Biology of comorbid depression and anxiety

University Of Michigan At Ann Arbor, Ann Arbor MI

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Abstract

This study focuses upon the stress biology of mood and anxiety disorders and will provide hormone data to test models of anxiety and depression and the co-morbid state proposed in the Specific Aims. Current research indicates that depression is accompanied by increased activation of the stress hormones (HPA axis) , while anxiety disorders, particularly Panic Disorder, is accompanied by abnormalities of the brain noradrenergic system, as reflected by a blunted growth hormone response to clonidine. We will study a group of well characterized pure depressed, pure panic and and mixed panic and depressed patients with the clonidine/growth hormone challenge to determine if all depressed patients manifest abnormalities in clonidine stimulated growth hormone release or if only those with both depression and panic symptoms manifest this abnormality. We will evaluate noradrenergic and stress "reactivity" to two simple challenges in pure depression, depression plus panic anxiety, panic disorder patients and normal controls. These challenges include orthostatic challenge and the Trier Social Stress Test (TSST). We hypothesize that panic disorder patients and depressed patients with anxiety will demonstrate exaggerated catecholamine response to orthostatic challenge i.e increased reactivity. We hypothesize that depressed patients will have altered HPA axis responses to stress response while Panic Disorder patients will have normal HPA axis response to the TSST.