Abstract
ObjectivesThe 2020 dietary guidelines specifically recommended a decrease in sugar intake. Reward-related, brain-based models of overeating and obesity suggest that increased intake of highly palatable foods is linked to decreased dopaminergic (striatal and prefrontal) brain functioning. This reduction acts to increase consumption of food to achieve pleasure. Here, we examined whether increased dietary intake of sugar and fat would be associated with increased activation in reward-related brain regions during anticipation of a sugar sweetened beverage (SSB), but decreased activation during SSB receipt. MethodsYoung adults (n = 100, age = 21.8 ± 2.4 y, BMI = 23.3 ± 3.5, 70% female) underwent an fMRI scan examining brain responses to receipt of a SSB, a tasteless rinse, and response cue-induced anticipation of these tastes. The Block Food Frequency Questionnaire (FFQ) was used to assess average dietary intake, % daily caloric intake from SSBs, sugar, sugar from SSBs and fat. These were correlated with whole-brain BOLD responses to SSB anticipation and receipt contrasts (e.g., SSB > rinse). Significance was corrected for multiple comparisons; pFWE < .05. ResultsIncreased consumption of sugar calories from SSBs was correlated with decreased activity in regions associated with dopamine (posterior midbrain, dorsolateral/orbitofrontal cortices) and taste processing regions (postcentral gyrus) during receipt of SSB (> rinse). ConclusionsThese results directly support previous research (Burger & Stice 2012; AJCN) demonstrating that increased consumption of highly palatable foods is associated with reduced dopaminergic brain response during consumption specifically of those foods. Critically, we demonstrate these effects with SSBs which are far more widely consumed. Our results were specific to increased intake of sugar calories from SSBs and not total calories from SSBs or total sugar calories, suggesting that added sugars in these beverages have the potential to lead to altered frontostriatal brain responses. Funding SourcesNIDDK R01DK112317.
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