comes to media, in order to reduce thin ideal internalization. The results showed that by creating more awareness of the media’s control of the societal ideal of attractiveness, the thin ideal internalization significantly dropped. In other words, less thin ideal images portrayed by the media resulted in less thin ideal internalization. Therefore, Thompson and Stice concluded that media affected greatly the thin ideal internalization.[39] [edit]Epidemiology There is little data on the prevalence of bulimia nervosa in-the-large, on general populations. Most studies conducted thus far have been on convenience samples from hospital patients, high school or university students. These have yielded a wide range of results: between 0.1% and 1.4% of males, and between 0.3% and 9.4% of females.[40] Studies on time trends in the prevalence of bulimia nervosa have also yielded inconsistent results.[41] According to Gelder, Mayou and Geddes (2005) bulimia nervosa is prevalent between 1 and 2 per cent of women aged 15–40 years. Bulimia nervosa occurs more frequently in developed countries (Gelder, Mayou and Geddes 2005). There is a perception that bulimia is most prevalent amongst girls from middle-class families,[42] however in a 2009 study girls from families in the lowest income bracket studied were 153 percent more likely to be bulimic than girls from the highest income bracket.[43] [edit]Treatment The treatment of this complex disorder is very critical, and thus the treatment providers should have expertise in eating disorders and adolescence health. There are two main types of treatment given to those suffering with bulimia nervosa; psychopharmacological and psychosocial treatments.[44] [edit]Psychotherapy There are several empirically supported psychosocial treatments for bulimia nervosa. Cognitive behavioral therapy (CBT), which involves teaching clients to challenge automatic thoughts and engage in behavioral experiments (for example, in session eating of "forbidden foods") has demonstrated efficacy both with and without concurrent antidepressant medication. Research suggests that cognitive-behavioral therapy (CBT) is the most effective psychotherapeutic treatment for bulimia nervosa. One exception was a study that suggested that interpersonal psychotherapy (IPT) might be as effective as CBT, although slower to achieve its effects.[45] By using CBT patients record how much food they eat and periods of vomiting with the purpose of identifying and avoiding emotional fluctuations that bring on episodes of bulimia on a regular basis (Gelder, Mayou and Geddes 2005). Barker (2003) states that research has found 40-60% of patients using cognitive behaviour therapy to become symptom free. He states in order for the therapy to work, all parties must work together to discuss, record and develop coping strategies. Barker (2003) claims by making people aware of their actions they will think of alternatives.[46][47] Patients undergoing CBT who exhibit early behavioral changes are most likely to achieve the best treatment outcomes in the long run.[48] Researchers have also reported some positive outcomes for interpersonal psychotherapy and dialectical behavior therapy.[49][50] Maudsley Family Therapy a.k.a. Family Based Treatment (FBT), developed at the Maudsley Hospital in London for the treatment of anorexia nervosa (AN) has been shown to have positive results for the treatment of bulimia nervosa. FBT has been shown through empirical research to be the most efficacious treatment of AN for patients under the age of eighteen and within three years of onset of illness. The studies to date using FBT to treat BN have been promising.[51] The use of Cognitive Behavioral Therapy (CBT) has been shown to be quite effective for treating bulimia nervosa (BN) in adults, but little research has been done on effective treatments of BN for adolescents.[52] Although CBT is seen as more cost efficient and helps individuals with BN in self-guided care, Family Based Treatment (FBT) might be more helpful to younger adolescents who need more support and guidance from their families. Adolescents are at the stage where their brains are still quite malleable and developing gradually.[53] Therefore, young adolescents with BN are less likely to realize the detrimental consequences of becoming bulimic and have less motivation to change,[54] which is why FBT would be useful to have families intervene and support the teens.[52] Working with BN patients and their families in FBT can empower the families by having them involved in their adolescent's food choices and behaviors, taking more control of the situation in the beginning and gradually letting the adolescent become more autonomous when they have learned healthier eating habits.