The idea of biological causation was both on the forefront [at least in the research laboratories] and in the background [in the ubiquitous Clinical Trials focused on symptomatic improvement rather than cause] – nowhere more apparent than in the treatment of depression. The DSM-III destroyed diagnostic distinctions among the clinical depressions – essentially shutting down biological research on the probably·biological depressive syndromes by diluting them with the larger group of probably·not·biological symptomatic depressions. The primary focus of psychiatric research turned from etiology to treatment effect and moved from academic centers to private enterprise – the clinical research industry.
By 2002, the psychopharmacology business was booming, managed care was in charge of clinical care, the psychoanalysts were elsewhere, but basic psychiatric research had gone nowhere in spite of the new technologies and much ado:
By David Kupfer, Michael First, and Darrel Regier, 2002
Need to Explore the Possibility of Fundamental Changes in the Neo-Kraepelinian Diagnostic Paradigm
The DSM-III diagnostic system adopted a so-called neo-Kraepelinian approach to diagnosis. The approach avoided organizing a diagnostic system around hypothetical but unproven theories about etiology in favor of a descriptive approach, in which disorders were characterized in terms of symptoms that could be elicited by patient report, direct observation, and measurement. The major advantage of adopting a descriptive classification was its improved reliability over prior classification systems using nonoperationalized definitions of disorders based on unproven etiological assumptions. From the outset, however, it was recognized that the primary strength of a descriptive approach was its ability to improve communication among clinicians and researchers, not its established validity.
Disorders in DSM-III were identified in terms of syndromes, symptoms that are observed in clinical populations to covary together in individuals. It was presumed that, as in general medicine, the phenomenon of symptom covariation could be explained by a common underlying etiology. As described by Robins and Guze , the validity of these identified syndromes could be incrementally improved through increasingly precise clinical description, laboratory studies, delineation of disorders, follow-up studies of outcome, and family studies. Once fully validated, these syndromes would form the basis for the identification of standard, etiologically homogeneous groups that would respond to specific treatments uniformly.In the more than 30 years since the introduction of the Feighner criteria by Robins and Guze, which eventually became the DSM-III, the goal of validating these syndromes and discovering common etiologies has remained elusive. Despite many proposed candidates, not one laboratory marker has been found to be specific in identifying any of the DSM-defined syndromes. Epidemiologic and clinical have shown extremely high rates of comorbidities among the disorders, undermining the hypothesis that the syndromes represent distinct etiologies. Furthermore, epidemiologic studies have shown a high degree of short-term diagnostic instability for many disorders. With regard to treatment, lack of treatment specificity is the rule rather than the exception…
Concerns have also been raised that researchers’ slavish adoption of DSM-IV definitions may have hindered research in the etiology of mental disaorders. Few question the value of having a well-described, well operationalized, and universally accepted diagnostic system to facilitate diagnostic comparisons across studies and to improve diagnostic reliability. However, reification of DSM-IV entities, to point that they are considered to be equivalent to diseases, is more likely to obscure than to elucidate research findings.
All these limitations in the current diagnostic paradigm suggest that research exclusively focused on refining the DSM-defined syndromes may never be successful in uncovering their underlying etiologies. For that to happen, an as yet unknown paradigm shift may need to occur. Therefore, another important goal of this volume is to transcend the limitations of the current DSM paradigm and to encourage a research agenda that goes beyond our current ways of thinking to attempt to integrate information from a wide variety of sources and technologies.
And that became the general approach of the DSM-5 Task Force – a search for something new. Rather than attempting to refine and revise the DSM-III/DSM-IV system and criteria [their assigned task], the DSM-V Task Force thought we needed something else – some as yet unknown paradigm shift and they focused on the ever exciting tools of neuroscience instead of the nuances of clinical diagnosis. They put on an series of expensive planning conferences that went on for four years – forgettable and forgotten. Little wonder that they developed an adversarial relationship with their predecessors who wondered at their secrecy and when they were going to get around to the task of revising.
And as they fiddled, Rome began to burn. The golden age of drug treatment morphed into an era of a corrupt academic/industrial complex with its conflicts of interest, ghost-writing, fallen KOLs, and suits galore alleging fraud in the pharmaceutical industry. Their early decision to put revision and refining on the back burner and pursue new vistas backfired when nothing new came along and their new, quirky diagnoses went up in smoke. They were left with an unrevised diagnostic system that failed its Field Tests, bringing the whole enterprise into question.