Article

Reward processing in anorexia nervosa

Monash Alfred Psychiatry Research Centre, Monash University, Central Clinical School, The Alfred, Australia.
Neuropsychologia (Impact Factor: 3.3). 02/2012; 50(5):567-75. DOI: 10.1016/j.neuropsychologia.2012.01.036
Source: PubMed

ABSTRACT

Individuals with anorexia nervosa (AN) demonstrate a relentless engagement in behaviors aimed to reduce their weight, which leads to severe underweight status, and occasionally death. Neurobiological abnormalities, as a consequence of starvation are controversial: evidence, however, demonstrates abnormalities in the reward system of patients, and recovered individuals. Despite this, a unifying explanation for reward abnormalities observed in AN and their relevance to symptoms of the illness, remains incompletely understood. Theories explaining reward dysfunction have conventionally focused on anhedonia, describing that patients have an impaired ability to experience reward or pleasure. We review taste reward literature and propose that patients' reduced responses to conventional taste-reward tasks may reflect a fear of weight gain associated with the caloric nature of the tasks, rather than an impaired ability to experience reward. Consistent with this, we propose that patients are capable of 'liking' hedonic taste stimuli (e.g., identifying them), however, they do not 'want' or feel motivated for the stimuli in the same way that healthy controls report. Recent brain imaging data on more complex reward processing tasks provide insights into fronto-striatal neural circuit dysfunction related to altered reward processing in AN that challenges the relevance of anhedonia in explaining reward dysfunction in AN. In this way, altered activity of the anterior cingulate cortex and striatum could explain patients' pathological engagement in behaviors they consider rewarding (e.g., self-starvation) that are otherwise aversive or punishing, to those without the eating disorder. Such evidence for altered patterns of brain activity associated with reward processing tasks in patients and recovered individuals may provide important information about mechanisms underlying symptoms of AN, their future investigation, and the development of treatment approaches.

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    • "Mesolimbic dopamine neurons are thought to be involved with reward (Wise, 2004), and Bergh and Södersten (1996) suggested that dieting, along with high levels of exercise, can lead to a stress response (Hotta et al., 1986; Rojo et al., 2006) that increases cortisol and corticotrophin releasing factor (Estour et al., 2010; Gwirtsman et al., 1989; Schorr et al., 2015; Shibuya et al., 2011). Stress then increases dopamine levels through these mechanisms (Holly et al., 2015; Wanat et al., 2008) and the nucleus accumbens, i.e., a region of the dopamine terminals in the ventral striatum, is in fact activated in anorexics (Fladung et al., 2010, 2013; Foerde et al., 2015; Frank, 2014; Keating et al., 2012; O'Hara et al., 2015; Wierenga et al., 2014, 2015). The elevated dopamine response is then thought to assist the sequence from rewarding behaviors such as dieting and exercise to become habits not unlike drug dependency or self-starvation by conditioning of this kind of reward to initially neutral stimuli (Bergh and Södersten, 1996; Everitt and Robbins, 2005; Jansen, 1998; Méquinion et al., 2015; Södersten et al., 2008). "
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    ABSTRACT: SÖDERSTEN, P., C. Bergh, M. Leon and M. Zandian. Dopamine and Anorexia Nervosa. NEUROSCI BIOBEHAV REV ab(c) XXX-XXX, 2015. - We have suggested that reduced food intake increases the risk for anorexia nervosa by engaging mesolimbic dopamine neurons, thereby initially rewarding dieting. Recent fMRI studies have confirmed that dopamine neurons are activated in anorexia nervosa, but it is not clear whether this response is due to the disorder or to its resulting nutritional deficit. When the body senses the shortage of nutrients, it rapidly shifts behavior toward foraging for food as a normal physiological response and the mesolimbic dopamine neurons may be involved in that process. On the other hand, the altered dopamine status of anorexics has been suggested to result from a brain abnormality that underlies their complex emotional disorder. We suggest that the outcomes of the treatments that emerge from that perspective remain poor because they target the mental symptoms that are actually the consequences of the food deprivation that accompanies anorexia. On the other hand, a method that normalizes the disordered eating behavior of anorexics results in much better physiological, behavioral and emotional outcomes.
    Full-text · Article · Nov 2015 · Neuroscience & Biobehavioral Reviews
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    • "There is evidence of broad perceptual disturbances in AN, beyond that related to body and shape. These include changes to pain thresholds (Bar, Berger, Schwier, Wutzler, & Beissner, 2013), taste sensation (Keating et al., 2012), sensitivity to disgust (Aharoni & Hertz, 2012), and perception of one's own (Kaye, Wierenga, Bailer, Simmons, & Bischoff-Grethe, 2013) and other's (Zucker et al., 2013) emotions. Interoceptive awareness, or interoception, refers to the typically unconscious maintenance and attention to the body's internal state of homeostasis, and is under the control of the insular cortex (Craig, 2009). "
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    Full-text · Article · Dec 2014 · Cortex
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    • "Though we can only provide a brief discussion of three such disorders here, the potential exists for many others . For instance, Obsessive-Compulsive disorder, where behavior may exhibit an overreliance on habits due to dysfunctional goaldirected circuitry (Gillan et al., 2011), and anorexia nervosa, where there is a tendency to deprive oneself of food, despite, or likely because of, hyperactivity in evaluative neural circuitry during food presentation (Keating et al., 2012), provide interesting examples. "
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