Anorexia nervosa overview
|
Anorexia nervosa Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Anorexia nervosa overview On the Web |
|
American Roentgen Ray Society Images of Anorexia nervosa overview |
|
Risk calculators and risk factors for Anorexia nervosa overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Anorexia nervosa is a psychiatric diagnosis that describes an eating disorder characterized by low body weight and body image distortion with an obsessive fear of gaining weight. Individuals with anorexia often control body weight by voluntary starvation, purging, vomiting, excessive exercise, or other weight control measures, such as diet pills or diuretic drugs. It primarily affects adolescent females all over the world, however approximately 10% of all afflicted are male. Anorexia nervosa is a complex condition, involving psychological, neurobiological, and sociological components.[1]
Anorexia Nervosa is a disease condition that can put a serious strain on many of the body's organs and physiological resources;[2][3][4] Anorexia puts a particular strain on the structure and function of the heart and cardiovascular system, with slow heart rate (bradycardia) and elongation of the QT interval seen early on. People with anorexia typically have a disturbed electrolyte balance, particularly low levels of phosphate, which has been linked to heart failure, muscle weakness, immune dysfunction, and ultimately death. Those who develop anorexia before adulthood may suffer stunted growth and subsequent low levels of essential hormones (including sex hormones) and chronically increased cortisol levels. Osteoporosis can also develop as a result of anorexia in 38-50% of cases,[5] as poor nutrition leads to the retarded growth of essential bone structure and low bone mineral density. Anorexia does not harm everyone in the same way. For example, evidence suggests that the results of the disease in adolescents may differ from those in adults.[2]
Changes in brain structure and function are early signs of the condition. Enlargement of the ventricles of the brain is thought to be associated with starvation, and is partially reversed when normal weight is regained.[6] 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.[7]
Causes
It is clear that there is no single cause for anorexia and that it stems from a mixture of social, psychological and biological 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]
Epidemiology 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[9][10] 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 90% of people with anorexia are female.[1]
Diagnosis
Electrocardiogram
Anorexia puts a particular strain on the structure and function of theheart and cardiovascular system, with slow heart rate (bradycardia) and elongation of the QT interval seen early on.
References
- ↑ 1.0 1.1 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.
- ↑ 2.0 2.1 Katzman DK. (2005) Medical complications in adolescents with anorexia nervosa: a review of the literature. International Journal of Eating Disorders, 37 Suppl, S52-9. PMID 15852321.
- ↑ Anorexia Vs Obesity in North America, retrieved May 25th 2007.
- ↑ Birmingham CL, Su J, Hlynsky JA, Goldner EM, Gao M. (2005) The mortality rate from anorexia nervosa. International Journal of Eating Disorders, 38 (2), 143-6. PMID 16134111.
- ↑ Legroux-Gerot I, Vignau J, Collier F, Cortet B. (2005) Bone loss associated with anorexia nervosa. Joint Bone Spine, 72 (6), 489-95. PMID 16242373.
- ↑ Palazidou E, Robinson P, Lishman WA. (1990) Neuroradiological and neuropsychological assessment in anorexia nervosa. Psychol Med, 20 (3), 521-7. PMID 2236361.
- ↑ 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.
- ↑ Tiggemann M and Pickering AS. (1996) Role of television in adolescent women's body dissatisfaction and drive for thinnessInt J Eat Disord, Sep;20(2):199-203.
- ↑ 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.
- ↑ Hoek HW. (2006) Incidence, prevalence and mortality of anorexia nervosa and other eating disorders. Curr Opin Psychiatry., 19 (4), 389-94. PMID 16721169.