[52] Adolescents with BN whom are either resistant to change or have not been successful with treatments such as CBT (Cognitive Behavioral Therapy) or IPT (Interpersonal Psychotherapy) could get recommended to try Cue Exposure (CE) by therapists.[55] In this type of therapy, a patient is presented in the beginning of each session with a "forbidden food", allowing the individual to pick up the item to feel and smell it, but they are not allowed to eat it. This will usually provoke a lot of stress and anxiety in the adolescent with BN, which ultimately leads them to have a feeling of intense hunger and wish to partake in binge eating. To help control their eating behaviors, the therapist attempts with CE to expose the adolescent to the food and condition them in order to not feel as much anxiety when presented with the food. If they do not feel as much stress or anxiety when the food is right in front of them, then they will be less likely to feel the need to binge and then purge. Some researchers have also claimed positive outcomes in hypnotherapy treatment.[56][57][58] [59] The Twelve-Step model, used for chemically dependent individuals, was applied to bulimic patients with good results. Researchers at [Ohio State University], in a preliminary study, incorporated the twelve-step model in their treatment of bulimic women in an inpatient unit. They reported positive outcomes.[60] [edit]Pharmacological treatment Some researchers have hypothesized a relationship to mood disorders and clinical trials have been conducted with tricyclic antidepressants,[61] MAO inhibitors, mianserin, fluoxetine,[62] lithium carbonate, nomifensine, trazodone, and bupropion. Research groups who have seen a relationship to seizure disorders have attempted treatment with phenytoin, carbamazepine, and valproic acid. Opiate antagonists naloxone and naltrexone, which block cravings for gambling, have also been used.[63] There has also been some research characterizing bulimia nervosa as an addiction disorder, and limited clinical use of topiramate, which blocks cravings for opiates, cocaine, alcohol and food.[64] Country Year Sample size and type Incidence Australia 2008 1,943 adolescents (ages 15–17) 1.0% male 6.4% female[21] Portugal 2006 2,028 high school students 0.3% female[65] Brazil 2004 1,807 students (ages 7–19) 0.8% male 1.3% female[66] Spain 2004 2,509 female adolescents (ages 13–22) 1.4% female[67] Hungary 2003 580 Budapest residents 0.4% male 3.6% female[68] Australia 1998 4,200 high school students 0.3% combined[69] USA 1996 1,152 college students 0.2% male 1.3% female[70] Norway 1995 19,067 psychiatric patients 0.7% male 7.3% female[71] Canada 1995 8,116 (random sample) 0.1% male 1.1% female[72] Japan 1995 2,597 high school students 0.7% male 1.9% female[73] USA 1992 799 college students 0.4% male 5.1% female[74] There are higher rates of eating disorders in groups involved in activities which idealize a slim physique, such as dance,[68] gymnastics, modeling, cheerleading, running, acting, swimming, diving, rowing and figure skating. Bulimia is thought to be more prevalent among Caucasians.,[75] however a more recent study showed that African-American teenage girls were 50 percent more likely than white girls to exhibit bulimic behavior, including both binging and purging.[76] [edit]Further reading For individuals and families being affected by bulimia nervosa, the following resources might be very helpful: http://www.nationaleatingdisorders.org/ http://www.eatingdisorders.org.au/ http://www.oa.org/ http://helpguide.org/mental/bulimia_signs_symptoms_causes_treatment.htm 3) Anorexia - Anorexia nervosa is an eating disorder characterized by immoderate food restriction and irrational fear of gaining weight, as well as a distorted body self-perception. It typically involves excessive weight loss. Anorexia nervosa usually develops during adolescence and early adulthood.[1] Due to the fear of gaining weight, people with this disorder restrict the amount of food they consume. This restriction of food intake 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 anorexia nervosa do not in fact, lose their appetites.[3] People suffering from anorexia have extremely high levels of ghrelin (the hunger hormone that tells the brain when it is time to eat) in their blood. The high levels of ghrelin suggests that their bodies are trying to desperately switch the hunger aspect on, however, that hungers call is being suppressed, ignored, or overridden. Nevertheless, one small single-blind study found that intravenous administration of ghrelin to anorexia nervosa patients increased food intake by 12–36% over the trial period.