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Revision as of 03:38, 7 August 2009

For other uses, see Anorexia nervosa (disambiguation).
Anorexia nervosa
SpecialtyPsychiatry, clinical psychology Edit this on Wikidata

Anorexia nervosa is a psychiatric illness that describes an eating disorder characterized by extremely low body weight and body image distortion with an obsessive fear of gaining weight. Individuals with anorexia nervosa are known to control body weight commonly through the means of voluntary starvation, excessive exercise, or other weight control measures such as diet pills or diuretic drugs. While the condition primarily affects adolescent females approximately 10% of people with the diagnosis are male. [1] Anorexia nervosa, involving neurobiological, psychological, and sociological components[2], is a complex condition that can lead to death in the most severe cases.

The term anorexia is of Greek origin: a (α, prefix of negation), n (ν, link between two vowels) and orexis (ορεξις, appetite), thus meaning a lack of desire to eat.[3]

"Anorexia nervosa" is frequently shortened to "anorexia" in the popular media. This is technically incorrect, as the term "anorexia" used separately refers to the medical symptom of reduced appetite (which therefore is distinguishable from anorexia nervosa in being non-psychiatric).

Diagnosis and clinical features

Established by the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) and the World Health Organization's International Statistical Classification of Diseases and Related Health Problems (ICD).


Furthermore, the DSM-IV-TR specifies two subtypes:

  • Restricting Type: during the current episode of anorexia nervosa, the person has not regularly engaged in binge-eating or purging behavior (that is, self-induced vomiting, or the misuse of laxatives, diuretics, or enemas). Weight loss is accomplished primarily through dieting, fasting, or excessive exercise.
  • Binge-Eating Type or Purging Type: during the current episode of anorexia nervosa, the person has regularly engaged in binge-eating OR purging behavior (that is, self-induced vomiting, or the misuse of laxatives, diuretics, or enemas).

The ICD-10 criteria are similar, but in addition, specifically mention

  1. 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).
  2. 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".
  3. If onset is before puberty, that development is delayed or arrested.

Presentation

There are a number of features that, although not necessarily diagnostic of anorexia, have been found to be commonly (but not exclusively) present in those with this eating disorder.[2][4]

Physical

Changes in brain structure and function are early signs often to be associated with starvation, and is partially reversed when normal weight is regained.[5] Anorexia is also linked to reduced blood flow in the temporal lobes, although since this finding does not correlate with current weight, it is possible that it is a risk trait rather than an effect of starvation.[6]

Other effects may include the following:

Psychological

  • Distorted body image
  • Poor insight
  • Self-evaluation largely, or even exclusively, in terms of their shape and weight
  • Pre-occupation or obsessive thoughts about food and weight
  • Perfectionism
  • Obsessive compulsive disorder (OCD)
  • Belief that control over food/body is synonymous with being in control of one's life
  • Refusal to accept that one's weight is dangerously low even when it could be deadly
  • Neuropsychological impairment at very low body weights

Emotional

Behavioral

  • Excessive exercise, food restriction
  • Secretive about eating or exercise behavior
  • Fainting
  • Social withdraw or being asocial
  • Self-harm, substance abuse or suicide attempts
  • Very sensitive to references about body weight
  • Aggressive when forced to eat "forbidden" foods
  • Weighing themselves and constantly checking themselves in the mirror

Diagnostic issues and controversies

The distinction between the diagnoses of anorexia nervosa, bulimia nervosa and eating disorder not otherwise specified (EDNOS) is often difficult to make in practice and there is considerable overlap between patients diagnosed with these conditions. Furthermore, seemingly minor changes in a patient's overall behavior or attitude (such as reported feeling of "control" over any binging behavior) can change a diagnosis from "anorexia: binge-eating type" to bulimia nervosa. It is not unusual for a person with an eating disorder to "move through" various diagnoses as his or her behavior and beliefs change over time.[4]

Additionally, it is important to note that an individual may still suffer from a health- or life-threatening eating disorder (e.g., sub-clinical anorexia nervosa or EDNOS) even if one diagnostic sign or symptom is still present. For example, a substantial number of patients diagnosed with EDNOS meet all criteria for diagnosis of anorexia nervosa, but lack the three consecutive missed menstrual cycles needed for a diagnosis of anorexia.[2]

Feminist writers such as Susie Orbach and Naomi Wolf have criticized the medicalization of extreme dieting and weight-loss as locating the problem within the affected women, rather than in a society that imposes concepts of unreasonable and unhealthy thinness as a measure of female beauty and gaining weight. Other writers have suggested that the disorder relates to issues of self-perception that are deeper than concerns with beauty and public perception.[7]

A vigorous debate exists on the topic of whether eating disorders are a choice or a biological illness. In 2006, Dr. Thomas Insel, director of the US National Institute of Mental Health, wrote an open letter to the National Eating Disorder Association stating "eating disorders are brain disorders."

