4.7 Article

Altered prefrontal activation during the inhibition of eating responses in women with bulimia nervosa

Journal

PSYCHOLOGICAL MEDICINE
Volume 53, Issue 8, Pages 3580-3590

Publisher

CAMBRIDGE UNIV PRESS
DOI: 10.1017/S0033291722000198

Keywords

Bulimia nervosa; fNIRS; inhibitory control; loss-of-control eating; prefrontal cortex

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This study used fNIRS to measure activation in the prefrontal cortices of individuals with bulimia nervosa (BN) and healthy controls (HC) during eating inhibition tasks. The results showed that individuals with BN made more errors in inhibiting eating responses. Those with more severe loss of control (LOC) eating and stronger binge eating feelings exhibited abnormal activation in specific brain regions associated with eating inhibition. Lower activation in specific brain region was also related to more frequent and severe LOC eating in the overall BN sample. These findings suggest that diminished prefrontal cortex activation may contribute to more severe eating-specific control deficits in BN.
Background The sense of 'loss of control' (LOC), or a feeling of being unable to stop eating or control what or how much one is eating, is the most salient aspect of binge eating. However, the neural alterations that may contribute to this experience and eating behavior remain poorly understood. Methods We used functional near-infrared spectroscopy (fNIRS) to measure activation in the prefrontal cortices of 23 women with bulimia nervosa (BN) and 23 healthy controls (HC) during two tasks: a novel go/no-go task requiring inhibition of eating responses, and a standard go/no-go task requiring inhibition of button-pressing responses. Results Women with BN made more commission errors on both tasks. BN subgroups with the most severe LOC eating (n = 12) and those who felt most strongly that they binge ate during the task (n = 12) showed abnormally reduced bilateral ventromedial prefrontal cortex (vmPFC) and right ventrolateral prefrontal cortex (vlPFC) activation associated with eating-response inhibition. In the entire BN sample, lower eating-task activation in right vlPFC was related to more frequent and severe LOC eating, but no group differences in activation were detected on either task when this full sample was compared with HC. BN severity was unrelated to standard-task activation. Conclusions Results provide initial evidence that diminished PFC activation may directly contribute to more severe eating-specific control deficits in BN. Our findings support vmPFC and vlPFC dysfunction as promising treatment targets, and indicate that eating-specific tasks and fNIRS may be useful tools for identifying neural mechanisms underlying dysregulated eating.

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