Title: Psychosocial stress, reward circuitry, and eating disorders: A biopsychosocial review of neurobiological mechanisms
Abstract:
Eating Disorders (EDs) are severe psychiatric conditions with high mortality rates, yet the specific biological pathways through which environmental stressors translate into pathological eating behaviors remain underdefined. This study used the biopsychosocial model to examine how psychosocial stress and social pressure interact to dysregulate the brain's reward circuitry. A systematic evaluation of nine academic publications specializing in neuroimaging, neuroendocrine, and reward-circuitry research was conducted. Findings indicated that psychosocial stress triggers hyperactivity of the Hypothalamic-Pituitary-Adrenal (HPA) axis, resulting in elevated cortisol levels that blunt mesolimbic reward responsiveness. This neuroendocrine response is associated with reduced activation of the nucleus accumbens and caudate during reward anticipation. In binge-type disorders, this "reward deficiency" may contribute to compensatory overeating as a biological attempt to normalize striatal dopamine function. Conversely, in restrictive-type disorders, the mechanism appears to involve a pathological top-down override of homeostatic hunger signals by the prefrontal cortex, often associated with altered connectivity involving the amygdala. This shift may be further reinforced by a reduced reward value of social cues, such as facial expressions, which individuals with anorexia nervosa may perceive as threatening. In conclusion, the findings suggest that HPA-axis-mediated mesolimbic reward dysregulation may represent an important biological pathway linking psychosocial stress and social pressure to eating disorder development and maintenance. These findings highlight the potential importance of stress-reduction interventions as part of efforts to restore normative reward-system functioning in individuals with eating disorders.
Keywords: Eating Disorders, HPA Axis, Cortisol, Reward Circuitry, Dopamine, Anorexia Nervosa, Psychosocial Stress, Biopsychosocial Model.


