nxious and Depressive Disorders and Their omorbidity: Effect on Central Nervous System oradrenergic Function

ackground: Although comorbidity of anxiety with depression is common, investigations of physiologic abnormalities related pecifically to comorbidity are rare. This study examined relationships of DSM-IV-defined depression, anxiety, and their comorbidity o noradrenergic function measured by blunting of the growth hormone (GH) response to the alpha2 adrenoreceptor agonist (and midazoline receptor agent) clonidine and by blood pressure and symptom responses. ethods: Fifteen subjects with pure social anxiety or panic disorder, 15 with pure major depression, and 18 with both depression and nxiety were compared with healthy control subjects matched for age and gender. Other factors known to affect GH (weight, menstrual tatus, prior antidepressant, or other drug exposure) were controlled. esults: Anxiety produced GH blunting, but depression was associated with normal GH responses. The comorbid state did not affect esults beyond the impact of anxiety. Preclonidine stress-related GH elevations were observed, to the greatest degree in anxious subjects. elevant symptom, but not blood pressure, changes were significantly associated with blunting. onclusions: With use of pure depression and anxiety groups and careful control of other factors known to affect GH, these results emonstrate central nervous system noradrenergic dysfunction in anxiety disorders. In contrast to less rigorously controlled studies, oradrenergic function in depression was normal.