[4] Anorexia nervosa has many complicated implications and may be thought of as a lifelong illness that may never be truly cured, but only managed over time. Anorexia nervosa is characterized by low body weight, inappropriate eating habits and obsession with having a thin figure. Individuals suffering from it may also practice repetitive weighing, measuring, and mirror gazing, alongside other obsessive actions to make sure they are still thin, a common practice known as "body checking".[5] Anorexia nervosa is often coupled with a distorted self image[6][7] which may be maintained by various cognitive biases[8] that alter how the affected individual evaluates and thinks about her or his body, food and eating.[9] Anorexia nervosa is characterized by the fear of gaining weight. Those suffering from this disorder often view themselves as "too fat" even if they are already underweight.[10] Persons with anorexia nervosa continue to feel hunger, but deny themselves all but very small quantities of food.[9] The average caloric intake of a person with anorexia nervosa is 600–800 calories per day, but extreme cases of complete self-starvation are known. It is a serious mental illness with a high incidence of comorbidity and similarly high mortality rates to serious psychiatric disorders.[10] Anorexia nervosa most often has its onset in adolescence and is more prevalent among adolescent females than adolescent males.[11] However, more recent studies show the onset age has decreased from an average of 13 to 17 years of age to 9 to 12.[12] While it can affect men and women of any age, race, and socioeconomic and cultural background,[13] anorexia nervosa occurs in 10 times more females than males.[14] The term anorexia nervosa was established in 1873 by Sir William Gull, one of Queen Victoria's personal physicians.[15] The term is of Greek origin: an- (ἀν-, prefix denoting negation) and orexis (ὄρεξις, "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 misleading. Many anorexics do enjoy eating and have certainly not lost their appetites as the term "loss of appetite" is normally understood; it is better to regard anorexia nervosa as a self-punitive addiction to fasting, rather than a literal loss of appetite. Contents [hide] 1 Signs and symptoms 2 Medical complications 3 Causes 3.1 Biological 3.2 Environmental 3.3 Relationship to autism 4 Diagnosis 4.1 Medical 4.2 Psychological 4.3 Differential diagnoses 5 Treatment 5.1 Dietary 5.2 Medication 5.3 Therapy 5.4 Alternative medicine 6 Prognosis 7 Epidemiology 8 History 9 Research 10 Notable cases 11 See also 12 References 13 Bibliography 14 Further reading 15 External links [edit]Signs and symptoms Anorexia nervosa is an eating disorder characterized by attempts to lose weight, sometimes to the point of starvation. A person with anorexia nervosa may exhibit a number of signs and symptoms, the type and severity of which may vary in each case and may be present but not readily apparent. Anorexia nervosa, and the associated malnutrition that results from self-imposed starvation, can cause severe complications in every major organ system in the body.[17][18][19] Hypokalaemia, a drop in the level of potassium in the blood, is a sign of anorexia nervosa. A significant drop in potassium can cause abnormal heart rhythms, constipation, fatigue, muscle damage and paralysis. Between 50% and 75% of individuals with an eating disorder experience depression. In addition, 1 in 4 individuals who are diagnosed with anorexia nervosa also exhibit obsessive compulsive disorder.[20] Symptoms for a typical patient include: Refusal to maintain a normal body mass index for their age[21] Amenorrhea, the absence of three consecutive menstrual cycles[21] Fearful of even the slightest weight gain and takes all precautionary measures to avoid weight gain and becoming overweight [21] Obvious, rapid, dramatic weight loss Lanugo: soft, fine hair growing on the face and body[22] Obsession with calories and fat content of food Preoccupation with food, recipes, or cooking; may cook elaborate dinners for others, but not eat the food themselves[23] Dieting despite being thin or dangerously underweight Rituals: cuts food into tiny pieces; refuses to eat around others; hides or discards 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 and quickly get rid of the calories[24][25] (see also bulimia nervosa). May engage in frequent, strenuous exercise[26] Perception of self to be overweight despite being told by others they are too thin and, in most cases, underweight. Becomes intolerant to cold and frequently complains of being cold from loss of insulating body fat or poor circulation resulting from extremely low blood pressure; body temperature lowers (hypothermia) in effort to conserve energy[27] Depression: may frequently be in a sad, lethargic state[28] Solitude: may avoid friends and family; becomes withdrawn and