Correlates of neural adaptation to food cues and taste: the role of obesity risk factors

Abstract

Identifying correlates of brain response to food cues and taste provides critical information on individual differences that may influence variability in eating behavior. However, few studies examine how brain response changes over repeated exposures and the individual factors that are associated with these changes. Using functional MRI, we examined how brain response to a palatable taste and proceeding cues changed over repeated exposures and how individual differences in weight, familial obesity risk, dietary restraint, and reward-responsiveness correlate with these changes. In healthy-weight adolescents (n=154), caudate and posterior cingulate cortex (PCC) response increased with repeated cue presentations, and oral somatosensory cortex and insula response increased with repeated milkshake tastes. The magnitude of increase over exposures in the left PCC to cues was positively associated with BMI-percentile (r=0.18, p=0.026) and negatively associated with dietary restraint scores (r=-0.24, p=0.003). Adolescents with familial obesity risk showed higher cue-evoked caudate response across time, compared to the low risk group (r=0.12, p=0.035). Reward-responsiveness positively correlated with right oral somatosensory cortex/insula response to milkshake over time (r=0.19, p=0.018). Results show that neural responses to food cues and taste change over time, and that individual differences related to weight gain are correlated with these changes.

Food reinforcement architecture: A framework for impulsive and compulsive overeating and food abuse

“…This shift of the reward creates a prediction error (violation of reward expectation) during taste, as the expected reward from the taste is gone. Similarly, in humans, when an arbitrary predictive visual cue (CS) is paired with a palatable food receipt (UCS), the striatal response to the cue increases over the pairings and the striatal response to the taste is decreased (Figure 2) [17,67].…”

“…Moreover, the posterior cingulate cortex response was positively associated with BMI percentile and negatively associated with dietary restraint scores. Furthermore, adolescents with familial obesity risk showed a higher cue‐evoked caudate response across time, compared with the low‐risk group [67]. Similarly, in young adults, the striatal response to an arbitrary cue increased over repeated parings with a food reward [17].…”

Eating healthy under work stress: A gene stress interaction model.

“…In contrast, Davis et al (2004) suggested that eating under stress reflects a high sensitivity to reward. The decrease of dopamine in the brain of stressed eaters has also been interpreted as a possible result of the downregulation of the adaptation of the dopaminergic system, reflecting that a high sensitivity to reward leads to neural adaptation after food stimulation (Bohon et al, 2009; Sadler et al, 2021; Smith et al, 2021). Regardless of whether the underlying mechanism is a lack of reward or increased sensitivity to reward, it is reasonable to assume that the DRD2 gene, a key element of the reward circuitry, may be associated with the different stress response patterns.…”

The role of reinforcement learning and value-based decision-making frameworks in understanding food choice and eating behaviors

“…This suggests that adults with overweight were more likely to attribute incentive salience to the cues that predicted chocolate milkshake receipt (i.e., sign-track) than those with healthy weight. Additionally, in adolescents, greater caudate and ventral pallidum activity is seen during Pavlovian cue-outcome learning for milkshake compared to water ( 49 , 50 ) with greater ventral pallidum activity predicting greater increases in BMI 2 years later ( 49 ). This finding parallels greater ventral pallidum activity in animal models of sign-tracking ( 30 ), suggesting that this may be a common neural pathway for sign-tracking and may be associated with tendency to develop obesity.…”