Acute stressors reduce neural inhibition to food cues and increase eating among binge eating disorder symptomatic women

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Abstract

Stressors can trigger binge-eating but researchers have yet to consider their effects on both neural responses to food cues and food consumption among those at risk. In this experiment, we examined the impact of acute stressors on neural activation to food images and subsequent food consumption within binge-eating disorder (BED) and non-eating disordered control groups. Eighteen women meeting DSM-IV BED criteria and 26 women serving as non-eating disordered controls were randomly assigned to unpleasant stressor (painful cold pressor test (CPT) followed by negative performance feedback) or less unpleasant stressor (non-painful sensory discrimination task followed by positive performance feedback) conditions. Subsequently, they were scanned with functional magnetic resonance imaging (fMRI) while viewing food and neutral images. After the scans, participants completed a self-report battery in an environment conducive to snacking. During exposure to food images, BED-symptomatic women in the unpleasant stressor condition reported more liking of high calorie food images and showed less activation in one inhibitory area, the hippocampus, compared to controls in this condition. BED-symptomatic women exposed to unpleasant stressors also consumed more chocolate than any other group during the post-scan questionnaire completion. Crucially, reduced hippocampal activation to high calorie food images predicted more chocolate consumption following fMRI scans within the entire sample. This experiment provides initial evidence suggesting unpleasant acute stressors contribute to reduced inhibitory region responsiveness in relation to external food cues and later food consumption among BED-symptomatic women.

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CITATION STYLE

APA

Lyu, Z., & Jackson, T. (2016). Acute stressors reduce neural inhibition to food cues and increase eating among binge eating disorder symptomatic women. Frontiers in Behavioral Neuroscience, 10(OCT). https://doi.org/10.3389/fnbeh.2016.00188

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