Monetary Reward Processing in Obese Individuals With and Without Binge Eating Disorder

Balodis, Iris M.; Kober, Hedy; Worhunsky, Patrick D.; White, Marney A.; Stevens, Michael C.; Pearlson, Godfrey D.; Sinha, Rajita; Grilo, Carlos M.; Potenza, Marc N.

doi:10.1016/j.biopsych.2013.01.014

Cited by 178 publications

(143 citation statements)

References 72 publications

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“…This finding is in accord with a previous fMRI study that assessed hedonic processing of general reward (i.e. monetary reward) in BED (Balodis et al, 2013). Thus, recurrent dieting and binge eating may lead to a sensitization of brain regions involved in hedonic valuation of food (i.e.…”

Section: Discussionsupporting

confidence: 91%

“…Furthermore, general reward processing (i.e. monetary reward) is not significantly altered in BTE patients compared with normal-weight controls (Wagner et al, 2010;Balodis et al, 2013). A previous study using repetitive transcranial magnetic stimulation (rTMS) found that stimulation of the dorsolateral prefrontal cortex reduces cue-induced food craving in patients with BTE (Van den Eynde et al, 2010), indicating a shared neural correlate of food craving across BTE disorders.…”

Section: Introductionmentioning

confidence: 91%

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Neural signature of food reward processing in bulimic-type eating disorders

Simon

Skunde

Walther

et al. 2016

Soc Cogn Affect Neurosci

100

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Clinical observations and similarities to addiction suggest heightened reward sensitivity to food in patients with bulimictype eating (BTE) disorders. Therefore, we investigated the expectation and receipt of food reward compared with monetary reward in patients with BTE. Fifty-six patients with BTE (27 patients with binge eating disorder and 29 with bulimia nervosa) and 55 matched healthy control participants underwent event-related functional magnetic resonance imaging while performing both food and monetary incentive delay tasks. BTE patients exhibited reduced brain activation in the posterior cingulate cortex during the expectation of food and increased activity in the medial orbitofrontal cortex, anterior medial prefrontal cortex and posterior cingulate cortex during the receipt of food reward. These findings were relevant to food because we found no significant group differences related to monetary reward. In the patients, higher brain activity in the medial orbitofrontal cortex during the receipt of food reward was related to higher levels of trait food craving and external eating. BTE patients exhibited increased hedonic processing during the receipt of food reward. These findings corroborate the notion that an altered responsiveness of the reward network to food stimuli is associated with BTE.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 91%

Neural signature of food reward processing in bulimic-type eating disorders

Simon

Skunde

Walther

et al. 2016

Soc Cogn Affect Neurosci

100

View full text Add to dashboard Cite

show abstract

“…Second, in MID paradigms − presumably reflecting phasic dopaminergic responses − reward anticipation differs in obese or binge-eating patients on the one hand and healthy non-obese controls on the other (Balodis et al, 2013;Stice et al, 2008aStice et al, , 2008bStoeckel et al, 2008). However, an apparent conundrum is the direction in which the striatal fMRI signal changes.…”

Section: Obesity-related Changes In Striatal Reward Processingmentioning

confidence: 99%

Altered reward anticipation: Potential explanation for weight gain in schizophrenia?

Grimm

Kaiser

Plichta

et al. 2017

Neuroscience & Biobehavioral Reviews

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a b s t r a c tObesity and weight gain are severe complications of mental illness, especially schizophrenia. They result from changes in lifestyle and nutrition, side effects of medication and other, less well-understood factors. Recent studies suggest that obesity and weight gain are linked to psychopathology. Specifically, severe psychopathology is associated with greater weight dysregulation, typically weight gain. However, our knowledge about the neuroscientific basis of weight gain in schizophrenia is currently limited. We propose that altered reward anticipation, which in turn is related to striatal dopaminergic dysregulation, may explain why obesity is more prevalent in individuals with mental illness. We review evidence that reward anticipation and weight change are linked by a core deficit in dopaminergic striatal circuits. Several lines of evidence, running from animal studies to preclinical and clinical studies, suggest that striatal dopaminergic neurotransmission is a major hub for the regulation of eating behavior and that dopamine links eating behavior to other motivated behavior. From this perspective, the present review outlines a unifying perspective on dopaminergic reward anticipation as a theoretical frame to link weight gain, medication effects and psychopathology. We derive important but open empirical questions and present perspectives for new therapeutic concepts.

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“…From a neurobiological point of view, BED is characterized by functional alteration in different brain areas, such as the prefrontal cortex [13][14][15], and several neurotransmitter systems, such as opioids and dopamine [for a review see 16].…”

Section: Introductionmentioning

confidence: 99%