Causes and contributory factors

It is clear that there is no single cause for anorexia and that it stems from a mixture of biological, social, and psychological factors. Current research is commonly focused on explaining existing factors and uncovering new causes. However, there is considerable debate over how much each of the known causes contributes to the development of anorexia. In particular, the contribution of perceived media pressure on women to be thin has been especially contentious.[8]

Physiological factors

Genetic factors

Family and twin studies have suggested that genetic factors contribute to about 50% of the variance for the development of an eating disorder[9] and that anorexia shares a genetic risk with clinical depression.[10] This evidence suggests that genes influencing both eating regulation, and personality and emotion, may be important contributing factors. In one study, variations in the norepinephrine transporter gene promoter were associated with restrictive anorexia nervosa, but not binge-purge anorexia (though the latter may have been due to small sample size).[11]

Several rodent models of anorexia have been developed which largely involve subjecting the animals to various environmental stressors or using gene knockout mice to test hypotheses about the effects of certain genes.[12] These models have suggested that the hypothalamic-pituitary-adrenal axis may be a contributory factor. However, these models have been criticised as food is being limited by the experimenter and not the animal and cannot take into account the complex cultural factors known to affect the development of anorexia nervosa.

Neurobiological factors

There are strong correlations between the neurotransmitter serotonin and various psychological symptoms such as mood, sleep, emesis (vomiting), sexuality and appetite. A recent review of the scientific literature has suggested that anorexia is linked to a disturbed serotonin system,[13] particularly to high levels at areas in the brain with the 5HT1A receptor - a system particularly linked to anxiety, mood and impulse control. Starvation has been hypothesised to be a response to these effects, as it is known to lower tryptophan and steroid hormone metabolism, which, in turn, might reduce serotonin levels at these critical sites and, hence, ward off anxiety. In contrast, studies of the 5HT2A serotonin receptor (linked to regulation of feeding, mood, and anxiety), suggest that serotonin activity is decreased at these sites. One difficulty with this work is that it is sometimes difficult to separate cause and effect, in that these disturbances to brain neurochemistry may be as much the result of starvation, than continuously existing traits that might predispose someone to develop anorexia. However, there is evidence that both personality characteristics (such as anxiety and perfectionism) and disturbances to the serotonin system are still apparent after patients have recovered from anorexia.[14] This suggests that these disturbances are likely to be causal risk factors.

Recent studies also suggest anorexia may be linked to an autoimmune response to melanocortin peptides which influence appetite and stress responses. [15]

Nutritional factors

Zinc deficiency causes a decrease in appetite that can degenerate in anorexia nervosa (AN), appetite disorders and, notably, inadequate zinc nutriture. The use of zinc in the treatment of anorexia nervosa has been advocated since 1979 by Bakan. At least five trials showed that zinc improved weight gain in anorexia. A 1994 randomized, double-blind, placebo-controlled trial showed that zinc (14 mg per day) doubled the rate of body mass increase in the treatment of AN.[16] Deficiency of other nutrients such as tyrosine and tryptophan (precursors of the monoamine neurotransmitters norepinephrine and serotonin, respectively), as well as vitamin B1 (thiamine) could contribute to this phenomenon of malnutrition-induced malnutrition.[16]

Psychological factors

There has been a significant amount of study on psychological factors that suggests how biases in thinking and perception help maintain or contribute to the risk of developing anorexia.

Anorexic eating behavior is thought to originate from feelings of fatness and unattractiveness[17] and is maintained by various cognitive biases that alter how the affected individual evaluates and thinks about their body, food and eating.

