Effects of the modern food environment on striatal function, cognition and regulation of ingestive behavior

Abstract

Emerging evidence from human and animal studies suggest that consumption of palatable foods rich in fat and/or carbohydrates may produce deleterious influences on brain function independently of body weight or metabolic disease. Here we consider two mechanisms by which diet can impact striatal circuits to amplify food cue reactivity and impair inhibitory control. First, we review findings demonstrating that the energetic properties of foods regulate nucleus accumbens food cue reactivity, a demonstrated predictor of weight gain susceptibility, which is then sensitized by chronic consumption of an energy dense diet. Second, we consider evidence for diet-induced adaptations in dorsal striatal dopamine signaling that is associated with impaired inhibitory control and negative outcome learning.

Integration of homeostatic signaling and food reward processing in the human brain

“…Our results add to the common observation that human eating behavior is closely related to reward processing in mesocorticolimbic reward circuits (73). …”

DRD2: Bridging the Genome and Ingestive Behavior

“…Likewise, this model predicts that a high fat diet also leads to impairments in DA-dependent cognition via influences on DRD2. This is an important consideration given emerging evidence that diabetes, obesity and diet are associated with cognitive impairments [4], and that many of these impairments rely upon DA signaling [125]. To date no study has directly evaluated the influence of diet on the association between the TaqIA A1 allele and adiposity, metabolic, and/or cognitive dysfunction.…”

Short-Term Consumption of Sucralose with, but Not without, Carbohydrate Impairs Neural and Metabolic Sensitivity to Sugar in Humans

“…Central to resolving this debate is defining and testing biologically plausible mechanisms by which LCSs could lead to metabolic impairment. Several have been proposed (Burke and Small, 2016;Davidson and Swithers, 2004;Pepino, 2015;Sylvetsky and Rother, 2018). The binding of LCSs to extra-oral taste…”