THE CATECHOLAMINE HYPOTHESIS OF AFFECTIVE DISORDERS: A REVIEW OF SUPPORTING EVIDENCE

¹ Clinical Associate, Section on Psychiatry, Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Md.

The "catecholamine hypothesis of affective disorders" proposes that some, if not all, depressions are associated with an absolute or relative decrease in catecholamines, particularly norepinephrine, available at central adrenergic receptor sites. Elation, conversely, may be associated with an excess of such amines. Evidence supporting this hypothesis was reviewed.

Data from pharmacological studies, mainly in animals, suggest that the actions of both major classes of antidepressant drugs are mediated through the catecholamines. The monoamine oxidase inhibitors increase brain concentrations of norepinephrine while imipramine-like agents potentiate the physiological effects of norepinephrine. Reserpine, a drug which can cause clinical depression, depletes catecholamines, but other amines may also be involved in its mechanism of action. A rigorous extrapolation from pharmacological studies to pathophysiology clearly cannot be made. Clinical studies relevant to the catecholamime hypothesis are limited and the findings are inconclusive.

It is not possible, therefore, to confirm definitively or to reject the catecholamine hypothesis on the basis of data currently available. In our present state of knowledge, however, the catecholamine hypothesis is of considerable heuristic value, providing the investigator and the clinician with a frame of reference integrating much of our experience with those pharmacological agents which produce alterations in human affective states.

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				E. L. Klaiber, D. M. Broverman, W. Vogel, and Y. Kobayashi Estrogen Therapy for Severe Persistent Depressions in Women Arch Gen Psychiatry, May 1, 1979; 36(5): 550 - 554. [Abstract] [PDF]

				J. D. van Scheyen and D. P. van Kammen Clomipramine-Induced Mania in Unipolar Depression Arch Gen Psychiatry, May 1, 1979; 36(5): 560 - 565. [Abstract] [PDF]

				D. R. Sweeney, J. W. Maas, and G. R. Heninger State Anxiety, Physical Activity, and Urinary 3-Methoxy-4-Hydroxyphenethylene Glycol Excretion Arch Gen Psychiatry, December 1, 1978; 35(12): 1418 - 1423. [Abstract] [PDF]

				J. J. Schildkraut, P. J. Orsulak, A. F. Schatzberg, J. E. Gudeman, J. O. Cole, W. A. Rohde, and R. A. LaBrie Toward a Biochemical Classification of Depressive Disorders: I. Differences in Urinary Excretion of MHPG and Other Catecholamine Metabolites in Clinically Defined Subtypes of Depressions Arch Gen Psychiatry, December 1, 1978; 35(12): 1427 - 1433. [Abstract] [PDF]

				J. J. Schildkraut, P. J. Orsulak, R. A. LaBrie, A. F. Schatzberg, J. E. Gudeman, J. O. Cole, and W. A. Rohde Toward a Biochemical Classification of Depressive Disorders: II. Application of Multivariate Discriminant Function Analysis to Data on Urinary Catecholamines and Metabolites Arch Gen Psychiatry, December 1, 1978; 35(12): 1436 - 1439. [Abstract] [PDF]

				S. G. Siris, D. P. van Kammen, and J. P. Docherty Use of Antidepressant Drugs in Schizophrenia Arch Gen Psychiatry, November 1, 1978; 35(11): 1368 - 1377. [Abstract] [PDF]

				D. Pickar, D. R. Sweeney, J. W. Maas, and G. R. Heninger Primary Affective Disorder, Clinical State Change, and MHPG Excretion: A Longitudinal Study Arch Gen Psychiatry, November 1, 1978; 35(11): 1378 - 1383. [Abstract] [PDF]

				F. Crews and C. Smith Presynaptic alpha-receptor subsensitivity after long-term antidepressant treatment Science, October 20, 1978; 202(4365): 322 - 324. [Abstract] [PDF]

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