Post-traumatic stress disorder may set the neurobiological stage for eating disorders: A focus on glutamatergic dysfunction.

Post-traumatic stress disorder (PTSD) is a trauma and stress-related disorder which has been shown to be highly comorbid with, and commonly a precedent of, the eating disorders anorexia nervosa, bulimia nervosa, and binge eating disorder. The objective of this review is to discuss a potential overlapping neurobiological mechanism for this comorbidity. Alterations in glutamatergic neurotransmission have been observed in all four of the aforementioned disorders. Excessive excitation via glutamate contributes to excitotoxicity, and over-activation of the hypothalamic-pituitary-adrenal axis, both of which have implications for the deterioration of various brain structures. Prominent structures impacted include the hippocampus, hypothalamus, and prefrontal cortex, all of which are integral to the regulation of stress and eating. The current review suggests that altered glutamate function by trauma or extreme stress may facilitate PTSD and subsequent eating disorder onset, and that glutamatergic modulation may be a key treatment for individuals suffering from these conditions. This overlapping mechanism may help inform future research on individuals with comorbid PTSD and eating disorders, and it could also help inform ways to potentially prevent the onset of these conditions.