Attenuated Neuroendocrine Response to Hypoglycemic Stress in Patients with Panic Disorder

Background/Aims: There is a lack of information on the effects of metabolic stress exposure on hormone release in patients with panic disorder. The aim of this study was to test the hypothesis that neuroendocrine activation during hypoglycemic stress is altered in panic disorder patients compared to healthy subjects. Methods: Hormone responses to an intravenous bolus of insulin (0.1 IU/kg) were evaluated in both fully remitted, medication-free panic disorder patients and healthy controls (n = 9/group). Blood samples for determination of cortisol, growth hormone, prolactin, adrenaline and noradrenaline concentrations were obtained at rest and over a 90-min period after insulin injection. Results: In patients with panic disorder, basal prestress hormone levels were comparable to those in healthy subjects with the exception of plasma adrenaline, which was higher in panic disorder patients compared to controls. The degree of hypoglycemia induced by insulin administration was similar in patients and healthy subjects. Hypoglycemia-induced increases in growth hormone, prolactin and cortisol concentrations were significantly attenuated in panic disorder patients compared to healthy individuals. No differences between patients and controls were observed in adrenalin release induced by hypoglycemia. Conclusions: The present data demonstrate that somatotropic, lactotropic and corticotropic activation during hypoglycemic stress is blunted in patients with panic disorder. It is suggested that in contrast to the effects of relatively mild stress conditions used in other studies published in the literature, intensive stressors inducing a broad spectrum of hormonal changes fail to provoke an adequate neuroendocrine response in patients with panic disorder.