Emotional feeding resulting from chronic exposure to psychosocial stressors is likely a key factor for excess food intake. This may be particularly important for women, who consistently report more stress-induced eating and have higher rates of obesity. The well-accepted notion is that emotional feeding of calorically dense diets is a form of self-medication to relieve the behavioral and physiological manifestations of stress. While this may be the case, it is also probable that emotional feeding is the result of compromised dopamine (DA) reward pathways, as exposure to chronic psychosocial stress increases susceptibility to an addictive phenotype by reducing DA 2 receptors (D2R) in mesolimbic regions, producing a hypodopaminergic condition. Furthermore, simply eating a calorically dense diet reduces D2R in these regions but only in some animals. Thus, self-medicating with high caloric diets may further compromise the stress-induced hypofunctional DA system. Clearly, this is not a healthy coping strategy for unresolved stress. An issue particularly important for women attempting to diet is whether these stress-induced changes, including impaired DA function, persist in the face of life style changes. Our preliminary data using social subordination in female rhesus monkeys as a model of chronic psychosocial stress in women suggests this may be the case, as subordinate females consume significantly more calories when given a high caloric diet (HCD) and this hyperphagia persists when a healthier diet is exclusively available. What is not known, however, is how this pattern continues under these healthy dietary conditions. Similarly, it is unknown if the alleviation of chronic psychosocial stress will restore caloric restraint, or if changes in systems regulating appetite, including DA, persist even after stress is resolved. Using socially housed female rhesus monkeys as a translational model for women, this project will identify mechanisms that sustain emotional feeding.
Aim 1 will determine whether chronic social stress induced by social subordination sustains excessive intake of a HCD and whether this is exacerbated by exposure to acute stressors.
Aim 2 will test the hypothesis that intake of a calorically dense diet will reduce DR2 availability in mesolimbic regions and this will be exacerbated by social subordination.
Aim 3 will test the hypothesis that estradiol will be more effective suppressing caloric intake in dominant females when a LCD is available but will promote caloric intake when an HCd is available, particularly in subordinate females. in a Aim 4 will use two intervention strategies to further elucidate how social stress sustains emotional feeding: 1) despite replacing a HCD with a healthier low caloric diet, hyperphagia and reduced D2R binding potential in subordinates will persist;and 2) reducing social stress by changing social status will improve but not normalize D2R availability or food intake Together, these studies will increase our understanding of factors that sustain emotional feeding, even in a healthy dietary environment.
The psychological and biological reasons why people find it so difficult to limit food intake are poorly understood. This project will examine the hypothesis that emotional feeding that results from exposure to chronic social stress changes brain neurochemicals that regulate reward pathways in the brain. These deficits lead individuals to overeat even when healthier diets and improved lifestyles are available. Together, the data will identify novel mechanisms for sustained food intake and thereby identify possible targets for therapeutic intervention.
