حساسیت به مجازات و پاداش در بی اشتهایی عصبی

Objective: The aim of this study was to investigate reinforcement sensitivity in anorexia nervosa (AN). It was tested whether self-reported punishment (PS) and reward sensitivity (RS) differed between adolescents with AN and healthy controls, and/or between AN-subtypes. In addition, the predictive validity of PS and RS was examined for AN symptoms one year later. Method: In total, 165 female adolescents admitted for treatment of AN or eating disorder not otherwise specified resembling AN and 72 controls participated in the study. Participants completed measurements for eating disorder severity and the Sensitivity to Punishment/Sensitivity to Reward Questionnaire (SPSRQ). Percentage of underweight and severity of AN symptoms were measured again after one year in individuals with AN. Results: Individuals with AN scored higher on PS and RS than controls. In addition, the AN purging type showed higher PS than the AN restrictive type, whereas there were no differences in RS between AN-subtypes. Regression analyses indicated that PS and RS were independently associated with the degree of eating disorder symptoms, whereas only PS was related to percentage underweight. Yet, neither RS nor PS were related to percentage of underweight and AN symptoms after one year. Discussion: Although the present study clearly demonstrated that heightened punishment and reward sensitivity are both linked to AN, there was no evidence that these characteristics are also involved in the course of AN symptoms.

Anorexia nervosa (AN) is a severe psychiatric disorder with the highest mortality rate among all psychiatric disorders (Sullivan, 1995). Unfortunately, the underlying processes that cause and maintain AN are still largely unknown. One of the puzzling features of AN is that patients succeed in restricting their food intake, while they actually are in a state of starvation. By nature, food has a high reward value, even more for people that have been deprived of food (e.g., Stroebe, Papies, & Aarts, 2008). So how do individuals with AN overcome their biological drive to eat? One explanation might be provided by the sensitivity of AN patients to environmental cues signaling reward or punishment. According to the Reinforcement Sensitivity Theory (e.g., Gray, 1987) individuals’ behaviors are guided by different brain systems. The behavioral inhibition system reacts to aversive/punishing stimuli and is thought to lead to avoidance behaviors. The behavioral activation system is sensitive to rewarding stimuli and assumed to guide approach behaviors. Heightened punishment sensitivity might be a risk factor for developing AN, because it could ‘help’ individuals to abstain from eating. For individuals who are high in punishment sensitivity and who base their self-esteem largely, or even exclusively, on their body shape and weight (Fairburn, 2008), the idea of gaining weight can become very threatening. As a consequence, they could start to avoid expected punishment (i.e. weight gain) through avoidance behaviors such as restriction of food intake, or excessive exercise, increasing the risk for developing AN. Prior findings suggest that patients with AN indeed show heightened punishment sensitivity supporting the hypothesis that heightened punishment sensitivity is a risk factor for developing AN (Beck et al., 2009, Claes et al., 2006, Harrison et al., 2010 and Jappe et al., 2011). However, up to now, studies mainly relied on adult samples. Yet, the impact/relevance of reward and punishment sensitivity may be different for younger, adolescent samples (e.g., adolescents generally seem to be more sensitive to appetitive stimuli: Spear and Varlinskaya, 2010 and Van Leijenhorst et al., 2010). In addition, and most critical for the present context, the first onset of AN often takes place during early adolescence and the heightened punishment sensitivity found in adults with AN might be the consequence of protracted AN rather than a premorbid risk factor. Therefore, the first goal of the present study is to examine whether punishment sensitivity is already heightened in young adolescents with AN. This would further support the idea that heightened punishment sensitivity might indeed be a risk factor for developing AN. In addition, an alternative explanation for the striking ability of AN patients to resist (or overcome) their drive to eat could be that they differ from healthy controls in their sensitivity to reward. Perhaps lowered reward sensitivity leads to a lower approach motivation to food cues, which increases the risk of developing AN. Results in this respect are still mixed. Some studies showed that individuals with AN of the restrictive type (AN-R) indeed displayed lower levels of reward sensitivity than controls, while individuals with AN of the purging/binging type (AN-P) showed higher levels of reward sensitivity than individuals with AN-R and/or controls (Beck et al., 2009, Claes et al., 2006 and Harrison et al., 2010). The latter could help explain why individuals with AN-P sometimes show episodes of binge eating. However, recently, Jappe and colleagues (2011) showed the opposite, namely that both types of women with AN displayed higher sensitivity to reward than healthy controls. They did not find differences in reward sensitivity between AN-R and AN-P. Consequently, the second goal of the present study is to examine reward sensitivity in a large group of AN patients, since in prior studies especially subgroups of AN-P were usually small. Because prior findings with respect to reward sensitivity in AN were mixed, we do not have a clear hypothesis. Although prior studies suggest that reward and punishment sensitivity generally are independent constructs (see e.g., Franken and Muris, 2006 and O’Connor et al., 2004), it is still unknown whether these constructs are also independently involved in AN, or whether they should be seen as overlapping risk factors. Furthermore, we explore whether perhaps the relationship between reward sensitivity and the onset of AN is moderated by punishment sensitivity, or vice versa (see e.g., Corr, 2002). Consequently, the third goal of this study is to test whether punishment and reward sensitivity as well as their interaction are independently related to severity of eating disorder symptoms. Our hypothesis is that both factors are independently linked to severity of AN. Finally, reward and punishment sensitivity might not only be risk factors for the onset of AN, but perhaps they also play a role in the persistence of AN over time. Therefore, the last goal is to examine whether in individuals with AN, punishment sensitivity, reward sensitivity, and/or their interaction predict AN symptoms later in time. More clarity with respect to the potential role of punishment and reward sensitivity as risk factors for the development and maintenance of AN-R and AN-P might be crucial for a better understanding of AN and its underlying processes.