One of the most well-known findings is that people with anorexia tend to over-estimate the size or fatness of their own bodies. A recent review of research in this area suggests that this is not a perceptual problem, but one of how the perceptual information is evaluated by the affected person.[18] Recent research suggests people with anorexia nervosa may lack a type of overconfidence bias in which the majority of people feel themselves more attractive than others would rate them. In contrast, people with anorexia nervosa seem to more accurately judge their own attractiveness compared to unaffected people, meaning that they potentially lack this self-esteem boosting bias.[19]

People with anorexia have been found to have certain personality traits that are thought to predispose them to develop eating disorders. High levels of obsession (being subject to intrusive thoughts about food and weight-related issues), restraint (being able to fight temptation), and clinical levels of perfectionism (the pathological pursuit of personal high-standards and the need for control) have been cited as commonly reported factors in research studies.[20]

It is often the case that other psychological difficulties and mental illnesses exist alongside anorexia nervosa in the sufferer. Clinical depression, obsessive compulsive disorder, substance abuse and one or more personality disorders are the most likely conditions to be comorbid with anorexia, and high-levels of anxiety and depression are likely to be present regardless of whether they fulfill diagnostic criteria for a specific syndrome.[21]

Research into the neuropsychology of anorexia has indicated that many of the findings are inconsistent across studies and that it is hard to differentiate the effects of starvation on the brain from any long-standing characteristics. Nevertheless, one reasonably reliable finding is that those with anorexia have poor cognitive flexibility[22] (the ability to change past patterns of thinking, particularly linked to the function of the frontal lobes and executive system).

Other studies have suggested that there are some attention and memory biases that may maintain anorexia.[23] Attentional biases seem to focus particularly on body and body-shape related concepts, making them more salient for those affected by the condition, and some limited studies have found that those with anorexia may be more likely to recall related material than unrelated material.

File:Fairburn et al Anorexia Model.png
Fairburn and colleagues psychological model of anorexia

Although there has been quite a lot of research into psychological factors, there are relatively few hypotheses which attempt to explain the condition as a whole.

Professor Chris Fairburn, of the University of Oxford and his colleagues have created a "transdiagnostic" model,[24] in which they aim to explain how anorexia, as well as related disorders such as bulimia nervosa and ED-NOS, are maintained. Their model is developed with psychological therapies, particularly cognitive behavioral therapy, in mind, and so suggests areas where clinicians could provide psychological treatment.

Their model is based on the idea that all major eating disorders (with the exception of obesity) share some core types of psychopathology which help maintain the eating disorder behavior. This includes clinical perfectionism, chronic low self-esteem, mood intolerance (inability to cope appropriately with certain emotional states) and interpersonal difficulties.

Social and environmental factors

Sociocultural studies have highlighted the role of cultural factors, such as the promotion of thinness as the ideal female form in Western industrialised nations, particularly through the media. 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.[25] A classic study by Garner and Garfinkel demonstrated that those 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,[26] and further research has suggested that those with anorexia have much higher contact with cultural sources that promote weight-loss.[27]

Although anorexia nervosa is usually associated with Western cultures, exposure to Western media is thought to have led to an increase in cases in non-Western countries. However, it is notable that other cultures may not display the same "fat phobic" worries about becoming fat as those with the condition in the West, and instead may present with low appetite with the other common features.[28]

There is a high rate of reported child sexual abuse experiences in clinical groups of who have been diagnosed with anorexia (up to 50% in those admitted to inpatient wards, with a lesser prevalence among people treated in the community). Although prior sexual abuse is not thought to be a specific risk factor for anorexia, those who have experienced such abuse are more likely to have more serious and chronic symptoms.[29]

The Internet has enabled anorexics and bulimics to contact and communicate with each other outside of a treatment environment, with much lower risks of rejection by mainstream society. A variety of websites exist, some run by sufferers, some by former sufferers, and some by professionals. The majority of such sites support a medical view of anorexia as a disorder to be cured, although some people affected by anorexia have formed online pro-ana communities that reject the medical view and argue that anorexia is a "lifestyle choice", using the internet for mutual support, and to swap weight-loss tips.[30] Such websites were the subject of significant media interest, largely focusing on concerns that these communities could encourage young women to develop or maintain eating disorders, and many were taken offline as a result.[31]

Prognosis

Anorexia is thought to have the highest mortality rate of any psychiatric disorder, with approximately 6% of those who are diagnosed with the disorder eventually die due to related causes.[32] The suicide rate of people with anorexia is also higher than that of the general population and is thought to be the major cause of death for those with the condition.[33]

