Food and Behaviour Research

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The neurocognitive mechanisms underlying food cravings and snack food consumption. A combined continuous theta burst stimulation (cTBS) and EEG study

Lowe CJ, Staines WR, Manocchio F, Hall PA (2018) Neuroimage.  15;177: 45-58. doi: 10.1016/j.neuroimage.2018.05.013. Epub 2018 May 6. 

Web URL: Read this and related abstracts on PubMed here


Regulation of food cravings is thought to be critical for modulating eating behavior, yet we do not fully understand the mechanisms by which cognitive control operates in the eating context.

The current study combined rTMS and EEG paradigms to examine the causal role of the left dorsolateral prefrontal cortex (dlPFC) in modulating visceral and behavioral responses to high calorie foods, and the mediational mechanisms underlying this relation. 28 right-handed female participants received both active and sham continuous theta burst stimulation (cTBS; a rTMS variant used to decrease cortical activity) targeting the left dlPFC in a counterbalanced order.

Prior to and following each stimulation session participants completed a flanker and food-cue presentation (high and low calorie food) task. Following cTBS participants had the opportunity to consume both high and low calorie foods during a taste test. Findings revealed a reliable effect of cTBS on food consumption, such that participants selectively ingested significantly more calories from appetitive calorie dense snack foods following active relative to sham cTBS; this effect did not translate to control (low calorie) food consumption.

In addition, attenuation of dlPFC activity resulted in the significant increase in N2 amplitude and P3b latency to incongruent flanker trials, and the selective significant increase in the P3a amplitude to and P3a amplitude bias for high calorie food stimuli. Results from the parallel mediation analysis revealed that only the indirect effect of flanker task performance was significant; the indirect effects of stimulation induced changes in the P3 bias for high calorie foods, the urge to consume high calorie foods, and the general liking ratings for high calorie foods were not significant.

These findings confirm the causal role of the left dlPFC in the modulation of calorie dense food consumption via inhibitory control capacity.


This study provides direct evidence that when activity in a particular brain region is reduced, cravings for unhealthy snack foods are increased.

The brain region in question is part of the frontal lobes - the dorsolateral pre-frontal cortex (DLPFC) - an area already known to be involved in various cognitive activities such as forward planning, and controlling impulses.

Impaired functioning of this region is implicated in various mental conditions, including ADHD, substance use disorders and other forms of impulsive and/or addictive behaviour.

Here, transcranial magentic stimulation was used to reduce DLPFC activity temporarily in healthy individuals, who then consumed more unhealthy, highy processed snacks afterwards.

By contrast, DLPFC suppression had no effect on the amount of healthy snacks they chose to consumed.

These findings add to the evidence that cravings for ultra-processed foods (high in refined sugars, starches and fats, as well as artificial additives) may involve some of the same brain mechanisms involved in other forms of addictive behaviour.

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