secretive Cheeks may become swollen because of enlargement of the salivary glands caused by excessive vomiting[29] Swollen joints[30] Abdominal distension Bad breath (from vomiting or starvation-induced ketosis) Hair loss or thinning[31] Fatigue [32] Dermatologic signs of anorexia nervosa[33] xerosis cutis telogen effluvium carotenoderma acne vulgaris hyperpigmentation seborrhoeic dermatitis acrocyanosis chilblains petechiae livedo reticularis interdigital intertrigo paronychia generalized pruritus acquired striae distensae angular stomatitis prurigo pigmentosa edema linear erythema craquele acrodermatitis enteropathica pellagra Possible medical complications of anorexia nervosa constipation[34] diarrhea[35] electrolyte imbalance[36] cavities[37] tooth loss[38] cardiac arrest[39] amenorrhoea[40] edema[41] osteoporosis[42] osteopenia[43] hyponatremia[44] hypokalemia[45] optic neuropathy[46] brain atrophy[47][48] leukopenia[49][50] [edit]Medical complications Anorexia nervosa can have serious implications if its duration and severity are significant and if onset occurs before the completion of growth, pubertal maturation or prior to attaining peak bone mass.[51] Complications specific to adolescents and children with anorexia nervosa can include the following: Growth retardation – height gain may slow and can stop completely with severe weight loss or chronic malnutrition. In such cases, provided that growth potential is preserved, height increase can resume and reach full potential after normal intake is resumed.[51] Height potential is normally preserved if the duration and severity of illness are not significant and/or if the illness is accompanied with delayed bone age (especially prior to a bone age of approximately 15 years), as hypogonadism may negate the deleterious effects of undernutrition on stature by allowing for a longer duration of growth compared to controls.[52] In such cases, 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 tissue levels compared to premorbid levels.[53][54][55] 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 pituitary gland. Suppression of gonadotrophins in patients with anorexia nervosa has been frequently documented.[51] However, a study demonstrated that growth hormone 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, similar to the resistance to growth hormone of bone-formation markers.[52] Instead, insulin-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 to affect height measures.[52] Reduction of Peak Bone Mass – bone accretion is the highest during adolescence, and if onset of anorexia nervosa occurs during this time and stalls puberty, bone mass may remain low.[51] Hepatic steatosis – fatty infiltration of the liver, is an indicator of malnutrition in children.[51] [edit]Causes Studies have hypothesized the continuance of disordered eating patterns may be epiphenomena of starvation. The results of the Minnesota Starvation Experiment showed 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 the neuroendocrine system, which results in a self-perpetuating cycle.[56][57][58][59] 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 from unintended weight loss that resulted from varied causes, such as a parasitic infection, medication side effects, and surgery. The weight loss itself was the triggering factor.[60][61] [edit]Biological Obstetric complications: various prenatal and perinatal complications may factor into the development of anorexia nervosa, such as maternal anemia, diabetes mellitus, preeclampsia, placental infarction, and neonatal cardiac abnormalities. Neonatal complications may also have an influence on harm avoidance, one of the personality traits associated with the development of AN.[62][63] Genetics: anorexia nervosa is believed to be highly heritable, with estimated inheritance rates ranging from 56% to 84%.[64][65][66] Association studies have been performed, studying 128 different polymorphisms related to 43 genes including genes involved in regulation of eating behavior, motivation and reward mechanics, personality traits and emotion. Consistent associations have been identified for polymorphisms associated with agouti-related peptide, brain derived neurotrophic factor, catechol-o-methyl transferase, SK3 and opioid receptor delta-1.[67] In one study, variations in the norepinephrine transporter gene promoter were associated with restrictive anorexia nervosa, but not binge-purge anorexia.[68] Recent 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 brain to anorexic (feeding suppressing) effects of the female sex hormone, estrogen.[69] This viewpoint has been recently supported by a report that abnormal forms of the estrogen receptor are more common in women with anorexia nervosa of the restricting type.