Incidence, prevalence and demographics

The majority of research into the incidence and prevalence of anorexia has been done in Western industrialized countries, so results are generally not applicable outside these areas. However, recent reviews[34][35] of studies on the epidemiology of anorexia have suggested an incidence of between 8 and 13 cases per 100,000 persons per year and an average prevalence of 0.3% using strict criteria for diagnosis. These studies also confirm the view that the condition largely affects young adolescent females, with females between 15 and 19 years old making up 40% of all cases. Furthermore, the majority of cases are unlikely to be in contact with mental health services. As a whole, about 10% of people with anorexia are male and about 90% of people with anorexia are female.[2] Anorexia, however, is not exclusively limited to any age or demographic. In March 2008, a British senior university lecturer with PhD in psychology and a professional background in health, Rosemary Pope, died from anorexia.[36] Anorexia has been reported occurring throughout a patient's life extending into the seventies and eighties.[37] In addition, onset can occur in one's sixties or later.[38] The Italian character actor, Giovanni Rovini, died of onset of symptoms commencing in his early nineties. [39]

Treatment

The first line treatment for anorexia is usually focused on immediate weight gain, especially with those who have particularly serious conditions that require hospitalization. In particularly serious cases, this may be done as an involuntary hospital treatment under mental health law, where such legislation exists. In the majority of cases, however, people with anorexia are treated as outpatients, with input from physicians, psychiatrists, clinical psychologists and other mental health professionals.

Medication treatments plays a much less prominent role in anorexia than for many other psychiatric disorders. There is some evidence for the benefit from pharmacologic treatments but the use of medication in anorexia is not all that well established. Many medications have been tried with mixed but mostly discouraging results. There are divergent reports on the use and efficacy of fluoxetine for anorexia relapse prevention. There has been some encouraging research on the use of antipsychotics in the treatment of anorexia, most namely olanzapine, risperidone and quetiapine.[citation needed] But on the whole there is no convincing evidence of the efficacy for any drug treatment for anorexia in either the acute or chronic phrase of the disorder. Anorexia is one of the few mental disorders of which this may be said. To date, no specific type of psychotherapy seems to show any overall advantage when compared to other types.

Family therapy has also been found to be an effective treatment for adolescents with anorexia[40] and in particular, a method developed at the Maudsley Hospital called the Maudsley Approach or Family-Based Treatment (FBT) is widely used and found to maintain improvement over time.[41]

An alternative approach to treatment has been proposed by Per Sodersten in Sweden, who has found that the main features of anorexia (slow, deliberate eating patterns, hyperactivity, and hypothermia) seem to reinforce the disorder. Sodersten's group suggests that keeping patients warm and normally active, and encouraging more normal meal-taking patterns, may be of aid (Sodersten P (2003) Anorexia nervosa: towards a neurbiologically based therapy. European J. Pharmacology, 480, 67-74.)

Drug treatments, such as SSRI or other antidepressant medication, have not been found to be generally effective for either treating anorexia,[42] or preventing relapse[43] although it has also been noted that there is a lack of adequate research in this area. It is common, however, for antidepressants to be prescribed, often with the intent of trying to treat the associated anxiety and depression.

Supplementation with 14 mg/day of zinc is recommended as routine treatment for anorexia nervosa due to a study showing a doubling of weight regain after treatment with zinc was begun. The mechanism of action is hypothesized to be an increased effectiveness of neurotransmission in various parts of the brain, including the amygdala, after adequate zinc intake begins resulting in increased appetite.[44]

There are various non-profit and community groups that offer support and advice to people who suffer from anorexia or who care for someone who does.

Family-Based Treatment or Maudsley Approach

Family-Based Treatment (FBT) has been shown to be an effective treatment for adolescents and young adults (younger than 19 years old) suffering from anorexia nervosa with a short history (less than 3 years).[45] Developed in the 1980s at the Maudsley Hospital in London, FBT is also known as the Maudsley Approach, Maudsley Treatment or Maudsley Method. A somewhat similar treatment method based on Maudsley called Behavioral Systems Family Therapy (BSFT) is also promising, according to studies. Another Maudsley offshoot, called Multiple-Family Day Treatment (MFDT), is currently being evaluated.[46]

"At this time, the evidence base is strongest for the Maudsley model of family therapy for anorexia nervosa," according to a 2008 paper published in the Journal of Clinical Child & Adolescent Psychology[47]. In 2008 published research on family-based interventions involving adolescents shows that "At 4-5 year follow-up, the majority (60-90%) will have fully recovered while only 10-15% will still be seriously ill. Outpatient family therapy compares quite favorably to other treatment modalities such as inpatient care where full recovery rates vary between 33% - 55%."[48]

