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Am J Psychiatry 1992; 149:999-1010
Copyright © 1992 by American Psychiatric Association
Transduction of psychosocial stress into the neurobiology of recurrent affective disorder
RM Post
Biological Psychiatry Branch, NIMH, Bethesda, MD 20892.
Early clinical observations and recent systematic studies overwhelmingly
document a greater role for psychosocial stressors in association with the
first episode of major affective disorder than with subsequent episodes.
The author postulates that both sensitization to stressors and episode
sensitization occur and become encoded at the level of gene expression. In
particular, stressors and the biochemical concomitants of the episodes
themselves can induce the protooncogene c- fos and related transcription
factors, which then affect the expression of transmitters, receptors, and
neuropeptides that alter responsivity in a long-lasting fashion. Thus, both
stressors and episodes may leave residual traces and vulnerabilities to
further occurrences of affective illness. These data and concepts suggest
that the biochemical and anatomical substrates underlying the affective
disorders evolve over time as a function of recurrences, as does
pharmacological responsivity. This formulation highlights the critical
importance of early intervention in the illness in order to prevent
malignant transformation to rapid cycling, spontaneous episodes, and
refractoriness to drug treatment.
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