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Understanding Eating Disorders

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Understanding Eating Disorders Hormones and Behavior 50 (2006) 572–578 www.elsevier.com/locate/yhbeh Understanding eating disorders Per Södersten ⁎, Cecilia Bergh, Michel Zandian Karolinska Institutet, Section of Applied Neuroendocrinology, Center for Eating Disorders, AB Mando, Novum, S-141 57 Huddinge, Sweden Received 16 May 2006; revised 20 June 2006; accepted 21 June 2006 Available online 4 August 2006 Abstract The outcome in eating disorders remains poor and commonly used methods of treatment have little, if any effect. It is suggested that this situation has emerged because of the failure to realize that the symptoms of eating disorder patients are epiphenomena to starvation and the associated disordered eating. Humans have evolved to cope with the challenge of starvation and the neuroendocrine mechanisms that have been under this evolutionary pressure are anatomically versatile and show synaptic plasticity to allow for flexibility. Many of the neuroendocrine changes in starvation are responses to the externally imposed shortage of food and the associated neuroendocrine secretions facilitate behavioral adaptation as needed rather than make an individual merely eat more or less food. A parsimonious, neurobiologically realistic explanation why eating disorders develop and why they are maintained is offered. It is suggested that the brain mechanisms of reward are activated when food intake is reduced and that disordered eating behavior is subsequently maintained by conditioning to the situations in which the disordered eating behavior developed via the neural system for attention. In a method based on this framework, patients are taught how to eat normally, their physical activity is controlled and they are provided with external heat. The method has been proven effective in a randomized controlled trial. © 2006 Elsevier Inc. All rights reserved. Keywords: Eating disorders; Starvation; Neuroendocrine adaptation; Behavior; Treatment Introduction Ben-Tovim et al. (2001) noted that when patients with eating disorders were evaluated five years after an initial Almost all patients with eating disorders (95%) are women. examination, it was not possible to determine an effect of the The aim of research on these women is to improve their treatments the patients had received in the intervening years. condition. If we fail to improve outcome, we most likely should And when the effects of the treatment of eating disorders are change our strategy. And failure to improve outcome is the result reviewed, which has been done many times, it is clear that when the field is reviewed. Hence, there is no evidence that there is no compelling evidence that existing treatments are outcome in anorexia nervosa has improved over the last 50 years effective. Thus, there is no evidence that behavioral treatments (Steinhausen, 2002) and the outcome in bulimia nervosa also have an effect on adult patients (Hay et al., 2003,2004) and the remains poor (Quadflieg and Fichter, 2003). Briefly, the chance claim that family-based behavioral treatment of young anorexic of recovery from eating disorders is less than 50% in ten years, patients is effective is based on weak evidence; the authors of about 25% of the patients become chronically ill and the the only study of its long term effect wrote that the mortality varies between 0% and 25% in published studies. improvement at follow-up could be “attributed to the natural Bringing patients into partial remission, i.e., patient may still outcome of the illness” (Eisler et al., 1997). It has been show some eating disorder symptoms, is considered easy, but suggested that cognitive behavioral therapy is effective in 50% or more relapse within less than a year. For these reasons, bulimia nervosa, but a recent, very thorough, series of studies eating disorders are considered chronic disorders. found that only 19% of a total of 194 bulimic patients who entered such treatment were in remission four months after treatment (Halmi et al., 2002). Treatment with psychopharma- ⁎ Corresponding author. Fax: +468 55640610. cological drugs has not been demonstrated to be effective on E-mail address: [email protected] (P. Södersten). any type of eating disorder (Pederson et al., 2003). 