FBT sees the parents of the ill person as the best ally for recovery. The effects of dieting (or insufficient food for a person's activity level) create for many people a self-perpetuating cycle that requires intervention. In this approach, parents are seen as the most committed and competent people in the patient's life and therefore best qualified to find ways to fight the illness, to regain healthy weight, to end unhealthy behaviors and to return their child to normal adolescent development unencumbered by the eating disorder.[citation needed]

FBT, with its emphasis on full weight restoration as the basis of recovery, differs from other approaches which rely on the patient's insight and motivation as necessary to recovery. FBT also challenges the traditional psychiatric view[vague] which holds that family and parental dysfunction are at the root of eating disorders and which questions the role of parents in the treatment. The approach is also appropriate for bulimia and for older patients whose families are able to take on this role.[citation needed]

Since its successful use in the UK, the treatment has spread to the United States, Australia, and Canada and is seen as a alternative model to costly inpatient or day hospital programs. Research has validated FBT for use with children and adolescents living at home. Modified versions of the approach have been used successfully with older patients, multi-family group trainings, Binge Eating Disorder patients, and for couples. Success rates for treatment are promising: small trials indicate 75-90% of patients are still well five years after treatment for anorexia, while most other treatments show only one third of patients in long-term recovery.[citation needed]

Methodology

In most cases, the treatment has three phases over a period of 6–12 months, led by an FBT therapist, and involve the entire family in hour-long weekly sessions. The parents are coached in how to help the patient eat (and/or stop purging and over-exercising) and siblings are encouraged to ally with the ill sibling. Patients are neither expected to nor asked to cooperate; in the first session of FBT/Maudsley therapy a meal is eaten in the therapist's office and the ill person is asked to resist eating to demonstrate the dynamics of the family around the meal.

The treatment for bulimia is slightly different: the patients, usually older and more ready to engage in therapy, are more involved with the problem-solving phase of recovery.

No one is blamed in FBT therapy; the illness is not seen as anyone's fault, and finding cause for the eating disorder is not part of the treatment at all. For many, the symptoms, behaviors and rituals seen in anorexia lighten in intensity or disappear completely as a result of refeeding and full weight restoration. Many patients make use of psychotherapy after weight restoration, but such therapy is not integral to FBT.

The three phases of treatment are:

  • Parents take control of decisions of what, when, and how much the ill patient eats. The goal is to refeed the patient, usually within 1–3 months.
  • After weight restoration is nearly achieved, control is carefully given back to the patient.
  • In the last phase, the therapist and family work to restore normal and age-appropriate lifestyle and relations between family members.

