Neurobiology of Overeating


The fact that some people are able to maintain a healthy weight, despite the omnipresence of high‐fat and high‐sugar foods, whereas others experience unhealthy weight gain, has prompted theories regarding individual difference factors that may increase risk for overeating. Some have proposed that individuals who experience less reward from food intake overeat to compensate for this reward deficit. Others have suggested that it is individuals who experience greater reward from food intake who are at risk for overeating. There is data from neuroimaging studies that investigate individual differences in response to food intake and food cues, as well as animal studies that support the reward deficit model, yet there is similar data to support the reward surfeit model. However, neither of these models fit with all of the data. We have therefore proposed a dynamic vulnerability model that appears to better account for the findings in the literature. This working model points to initial vulnerability factors as well as neural adaptations to overeating which may perpetuate overeating in a feed forward manner.

Key Concepts:

  • Advances in neuroimaging techniques allows for the direct assessment of how food reward can impact eating behaviour.

  • Multiple, conflicting theories of food reward and obesity have been presented.

  • Emerging animal and prospective human data suggest that reduced reward when consuming foods and hyper‐responsivity to food cues may evolve from overeating and perpetuate further overeating.

  • Initial hyper‐responsivity of brain regions that encode the reward value of food cues, coupled with greater responsivity of gustatory/oral somatosensory regions may be initial vulnerability factors of overeating.

  • Reduced inhibitory activation in response to food stimuli, and genotypes associated with compromised dopamine function may increase risk for overeating/weight gain.

  • Collectively, data point toward a dynamic vulnerability of overeating and obesity.

Keywords: neuroimaging; functional MRI; food reward; obesity; striatum; dopamine; addiction

Figure 1.

Decreased activation in the caudate in response to milkshake receipt (contrasted with tasteless receipt) by weight change group over a 6‐month period. Those that gained weight (solid line) showed decreases in activation, whereas those that lost weight (dashed line) or were weight stable (dotted line) showed slight increases in activation in this region (Stice et al., ).

Figure 2.

Reduced striatal responsivity to milkshake receipt as a function of frequency of ice cream consumption (tasteless solution receipt>milkshake receipt contrast). Participant's frequency of ice cream intake was associated with reduced responsivity to milkshake receipt in the (a) bilateral putamen, (b) right caudate and (c) the graph of activation (Burger and Stice, ).

Figure 3.

Activation in the orbitofrontal cortex in response to initial orientation to appetising food images (contrasted with pictures of glasses of water) related to weight change over a one‐year period (Yokum et al., ).

Figure 4.

Dynamic vulnerability model of obesity.



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Stice, Eric, and Burger, Kyle S(Jun 2012) Neurobiology of Overeating. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0024012]