As Co-Chair of the Program Committee for the annual meeting of the American Society of Clinical Psychopharmacology (ASCP) (the meeting was formerly called “NCDEU”), I realized that we had seldom covered autism among our scientific topics. I invited Dr. Michael Murray, who directs the autism program at Penn State, to chair a panel. Mike accepted and invited Drs. Allison Jack from Yale and David Beversdorf from the University of Missouri to join him on the panel, and he asked me to serve as Discussant. I have seldom seen a patient with autism spectrum disorder (ASD) and have never conducted research on it. But I viewed this as a learning opportunity and attended the session on June 22nd. What struck me was how far this field has progressed over my 50-year career, along with the rest of psychiatry.
When I attended medical school in the 1960s, a dominant school of thought held that autism resulted from cold mothers. Analogously, schizophrenia was caused by bad mothers and/or by family communications that “taught” children to think psychotically. Fortunately, brain science has advanced. Now we recognize that peculiar family communications may reflect expression of aberrant genes, and an offspring with schizophrenia is showing a phenotype of those genes. Similarly, one or both parents may be on the autism spectrum genetically, and as a result, one or more children may have the full-blown disorder.
When I was a psychiatry resident in the early 1970s, my mentor Gerald Klerman wished for a moratorium on new psychiatric theories. Gerry thought we should test the extant ones before any new theories were promulgated. Back then, there was little science to underpin our diagnoses and treatments. Instead, the literature was replete with anecdotes, case studies, and personal testimonies.
With this backdrop, the ASD panel was refreshing and encouraging. Many or most cases of ASD probably reflect genetic abnormalities that impair social interactions and communication. The ultimate triumph in 5 or 50 years may be identifying the abnormal genes in utero and correcting them prenatally. But until then, much can be done to improve the lives of ASD patients and their families.
Panelists described rigorous studies with oral propranolol, intranasal oxytocin, and a social skills intervention. The research was elegant—employing state-of-the-art behavioral techniques, physiologic monitoring, and parallel work in animal models. Graphs, tables, and P values were augmented by poignant vignettes with patients, showing benefit from new interventions—interventions that build on preclinical and clinical research.
Our field has matured—in the ways we think about emotional and behavioral disorders, define and describe them, and attempt to intervene and assess effectiveness. The benefits of that maturation accrue to patients—including those with autism.
-Alan J. Gelenberg, M.D.
Editor, Biological Therapies in Psychiatry
Professor Emeritus, University of Arizona
Editor-in-Chief, Journal of Clinical Psychiatry