See also

References

  1. ^ "The Numbers Count: Mental Disorders in America". The National Institute of Mental Health. Retrieved 2008-10-09.
  2. ^ a b c d Lask B, and Bryant-Waugh, R (eds) (2000) Anorexia Nervosa and Related Eating Disorders in Childhood and Adolescence. Hove: Psychology Press. ISBN 0-86377-804-6.
  3. ^ Costin, Carolyn.~ (1999) The Eating Disorder Sourcebook. Linconwood: Lowell House. 6.
  4. ^ a b Gowers S, Bryant-Waugh R. (2004) Management of child and adolescent eating disorders: the current evidence base and future directions. J Child Psychol Psychiatry, 45 (1), 63-83. PMID 14959803
  5. ^ Palazidou E, Robinson P, Lishman WA. (1990) Neuroradiological and neuropsychological assessment in anorexia nervosa. Psychol Med, 20 (3), 521-7. PMID 2236361.
  6. ^ Lask B, Gordon I, Christie D, Frampton I, Chowdhury U, Watkins B. (2005) Functional neuroimaging in early-onset anorexia nervosa. Int J Eat Disord, 37 Suppl, S49-51. PMID 15852320.
  7. ^ Jacobson, K. (2006) The Interpersonal Experience of Human Spatiality: A Phenomenological Interpretation of Anorexia Nervosa. Chiasmi International 8, 157-74
  8. ^ Tiggemann M and Pickering AS. (1996) Role of television in adolescent women's body dissatisfaction and drive for thinness Int J Eat Disord, Sep;20(2):199-203.
  9. ^ Klump KL, Kaye WH, Strober M (2001) The evolving genetic foundations of eating disorders. Psychiatr Clin North Am, 24 (2), 215-25. PMID 11416922.
  10. ^ Wade TD, Bulik CM, Neale M, Kendler KS. (2000) Anorexia nervosa and major depression: shared genetic and environmental risk factors. Am J Psychiatry, 157 (3), 469-71. PMID 10698830.
  11. ^ Urwin, R.E., Bennetts, B., Wilcken, B. et al. (2002). "Anorexia nervosa (restrictive subtype) is associated with a polymorphism in the novel norepinephrine transporter gene promoter polymorphic region," Molecular Psychiatry, 7(6), 652–657.
  12. ^ Siegfried Z, Berry EM, Hao S, Avraham Y. (2003) Animal models in the investigation of anorexia. Physiol Behav, 79 (1), 39-45. PMID 12818708.
  13. ^ Kaye WH, Frank GK, Bailer UF, Henry SE, Meltzer CC, Price JC, Mathis CA, Wagner A. (2005) Serotonin alterations in anorexia and bulimia nervosa: new insights from imaging studies. Physiol Behav, 85 (1), 73-81. PMID 15869768.
  14. ^ Kaye WH, Bailer UF, Frank GK, Wagner A, Henry SE. (2005) Brain imaging of serotonin after recovery from anorexia and bulimia nervosa. Physiol Behav, 86(1-2), 15-7. PMID 16102788.
  15. ^ Fetissov SO, Harro J, Jaanisk M, Jarv A, Podar I, Allik J, Nilsson I, Sakthivel P, Lefvert AK, Hokfelt T. (2005) Autoantibodies against neuropeptides are associated with psychological traits in eating disorders. Proc Natl Acad Sci U S A, 102 (41), 14865-70. PMID 16195379.
  16. ^ a b Shay NF, Mangian HF (2000). "Neurobiology of zinc-influenced eating behavior". The Journal of nutrition. 130 (5S Suppl): 1493S–9S. PMID 10801965. {{cite journal}}: Unknown parameter |month= ignored (help)
  17. ^ Rosen JC, Reiter J, Orosan P. (1995) Assessment of body image in eating disorders with the body dysmorphic disorder examination. Behav Res Ther, 1, 77-84. PMID 7872941.
  18. ^ Skrzypek S, Wehmeier PM, Remschmidt H. (2001) Body image assessment using body size estimation in recent studies on anorexia nervosa. A brief review. Eur Child Adolesc Psychiatry, 10 (4), 215-21. PMID 11794546.
  19. ^ Jansen A, Smeets T, Martijn C, Nederkoorn C. (2006) I see what you see: the lack of a self-serving body-image bias in eating disorders. Br J Clin Psychol, 45 (1), 123-35. PMID 16480571.
  20. ^ Wonderlich SA, Lilenfeld LR, Riso LP, Engel S, Mitchell JE. (2005) Personality and anorexia nervosa. Int J Eat Disord, 37 Suppl, S68-71. PMID 15852324.
  21. ^ O'Brien KM, Vincent NK. (2003) Psychiatric comorbidity in anorexia and bulimia nervosa: nature, prevalence, and causal relationships. Clin Psychol Rev, 23 (1), 57-74. PMID 12559994
  22. ^ Tchanturia K, Campbell IC, Morris R, Treasure J. (2005) Neuropsychological studies in anorexia nervosa. Int J Eat Disord, 37 Suppl, S72-6. PMID 15852325.
  23. ^ Cooper MJ (2005) Cognitive theory in anorexia nervosa and bulimia nervosa: progress, development and future directions. Clin Psychol Rev, 25 (4), 511-31. PMID 15914267.