0018-506X/$ - see front matter © 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.yhbeh.2006.06.030 P. Södersten et al. / Hormones and Behavior 50 (2006) 572–578 573 Why is it that all the efforts to understand the cause of eating description of anorexia nervosa, Bruch (1962) described bulimic disorders have yielded treatment strategies with such limited behavior as part of anorexia, and Russell (1979), who introduced success? We suggest that the reason is that the physiological bulimia nervosa as a separate eating disorder diagnosis, referred responses to shortage of food, which is the main evolutionary to it as a special form of anorexia. About 20% of patients with pressure under which human biology has evolved, has been anorexia display bulimic behavior, i.e., bingeing and purging, ignored in clinical accounts of anorexia and bulimia nervosa. and most bulimic patients have a history of anorexia and their bulimic behavior is preceded by brief episodes of starvation. We Feast, famine and thrifty genes view anorexia and bulimia as two phases of the same disorder. There are two main reasons why they have been kept separate. It is estimated that presently one billion of the world's Firstly, anorexic patients are underweight and bulimic patients population (17%) is malnourished (Behrman et al., 2006). This are normal weight and so the patients are conspicuously, but number is decreasing and starvation has probably been even only superficially, different. Secondly, the failure to treat eating more common during early evolution. Most likely, humans disorders leads to the introduction of more diagnostic groups have been exposed to erratic fluctuations in food availability and the belief that they are all different. and only those who have been able to cope have survived (Diamond, 2003). Those are bearers of “thrifty” genes that The traditional explanatory model of eating disorders make intake of large amounts of food possible in times of plenty and hence make survival possible in the subsequent and Rather than viewing all symptoms of anorexia nervosa as inevitable periods of famine (Diamond, 2003; see also signs of starvation, the psychiatric symptoms are often analyzed Schneider, this issue). It seems likely that the phenotypic separately and thought of as causes of eating disorders. For expression of thrifty genes includes the capacity for inter- example, Bruch (1962) noted hyperactivity in anorexia but no mittent high levels of physical activity as well (Chakravarthy differences between anorexia and other forms of malnutrition, and Booth, 2004). But “thrifty” genes are thrifty only under nor indications of organic damage. Yet, she chose to interpret normal conditions and to our disadvantage in present day her observations as indicating that the behavior of her patients society where food is continuously abundant. Hence, the was “closely related to schizophrenia”. Probably for this reason, increase in body weight, reduction of physical activity, obesity her attempts to treat her patients failed. In fact, Bruch (1962) and, eventually, obesity-induced diseases such type 2 diabetes reported that “patients got worse after treatment”. (Diamond, 2003). However, while genes that are “thrifty” The model that Bruch (1962) used to explain and treat eating under certain conditions can facilitate the development of disorders remains essentially unchanged today. In that model, disease under other conditions it is questionable if such genes anorexia is considered a mental disorder, which is caused by should be referred to as “disease” genes. another mental disorder, e.g., schizophrenia causes anorexia nervosa. The model is, however, quite difficult to understand. Is The phenotypic expression of anorexia nervosa it for example, applicable to other, perhaps all, mental disorders, such that one disorder causes another? If so, the model must be Anorexia nervosa starts by a reduction of food intake. An expanded to: a mental disorder causes a mental disorder causes increase in physical activity then follows, a phenomenon that a mental disorder … etc. And the question arises: where does the has been demonstrated in a wide variety of animal species “first” mental disorder come from? Clearly an uncomfortable (Mistlberger, 1987). This effect may be related to stimulation of situation. dopamine transmission in the striatum (Bassareo and Di Chiara, 1999). Also, ovarian cyclicity ceases (Wade and Jones, 2004), Anorexic genes and the neurotransmitters that mediate the and this can also occur in normal weight women who are symptoms excessively active, e.g., those engaging in athletic sports. Increased physical activity and amenorrhea are physiological A modern version of the explanatory model of Bruch (1962) responses to food shortage, not signs of disease. Subsequently, has been formulated by Kaye et al. (2003, 2004), who lowering of body temperature and slowing of heart rate occur as hypothesize that there are genes that predispose individuals to anorexia develops. No one disagrees that these physiological develop a variety of anxiety disorders and that the time line of changes are caused by the shortage of food. But what about the the phenotypic expression of these genes is (1) childhood psychiatric symptoms of anorexia nervosa? Patients suffering obsessive–compulsive disorder (OCD), (2) anorexia
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