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


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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    ABSTRACT: Anorexia Nervosa (AN) is a serious psychiatric condition marked by firmly entrenched and maladaptive behaviours and beliefs about body, weight and food, as well as high rates of psychiatric comorbidity. The neural roots of AN are now beginning to emerge, and appear to be related to dysfunctional, primarily limbic, circuits driving pathological thoughts and behaviours. As a result, the significant physical symptoms of AN are increasingly being understood at least partially as a result of abnormal or dysregulated emotional processing. This paper reviews the nature of limbic dysfunction in AN, and how structural and functional imaging has implicated distinct emotional and perceptual neural circuits driving AN symptoms. We propose that top-down and bottom-up influences converge on key limbic modulatory structures, such as the subcallosal cingulate and insula, whose normal functioning is critical to affective regulation and emotional homeostasis. Dysfunctional activity in these structures, as is seen in AN, may lead to emotional processing deficits and psychiatric symptoms, which then drive maladaptive behaviours. Modulating limbic dysregulation may therefore be a potential treatment strategy in some AN patients.
    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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    ABSTRACT: The ability to learn contingencies between actions and outcomes in a dynamic environment is critical for flexible, adaptive behavior. Goal-directed actions adapt to changes in action-outcome contingencies as well as to changes in the reward-value of the outcome. When networks involved in reward processing and contingency learning are maladaptive, this fundamental ability can be lost, with detrimental consequences for decision-making. Impaired decision-making is a core feature in a number of psychiatric disorders, ranging from depression to schizophrenia. The argument can be developed, therefore, that seemingly disparate symptoms across psychiatric disorders can be explained by dysfunction within common decision-making circuitry. From this perspective, gaining a better understanding of the neural processes involved in goal-directed action, will allow a comparison of deficits observed across traditional diagnostic boundaries within a unified theoretical framework. This review describes the key processes and neural circuits involved in goal-directed decision-making using evidence from animal studies and human neuroimaging. Select studies are discussed to outline what we currently know about causal judgments regarding actions and their consequences, action-related reward evaluation, and, most importantly, how these processes are integrated in goal-directed learning and performance. Finally, we look at how adaptive decision-making is impaired across a range of psychiatric disorders and how deepening our understanding of this circuitry may offer insights into phenotypes and more targeted interventions.
    Full-text · Article · May 2014 · Frontiers in Systems Neuroscience
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