Differential activation of the frontal pole to high vs low calorie foods: The neural basis of food preference in Anorexia Nervosa?

Abstract

Neuroimaging studies in anorexia nervosa (AN) suggest that altered food reward processing may result from dysfunction in both limbic reward and cortical control centers of the brain. This fMRI study aimed to index the neural correlates of food reward in a subsample of individuals with restrictive AN: twelve currently ill, fourteen recovered individuals and sixteen healthy controls. Participants were shown pictures of high and low-calorie foods and asked to evaluate how much they wanted to eat each one following a four hour fast. Whole-brain task-activated analysis was followed by psychophysiological interaction analysis (PPI) of the amygdala and caudate. In the AN group, we observed a differential pattern of activation in the lateral frontal pole: increasing following presentation of high-calorie stimuli and decreasing in during presentation of low-calorie food pictures, the opposite of which was seen in the healthy control (HC) group. In addition, decreased activation to food pictures was observed in somatosensory regions in the AN group. PPI analyses suggested hypo-connectivity in reward pathways, and between the caudate and both somatosensory and visual processing regions in the AN group. No significant between-group differences were observed between the recovered group and the currently ill and healthy controls in the PPI analysis. Taken together, these findings further our understanding of the neural processes which may underpin the avoidance of high-calorie foods in those with AN and might exacerbate the development of compulsive weight-loss behavior, despite emaciation.

Same, same but different: Attention bias for food cues in adults and adolescents with anorexia nervosa

“…Our findings add to previous research demonstrating cognitive (down‐)regulation upon confrontation with food cues in AN. For example, when hungry, AN patients displayed weaker activation of the right visual occipital cortex than healthy controls (Santel, Baving, Krauel, Münte, & Rotte, ) and showed, in general, hypoconnectivity in circuitry responsible for modulating responses to food cues (Scaife, Godier, Reinecke, Harmer, & Park, ).…”

Neurobiological signature of intimacy in anorexia nervosa

“…Furthermore, studies of REC by Bang et al on socioemotional processing (threat detection and emotional conflict) yielded similar phenomena of decreased modulation (Bang, Rø, & Endestad, , ). Looking at recent studies evaluating disorder‐specific paradigms (food images), it seems that there is preserved modulation (Oberndorfer et al, ; Sanders et al, ; Scaife, Godier, Reinecke, Harmer, & Park, ). One might therefore postulate that AN patients show preserved cerebral modulation with disorder‐specific paradigms, and this is reduced in more general emotion‐related paradigms.…”

Resting state functional connectivity of networks associated with reward and habit in anorexia nervosa

“…Although differences in the function of ventral frontostriatal circuitry between AN and HC participants have been frequently identified and hypothesized to reflect reward system disturbances in AN, the direction of these effects has been inconsistent (O’Hara, Campbell, & Schmidt, 2015). For instance, some studies have demonstrated over-responsivity (Cowdrey, Park, Harmer, & McCabe, 2011; Frank et al, 2012) and others under-responsivity (Brooks et al, 2011; Holsen et al, 2012; Scaife, Godier, Reinecke, Harmer, & Park, 2016) of regions associated with reward processing in response to food cues. Such incongruities in the literature indicate that there is unexplained complexity, and potentially heterogeneity, in the precise pattern of ventral frontostriatal involvement in AN that warrants further research.…”