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April 21, 2003. Richard Gottlieb has made much of the ability of SSRI medications to modify aggression and has elevated this observation to the status of an hypothesis. There is no clinical doubt that SSRIs can modify aggression in some patients, and that such a modification is also found to be true with older antidepressants, such as tricyclics and monoamine oxidase inhibitors. Indeed, the success of any member of any class of antidepressants depends on its ability to modify aggression in the given depressed patient. What has so far eluded psychopharmacologists is the ability to predict which antidepressant will work in which patient. Some mood stabilizers, such as lithium carbonate and depakote, are also able to modify aggression in ways that prevent the recurrence of both mania and depression in bipolar patients. Such observations suggest that affective disorders generally are diseases of dysregulation of energy: too much or too little in the system clinically representing mania on the one hand, or depression on the other. With this broadened hypothesis, one is able to explain why some patients seem to have affective disorders based on the length of time light strikes the retina, others based on a discontinuity between external and internal clocking systems, and still others based on shifts of internal self-regard. The initiating agent in each case may differ, but the end result is an affective disorder with similar end-state symptoms, regardless of initiating event.
The broadening of Gottlieb's SSRI hypothesis would lead to the research he suggests, as well as to an approach to affective states that is even broader in scope, embracing affective states determined entirely by physiological factors, others whose determination is purely psychological, and still others with contributions from both physiological and psychological parameters.