[70] epigenetics: Epigenetic mechanisms: are means by which genetic mutations are caused by environmental effects that alter gene expression via methods such as DNA methylation, these are independent of and do not alter the underlying DNA sequence. They are heritable, as was shown in the Överkalix study, but also may occur throughout the lifespan, and are potentially reversible. Dysregulation of dopaminergic neurotransmission and Atrial natriuretic peptide homeostasis resulting from epigenetic mechanisms has been implicated in various eating disorders.[71] "We conclude that epigenetic mechanisms may contribute to the known alterations of ANP homeostasis in women with eating disorders."[71][72] Dysregulation of the dopamine and serotonin pathways has been implicated in the etiology, pathogenesis and pathophysiology of anorexia nervosa.[73][74][75][76] serotonin dysregulation;[77] particularly high levels in those areas in the brain with the 5HT1A receptor – a system particularly linked to anxiety, mood and impulse control. Starvation has been hypothesized to be a response to these effects, as it is known to lower tryptophan and steroid hormone metabolism, which might reduce serotonin levels at these critical sites and ward off anxiety. Other studies of the 5HT2A serotonin receptor (linked to regulation of feeding, mood, and anxiety), suggest that serotonin activity is decreased at these sites. There is evidence that both personality characteristics associated with AN, and disturbances to the serotonin system are still apparent after patients have recovered from anorexia.[78] Brain-derived neurotrophic factor (BDNF) is a protein that regulates neuronal development and neuroplasticity, it also plays a role in learning, memory and in the hypothalamic pathway that controls eating behavior and energy homeostasis. BDNF amplifies neurotransmitter responses and promotes synaptic communication in the enteric nervous system. Low levels of BDNF are found in patients with AN and some comorbid disorders such as major depression.[79][80] Exercise increases levels of BDNF[81] leptin and ghrelin; leptin is a hormone produced primarily by the fat cells in white adipose tissue of the body it has an inhibitory (anorexigenic) effect on appetite, by inducing a feeling of satiety. Ghrelin is an appetite inducing (orexigenic) hormone produced in the stomach and the upper portion of the small intestine. Circulating levels of both hormones are an important factor in weight control. While often associated with obesity both have been implicated in the pathophysiology of anorexia nervosa and bulimia nervosa.[82] cerebral blood flow (CBF); neuroimaging studies have shown reduced CBF in the temporal lobes of anorectic patients, which may be a predisposing factor in the onset of AN.[83] autoimmune system; Autoantibodies against neuropeptides such as melanocortin have been shown to affect personality traits associated with eating disorders such as those that influence appetite and stress responses.[84] Infections: Some people are hypothesized to have developed anorexia abruptly as a reaction to a streptococcus or mycoplasma infection. PANS is an acronym for Pediatric acute-onset neuropsychiatric syndrome, a hypothesis describing children who have abrupt, dramatic onset of obsessive-compulsive disorder (OCD) or anorexia nervosa coincident with the presence of two or more neuropsychiatric symptoms.[85] Nutritional deficiencies Zinc deficiency may play a role in anorexia. It is not thought responsible for causation of the initial illness but there is evidence that it may be an accelerating factor that deepens the pathology of the anorexia. A 1994 randomized, double-blind, placebo-controlled trial showed that zinc (14 mg per day) doubled the rate of body mass increase compared to patients receiving the placebo.[86] [edit]Environmental Sociocultural studies have highlighted the role of cultural factors, such as the promotion of thinness as the ideal female form in Western industrialized nations, particularly through the media.[87] A change in culture can cause anorexia nervosa in teenage girls who live in a Western culture and are from immigrant families.[88] A recent epidemiological study of 989,871 Swedish residents indicated that gender, ethnicity and socio-economic status were large influences on the chance of developing anorexia, with those with non-European parents among the least likely to be diagnosed with the condition, and those in wealthy, white families being most at risk.[89] People in professions where there is a particular social pressure to be thin (such as models and dancers) were much more likely to develop anorexia during the course of their career,[90] and further research has suggested that those with anorexia have much higher contact with cultural sources that promote weight-loss.