Recently, a psychiatric study on first episodes of psychosis made front-page news. People seemed quite surprised by the finding: that lower doses of psychotropic drugs, when combined with individual psychotherapy, family education and a focus on social adaptation, resulted in decreased symptoms and increased wellness.
But the real surprise — and disappointment — was that this was considered so surprising. The study, by Dr. John M. Kane of Hofstra North Shore-LIJ School of Medicine and his colleagues, simply gave empirical support to the longstanding "biopsychosocial" model of illness, which acknowledges that, in ways not fully understood, biology, psychology and social forces can all affect mental health. This model has long been the basis of treatment for experienced, pragmatically minded clinicians.
Unfortunately, such clinical pragmatism has seriously declined in the United States, as psychiatry has veered toward pharmacology. After the emergence of Prozac and the newer antipsychotic drugs like Risperidone some two decades ago, there was a sustained effort by academic research leaders in American psychiatry to promote these successes, and to fight the stigmatization of the mentally ill by forgoing the complexities of the biopsychosocial model for a simpler, more authoritative claim: Mental illness is a brain disease.
Inherent to this proposition is the implication that psychological and social events somehow are not also brain events. Acknowledgment of any nonexplicitly neural factors is seen as opening the door to those who dismiss mental illness as metaphysical, fake or the result of a moral failing. By these lights, meaningful interventions for those struggling with mental illness must be biochemical or anatomical.