Variability in reward responsivity and obesity: evidence from brain imaging studies

Abstract

Advances in neuroimaging techniques have provided insight into the role of the brain in the regulation of food intake and weight. Growing evidence demonstrate that energy dense, palatable foods elicit similar responses in reward-related brain regions that mimic those of addictive substances. Currently, various models of obesity's relation to reward from food have been theorized. There is evidence to support a theory of hypo-responsivity of reward regions to food, where individuals consume excess amounts to overcome this reward deficit. There is also data to support a theory of hyper-responsivity of reward regions, where individuals who experience greater reward from food intake are at risk for overeating. However, these seemingly discordant theories are static in nature and do not account for the possible effects of repeated overeating on brain responsivity to food and initial vulnerability factors. Here we review data that support these theories and propose a dynamic vulnerability model of obesity that appears to offer a parsimonious theory that accommodates extant findings.

Figure 1

Differential activation in the caudate in response to milkshake receipt (contrasted with tasteless receipt) across weight change over one year by TaqIA A1 status. Those with the A1 allele (dashed line) show decreases in activation as weight increases, whereas those without the A1 allele (solid line) show increases in activation as weight increases [22].

Figure 2

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 [34].

Figure 3

Activation in the orbitofrontal cortex in response to initial orientation to appetizing food images (contrasted with pictures of glasses of water) related to weight change over a one-year period [48].

Figure 4

Differential activation in the frontal operculum in response to appetizing food pictures (contrasted with pictures of glasses of water) across weight change over one year by TaqIA A1 status. Those with the A1 allele (dashed line) show increases in activation as weight decreases, whereas those without the A1 allele (solid line) show increases in activation as weight increases [40].

Figure 5

Greater activation in the A) caudate and B) frontal operculum in adolescents at a high risk for obesity vs. adolescents at a low risk for obesity in response to milkshake receipt (contrasted with tasteless receipt). Despite no difference in current BMI, adolescents at high risk for obesity show greater activation in these reward and gustatory related regions to a palatable food [52].

Figure 6

Dynamic vulnerability model of obesity