[91] Anorexia nervosa is more likely to occur in a person's pubertal years, especially for girls.[92] Female students are 10 times more likely to suffer from anorexia nervosa than male students. According to a survey of 1799 Japanese female high school students, "85% who were a normal weight wanted to be thinner and 45% who were 10–20% underweight wanted to be thinner."[93] Teenage girls concerned about their weight and who believe that slimness is more attractive among peers trend to weight-control behaviors. Teen girls are learning from each other to consume low-caloric, low-fat foods and diet pills. This results in lack of nutrition and a greater chance of developing anorexia nervosa.[94] It has also been noted that anorexia nervosa is more likely to occur in populations in which obesity is more prevalent. It has been suggested that anorexia nervosa results from a sexually selected evolutionary drive to appear youthful in populations in which size becomes the primary indicator of age.[95] There is also evidence to suggest that patients who have anorexia nervosa can be characterised by alexithymia[96] and also a deficit in certain emotional functions. A research study showed that this was the case in both adult and adolescent anorexia nervosa patients.[97] There is a high rate of reported child sexual abuse experiences in clinical groups of who have been diagnosed with anorexia. The connection between eating disorders and abuse has been convincingly evidenced by a number of studies, including one published in Epidemiology (and strengthened by blind hypothesis survey), which showed in a comparison of women with no history of eating disorders, women with a history of eating disorders were twice as likely to have reported childhood sexual abuse.[98] While the joint effect of both physical and sexual abuse resulted in a nearly 4-fold risk of eating disorders that met DSM-IV criteria.[98] It is thought that links between childhood abuse and sexual abuse are complex, such as by influencing psychologic processes that increase a woman's susceptibility to the development of an eating disorder, or perhaps by producing changes in psychobiologic process and neurotransmitting function, associated with eating behaviour.[98] Recent efforts have been made to dispel some of the myths around anorexia nervosa and eating disorders, such as the misconception that families, in particular mothers, are responsible for their daughter developing an eating disorder.[99] [edit]Relationship to autism A summary of the strategy Zucker et al. (2007) used to assess the relationship between anorexia nervosa and the autism spectrum.[100] Since Gillberg's (1983 & 1985)[101][102] and others' initial suggestion of relationship between anorexia nervosa and autism,[103][104] a large-scale longitudinal study into teenage-onset anorexia nervosa conducted in Sweden confirmed that 23% of people with a long-standing eating disorder are on the autism spectrum.[105][106][107][108][109][110][111] Those on autism spectrum tend to have a worse outcome,[112] but may benefit from the combined use of behavioural and pharmacological therapies tailored to ameliorate autism rather than anorexia nervosa per se.[113][114] 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 flexibility, emotion regulation and understanding facial expressions.[115][116][117][118][119][120] 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).[100] A pilot study into the effectiveness Cognitive Behaviour Therapy, which based its treatment protocol on the hypothesised relationship between anorexia nervosa and an underlying autistic like condition, reduced perfectionism and rigidity in 17 out of 19 participants.[121] [edit]Diagnosis [edit]Medical The initial diagnosis should be made by a competent medical professional. There are multiple medical conditions, such as viral or bacterial infections, hormonal imbalances, neurodegenerative diseases and brain tumors which may mimic psychiatric disorders including anorexia nervosa. According to an in depth study conducted by psychiatrist Richard Hall as published in the Archives of General Psychiatry: Medical illness often presents with psychiatric symptoms. It is difficult to distinguish physical disorders from functional psychiatric disorders on the basis of psychiatric symptoms alone. Detailed physical examination and laboratory screening are indicated as a routine procedure in the initial evaluation of psychiatric patients. Most patients are unaware of the medical illness that is causative of their psychiatric symptoms. The conditions of patients with medically induced symptoms are often initially misdiagnosed as a functional psychosis.[122][123] 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.