Academic journal article Journal of Eating Disorders

Neurobiological Model of the Persistence of Anorexia Nervosa

Academic journal article Journal of Eating Disorders

Neurobiological Model of the Persistence of Anorexia Nervosa

Article excerpt

Author(s): Joanna E. Steinglass[sup.1] and B. Timothy Walsh[sup.1]

Background

Anorexia Nervosa (AN) is characterized by the maintenance of an undernourished, or starved, state. Affecting approximately 1 % of women [1] across all socioeconomic classes [2], AN is characterized by severe restriction of food intake resulting in an inappropriately low body weight, fear and anxiety about weight gain, and preoccupation with body shape and weight [3]. The recurrent intake of a diet that is inadequate to sustain a healthy weight is the central behavior maintaining this condition. To understand this disturbance, it is useful to consider the neural mechanisms that promote the persistent choice of inadequate caloric intake, a behavior that clearly becomes maladaptive and self-destructive. Here, we review a cognitive neuroscience model of AN that focuses on the persistence of maladaptive behavior.

AN commonly begins during adolescence, with a peak age at first presentation between 14 and 18 years [4, 5]. Unlike many psychiatric illnesses, in which early onset signifies a more severe course of illness, adolescents with AN have a better prognosis than adults: studies of adolescents receiving treatment for AN show that, at 1 year of follow-up, approximately 75 % are in partial or full remission [6-8]. However, when the disease progresses into adulthood, the treatment outlook is disheartening [8, 9]. No pharmacotherapies have proven effective, psychosocial interventions are often inadequate, and relapse rates are high - up to 50 % of adult patients require rehospitalization within a year of discharge [10, 11]. Mortality among young women with AN is at least six times that expected for their age [12], the highest of any psychiatric disorder, and the likelihood of death increases with duration of illness [13]. A better understanding of the neural underpinnings of AN may help to develop novel treatments and improve outcomes for these severely ill individuals.

Review

The importance of eating behavior in AN

Eating is a multifaceted behavior, affected by multiple social, psychological and biological factors. The neurobiological value of food as a primary reward has been long noted [14-16], and much is understood regarding appetitive and inhibitory control around normal eating [17-19]. Yet, models of the neural mechanisms of normal eating have not contributed greatly to the understanding of eating disorders - perhaps because these models, largely based on studies of rodents, do not clarify the influences that promote maladaptive eating behavior among humans with eating disorders [19].

The aberrations in eating behavior that occur among individuals with eating disorders have been usefully examined via objective assessment in eating laboratories. Most such studies have compared the eating of individuals without eating disorders to that of individuals with binge eating, such as occurs in bulimia nervosa (BN) and binge eating disorder (BED). Laboratory studies have documented that individuals with BN and with BED consume significantly more calories than controls when asked to binge, and that some satiety cues are abnormal. These studies have also documented that, when not binge eating, individuals with BN tend to consume fewer calories than healthy volunteers [20, 21]. These studies laid a foundation for using the laboratory setting to examine abnormally reduced food intake such as occurs in AN.

Restrictive caloric intake in AN has been objectively assessed [22, 23]. One of the first observational studies of intake among individuals with AN demonstrated lower caloric intake compared with healthy controls (HC) (1289 [+ or -] 150 vs 2220 [+ or -] 108 kcal, p < 0.05) as well as restricted fat intake (17.6 [+ or -] 2.3 % vs 28.4 [+ or -] 1.3 % of total calories consumed, p < 0.05) [24]. Additional studies of eating behavior have demonstrated significantly restricted dietary intake among individuals with AN, not only when acutely ill but also immediately after weight restoration. …

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