Ross J Baldessarini, MD
The Canadian Journal of Psychiatry, Vol 59, No 8, August 2014.
p. 402 “A further effect of the discovery of the several new classes of psychotropics in and following the 1950’s is that a new kind of biological theorizing became dominant in academic psychiatry – one that I have termed pharmacocentric. 1,9 The basic idea is that, as the science of drug action (pharmacodynamics) has made initial small advances, it has been irresistibly tempting to argue that the opposite of the drug action may be a clue to pathophysiology. Among other examples, this kind of thinking led to the dopamine-excess theory of psychotic disorders and mania based on the antidopaminergic actions of most antipsychotic-anti-manic drugs, to the various monoamine deficiency hypotheses concerning depression and some anxiety disorders based on speculations about the norepinephrine- or serotonin potentiating actions of most antidepressants. Although such theorizing stimulated a generation of clever experimentation, findings of research aimed at testing them at the clinical level has remained inconsistent and unconvincing. This outcome should not be any more surprising than, for example, expecting to discover the pneumococcus from detailed knowledge of the molecular pharmacology of willow bark and its antipyretic salicylates.
An extension of such speculations sometimes extends into clinical practice, as diagnoses and rationales for particular treatments are presented to patients couched in concepts arising from pharmacodynamics but representing little more than NEUROMYTHOLOGY. Again, the fundamental fact is that the disorders considered to lie within the province of psychiatry remain idiopathic.”