[124] urinalysis: a variety of tests performed on the urine used in the diagnosis of medical disorders, to test for substance abuse, and as an indicator of overall health[125] ELISA: Various subtypes of ELISA used to test for antibodies to various viruses and bacteria such as Borrelia burgdoferi (Lyme Disease)[126] Western Blot Analysis: Used to confirm the preliminary results of the ELISA[127] 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 such as potassium, chlorine and sodium and tests specific to liver and kidney function.[128] glucose tolerance test: Oral glucose tolerance test (OGTT) used to assess the body's ability to metabolize glucose. Can be useful in detecting various disorders such as diabetes, an insulinoma, Cushing's Syndrome, hypoglycemia and polycystic ovary syndrome[129][130] Secritin-CCK Test: Used to assess function of pancreas and gall bladder[131][132] Serum cholinesterase test: a test of liver enzymes (acetylcholinesterase and pseudocholinesterase) useful as a test of liver function and to assess the effects of malnutrition[133] 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, kidney function, bleeding disorders, Crohn's Disease[134] 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 cases.[135] Creatine Kinase Test (CK-Test): measures the circulating blood levels of creatine kinase an enzyme found in the heart (CK-MB), brain (CK-BB) and skeletal muscle (CK-MM).[136][137] Blood urea nitrogen (BUN) test: urea nitrogen is the byproduct of protein metabolism first formed in the liver then removed from the body by the kidneys. The BUN test is used primarily to test kidney function. A low BUN level may indicate the effects of malnutrition.[138] BUN-to-creatinine ratio: A BUN to creatinine ratio is used to predict various conditions. 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 liver.[139][140][141] electrocardiogram (EKG or ECG): measures electrical activity of heart can be used to detect various disorders such as hyperkalemia[142] electroencephalogram (EEG): measures the electrical activity of the brain. Can be used to detect abnormalities such as those associated with pituitary tumors[143][144] Upper GI Series: test used to assess gastrointestinal problems of the middle and upper intestinal tract[145] Thyroid Screen TSH, t4, t3 :test used to assess thyroid functioning by checking levels of thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3)[146] Parathyroid hormone (PTH) test: tests the functioning of the parathyroid by measuring the amount of (PTH) in the blood. Test is used to diagnose parahypothyroidism. PTH also controls the levels of calcium and phosphorus in the blood (homeostasis).[147] barium enema: an x-ray examination of the lower gastrointestinal tract[148] neuroimaging; via the use of various techniques such as PET scan, fMRI, MRI and SPECT imaging should be included in the diagnostic procedure for any eating disorder to detect cases in which a lesion, tumor or other organic condition has been either the sole causative or contributory factor in an eating disorder.[citation needed] [edit]Psychological Not only does starvation result in physical complications, but mental complications as well.[149] It has been shown that eating disorders such as anorexia nervosa are reinforced by reward and attention. P. Sodersten and colleagues suggest that effective treatment of this disorder depends on re-establishing reinforcement for normal eating behaviours instead of unhealthy weight loss.[3] Anorexia nervosa is classified as an Axis I[150] disorder in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM-IV), published by the American Psychiatric Association. The DSM-IV should not be used by laypersons to diagnose themselves. DSM-IV-TR: diagnostic criteria for AN includes intense fear of gaining weight, a refusal to maintain body weight above 85% of the expected weight for a given age and height, and three consecutive missed periods and either refusal to admit the seriousness of the weight loss, or undue influence of shape or weight on one's self-image, or a disturbed experience in one's shape or weight. There are two types: the binge-eating/purging type is characterized by overeating or purging, and the restricting type is not.[151] Criticism of DSM-IV There has been criticisms over various aspects of the diagnostic criteria utilized for anorexia nervosa in the DSM-IV. Including the requirement of maintaining a body weight below 85% of the expected weight and the requirement of amenorrhea for diagnosis; some women have all the symptoms of AN and continue to menstruate.[152] Those who do not meet these criteria are usually classified as eating disorder not otherwise specified; this may affect treatment options and insurance reimbursments.