  24. ^ Fairburn CG, Cooper Z, Shafran R. (2003) Cognitive behavior therapy for eating disorders: a "transdiagnostic" theory and treatment. Behav Res Ther, 41 (5), 509-28. PMID 12711261.
  25. ^ Lindberg L, Hjern A. (2003) Risk factors for anorexia nervosa: a national cohort study. International Journal of Eating Disorders, 34 (4), 397-408. PMID 14566927
  26. ^ Garner DM, Garfinkel PE. (1980) Socio-cultural factors in the development of anorexia nervosa. Psychol Med, 10 (4), 647-56. PMID 7208724.
  27. ^ Toro J, Salamero M, Martinez E. (1994) Assessment of sociocultural influences on the aesthetic body shape model in anorexia nervosa. Acta Psychiatrica Scandinavica, 89 (3), 147-51. PMID 8178671.
  28. ^ Simpson KJ. (2002) Anorexia Nervosa and culture. J Psychiatr Ment Health Nurs, 9 (1), 65-71. PMID 11896858.
  29. ^ Carter JC, Bewell C, Blackmore E, Woodside DB. (2006) The impact of childhood sexual abuse in anorexia nervosa. Child Abuse Negl, 30 (3), 257-69. PMID 16524628.
  30. ^ Norris ML, Boydell KM, Pinhas L, Katzman DK. (2006) Ana and the internet: A review of pro-anorexia websites. International Journal of Eating Disorders, 39(6):443-7. PMID 16721839.
  31. ^ Reaves, J. (2001). Anorexia goes high tech. Time (July). Retrieved on April 16, 2007.
  32. ^ Herzog, David B; Greenwood, Dara N; Dorer, David J; Flores, Andrea T; Ekeblad, Elizabeth R; Richards, Ana; Blais, Mark A; Keller, Martin B (2000), "Mortality in eating disorders: A descriptive study", International Journal of Eating Disorders, 28 (1): 20–26, doi:10.1002/(SICI)1098-108X(200007)28:1<20::AID-EAT3>3.0.CO;2-X
  33. ^ Pompili, M; Mancinelli, I; Girardi, P; Ruberto, A; Tatarelli, R (2004), "Suicide in anorexia nervosa: A meta-analysis", International Journal of Eating Disorders, 36 (1), John Wiley: 99–103, doi:10.1002/eat.20011
  34. ^ Bulik CM, Reba L, Siega-Riz AM, Reichborn-Kjennerud T. (2005) Anorexia nervosa: definition, epidemiology, and cycle of risk. Int J Eat Disord, 37 Suppl, S2-9. PMID 15852310.
  35. ^ Hoek HW. (2006) Incidence, prevalence and mortality of anorexia nervosa and other eating disorders. Curr Opin Psychiatry., 19 (4), 389-94. PMID 16721169.
  36. ^ "Professor, 49, died from anorexia". BBC. 2008-04-22. Retrieved 2008-04-23.
  37. ^ AJ Giannini, N Telew. Anorexia nervosa in geriatric patienys. Geriatric Medicine Today. 6:75-78, 1987.
  38. ^ AJ Giannini. Drug abuse and depression:possible models for geriatric anorexia. Neurobiology of Aging. 9:26-27, 1988.
  39. ^ AJ Giannini, AE Slaby. The Eating Disorders. NY, Springer-Verlag,1993. ISBN 3-540-94002-2
  40. ^ Lock J, Le Grange D. (2005) Family-based treatment of eating disorders. Int J Eat Disord, 37 Suppl, S64-7. PMID 15852323.
  41. ^ Le Grange D. (2005) The Maudsley family-based treatment for adolescent anorexia nervosa. World Psychiatry, 4 (3), 142-6. PMID 16633532.
  42. ^ Claudino AM, Hay P, Lima MS, Bacaltchuk J, Schmidt U, Treasure J. (2006) Antidepressants for anorexia nervosa. Cochrane Database Syst Rev, 1, CD004365. PMID 16437485.
  43. ^ Walsh BT, Kaplan AS, Attia E, Olmsted M, Parides M, Carter JC, Pike KM, Devlin MJ, Woodside B, Roberto CA, Rockert W. (2006) Fluoxetine after weight restoration in anorexia nervosa: a randomized controlled trial. JAMA, 295(22), 2605-12. PMID 16772623.
  44. ^ Birmingham CL, Gritzner S (2006) How does zinc supplementation benefit anorexia nervosa? Eating and Weight Disorders, 11 (4), e109-111. PMID 17272939
  45. ^ Christopher Dare; Ivan Eisler, "Family Therapy and Eating Disorders", Eating Disorders and Obesity (Ed. Christopher Fairburn & Kelly Brownell) (2 ed.): pp 314-319 {{citation}}: |pages= has extra text (help)
  46. ^ Le Grange. The Maudsley family-based treatment for adolescent anorexia nervosa. World Psychiatry. 2005 October; 4(3): 142–146
  47. ^ Keel, Pamela K. and Haedt, Alissa. Journal of Clinical Child & Adolescent Psychology, Volume 37, Issue 1 January 2008 , pages 39 - 61
  48. ^ Le Grange, Daniel and Eisler, Ivan. Family Interventions in Adolescent Anorexia Nervosa. "Child Adolesc Psychiatric Clin N Am". 18 (2008): 159-173

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