Principal Investigator: Laura M. Holsen
Many people experience altered eating behaviors under stress. Stress-related overeating has been suggested as a mechanism potentiating weight gain. It is known that stress affects behavior related to food , changing our preference for or intake of palatable food, but the brain networks that orchestrate these behavior changes are not well understood. Therefore, we investigated brain functional connectivity (FC) from regions that play key roles in maintaining homeostatic state of our body and in processing rewards. First, subjects were exposed to an interpersonal stress manipulation outside the MRI scanner. Then, they completed a task in an MRI scanner during which they experienced conditions involving expectation and receipt of food reward under psychosocial stress. We found that anticipation of food reward was associated with alterations in the coordinated activity between different networks (homeostatic, emotion, reward) and executive control regions under psychosocial stress. Our results contribute to the understanding of neural circuit synchrony involved in stress-induced food reward and may inform mechanisms underlying changes in eating behavior under stress. These findings may also contribute to the development of novel treatments for stress-related eating disorders.
Stress-related overeating has been suggested as a mechanism potentiating weight gain. Psychosocial stress impacts behavioral aspects of food reward, yet the coordinated activity of neural circuits which orchestrate these behaviors is not well understood. We investigated functional connectivity (FC) of homeostatic/mesolimbic reward pathways during food reward processing under psychosocial stress.
39 healthy adults completed a study involving exposure to acute psychosocial stress, followed by functional MRI scanning during a food incentive delay task. Data were analyzed to investigate FC between homeostatic (hypothalamus) and mesolimbic regions [amygdala, nucleus accumbens (NAcc)] and whole brain.
During food reward anticipation , we observed stress-induced decreases in hypothalamus FC to superior/middle frontal gyrus (p=0.01), in amygdala FC to superior frontal gyrus (p=0.04), and in NAcc FC to precentral gyrus (p=0.02), with increases in amygdala FC to precuneus (p<0.01) and NAcc FC to superior/middle frontal gyrus (p<0.01). During food reward receipt, amygdala showed increased FC to orbitofrontal cortex (p=0.02) and hippocampus (p=0.02), and decreased FC to superior frontal gyrus (p=0.05).
We found that stress induced alterations in the balance between homeostatic/mesolimbic reward and prefrontal cognitive control FC during anticipation and receipt of food reward. These findings may inform mechanisms underlying changes in eating under stress.