[153] The validity of the AN subtype classification has also been questioned because of the considerable diagnostic overlap between the binge-eating/purging type and the restricting type and the propensity of the patient to switch between the two.[154][155] Criticisms of DSM-IV and Diagnosing Adolescents with Anorexia Nervosa – There have been criticisms over the diagnostic criteria utilized for anorexia nervosa in the DSM- IV and its applicability in diagnosing adolescents with anorexia nervosa. Several criticisms of the DSM-IV in diagnosing adolescents with anorexia nervosa are: Fulfillment of DSM- IV criteria B and C for anorexia nervosa are dependent on complex abstract reasoning, the capacity to describe internal experiences, and the ability to perceive risk.[156] While formal thought emerges between ages 11–13, complex abstract reasoning continues to develop late into adolescence. The ability to perceive risk also continues to develop through adolescence, as some preadolescents have difficult perceiving the relative risk of alternative outcomes.[156] 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 deny the seriousness of low body weight despite their behaviors that contribute to harmful weight loss, which are necessary to fulfill criteria B and C.[157] These developmental factors may impede an adolescent or child from receiving a diagnosis 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 account when revising the current criteria. One proposed amendment would be to allow behavioral indicators as a means of substituting internally referenced cognitive criteria.[156] Another criticism focuses on the current weight criteria specified to receive a diagnosis of anorexia nervosa. Critics state that there is wide variability in the rate, timing and magnitude of both height and weight gain during normal puberty.[158] Physical development varies greatly during puberty, making it a challenge to define an optimal weight range for a growing child or adolescents.[157] 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 involving hypothalamic-pituitary-gonadal axis is manifest in women as amenorrhoea and in men as loss of sexual interest and potency. There may also be elevated levels of growth hormones, raised cortisol levels, changes in the peripheral metabolism of thyroid hormone and abnormalities of insulin secretion". 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 writes, "The state of starvation is associated by marked psychological changes... camouflaged by rationalizations." She identifies the family interaction becomes 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" and "primary" cases of anorexia nervosa. The atypical cases of anorexia were brought about by a range of stimuli (from schizophrenia to depression, as noted above). (Bruch 227). In contrast to the atypical group, Bruch observed primary, or genuine anorexia nervosa, "amazingly uniform". The first outstanding symptom is "disturbance of delusional proportions in the body image". The second outstanding characteristic is "disturbance in the accuracy of their perception or cognitive interpretation of stimuli arising from the body... failure to recognize hunger and denial of fatigue". The third outstLikes: Everybody else. P.S. Erica Campbell is the most beautiful woman in the world. End of story. That's my opinion. :) Dislikes: The "constantly-hating crowd" of losers.Favorite Music: My favorite bands right now are Ke$ha and Dazzle Vision, also 45 Grave (from way back), Switchblade Symphony, and 7 Seconds, but I'm always going to be a fan of Lindsay Lohan (because you make me fall in love with everybody on Earth again), Pink (the punk), Lady Gaga (befcause she's so real) and Jennifer Lopez (only because she's so beautiful and her voice is so raw). I also like Merril Bainbridge, Katie Melau, Rick Ross, David Rush, Belly, Beastie Boys, FraMnkie Goes To Hollywood, Duran Duran, Pet Shop Boys, and Led Zepplin. Punk's close to my heart, even though I listen to it very little these days. Tthese bands were my formative musical influences: T.S.O.L., Agent Orange, Brimstone (the Orangevale, CA underground post-punk goth band), Hollowman (the original Sacramento/LA band), Van Halen, 7 Seconds, 45 Grave, Circle Jerks, Dead Kennedys, MIA (referring to the original underground punk band that is now truly M.I.A.!!! Where are you guys?), The Vandals, and NENA. Other favorites include: Amy Winehouse (Rest In Peace), Johnny Cash and lots to come as soon as I can type them in. I should probably categorize this later, since I don't think that Mariah Carey would enjoy sitting next to Jello Biafra on this list! :)Homepage: http://www.redbgenetics.com/ Link 1: https://twitter.com/
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