{"id":42759,"date":"2014-01-03T09:29:24","date_gmt":"2014-01-03T14:29:24","guid":{"rendered":"http:\/\/1boringoldman.com\/?p=42759"},"modified":"2014-01-03T09:43:35","modified_gmt":"2014-01-03T14:43:35","slug":"dsm-5-retrospective-i","status":"publish","type":"post","link":"https:\/\/1boringoldman.com\/index.php\/2014\/01\/03\/dsm-5-retrospective-i\/","title":{"rendered":"DSM-5 retrospective I…"},"content":{"rendered":"\n

Something very unusual happened in the process of the revision of the psychiatric diagnostic manual – the DSM-5 revision published last May. The leaders of the previous revisions, Robert Spitzer [DSM-III, DSM-IIIR] and Allen Frances [DSM-IV], both became outspoken critics of the enterprise and went public with their dissatisfaction. Dr. Spitzer was refused access the the minutes of the DSM-V meetings, and then found out that all the members of the Task Force had signed confidentiality agreements. In a series of articles in the Psychiatric News in 2008 and early 2009, he repeatedly pointed out that secrecy was unprecedented and incompatible with the charge of the Task Force. Dr. Allen Frances declined to join Dr. Spitzer’s campaign until May when he learned about some of the things the DSM-5 Task Force were contemplating, and he went public with his concerns with what became the very public campaign that continues to the present [see dangerous men…<\/a>]. The response from the APA was silence, defensiveness, or attacks – but never engagement.<\/p>\n

As this increasingly loud controversy filled our airways, I went back and read the book that had introduced the whole DSM-5 process in 2002, A Research Agenda for the DSM-V<\/a> [available as a pdf]. I’ve mentioned this book repeatedly but have never gotten much of a response. I think it’s a book of dirty tricks that contains the roots of what came later. From the Introduction [page 18<\/a> of the PDF]:<\/div>\n
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Need to Explore the Possibility of Fundamental Changes in the Neo-Kraepelinian Diagnostic Paradigm<\/font><\/strong><\/div>\n

… 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 [1970], the validity of these identified syndromes could be incrementally improved through increasingly precise clinical description, laboratory studies, delimitation 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.<\/p>\n

In the more than 30 years since the introduction of the Feighner criteria by Robins and Guze, which eventually led to 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 studies 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. <\/p>\n

The efficacy of many psychotropic medications cuts across the DSM-defined categories. For example, the selective serotonin reuptake inhibitors [SSRIs] have been demonstrated to be efficacious in a wide variety of disorders, described in many different sections of DSM, including major depressive disorder, panic disorder, obsessive-compulsive disorder, dysthymic disorder, bulimia nervosa, social anxiety disorder, posttraumatic stress disorder, generalized anxiety disorder, hypochondriasis, body dysmorphic disorder, and borderline personality disorder. Results of twin studies have also contradicted the DSM assumption that separate syndromes have a different underlying genetic basis. For example, twin studies have shown that generalized anxiety disorder and major depressive disorder may share genetic risk factors [Kendler 1996]…<\/div>\n<\/blockquote>\n
I would never be a person accused of defending the DSM-III or the Feighner Criteria, but my reading of Kupfer et al is that they’re making a Straw Man Argument<\/em> here – presenting things in a certain way so as to be able to shoot them down. And they don’t mention what Dr. Spitzer said in the Introduction to his DSM-III:<\/div>\n
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For most of the DSM-III disorders, however, the etiology is unknown. A variety of theories have been advanced, buttressed  by evidence – not always convincing – to explain how these disorders came about. The approach taken in DSM-III is atheoretical with regard to etiology or pathophysiological process except for those disorders for which this is well established and therefore included in the definition of the disorder. Undoubtedly, with time, some of the disorders of unknown etiology will be found to have specific biological etiologies, others to have specific psychological causes, and still others to result mainly from a particular interplay of psychological, social, and biological factors. The major justification for the generally atheoretical approach taken in DSM-III with regard to etiology is that the inclusion of etiological theories would be an obstacle to use of the manual by clinicians of varying theoretical orientations, since it would not be possible to present all reasonable etiologic theories for each disorder.<\/div>\n
Robert Spitzer, in the DSM-III, p 6.<\/div>\n<\/blockquote>\n
There are plenty of other more likely explanations for the disappointments they mention with the previous DSMs. There’s a major flaw in the DSM system that would explain much of what they complain about. The creation of the omnibus unitary Major Depressive Disorder [MDD] destroyed the most likely candidate for biomarkers, Endogenous Depression or Melancholia, a category Dr. Kupfer himself had studied productively in the past [REM latency: a psychobiologic marker for primary depressive disease<\/a>]. Who ever said that the conditions listed in the DSM were biological or genetic in origin? We hypothesis that some are, pending confirmation. I agree with some of those hypotheses. But what is it about the medications that suggests disease specificity? More likely, they are symptomatic medications, unrelated to underlying etiology. And the more basic concern that the biologic measures don’t map onto DSM categories as Drs. Robins and Guze predicted may well have the same significance – the biological hypotheses are simply incorrect.<\/div>\n

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It’s an odd book in that it looks at thirty years of evidence of a failed set of hypotheses and concludes that the hypothesis is right but we’re just not collecting the right evidence – the truth was in the hypothesis, not in the test results. Ergo, the diagnostic system based on the predictions was wrong, because it didn’t produce the expected results themselves. I’m of course making something of a Straw Man Argument<\/em> myself here. I support the research into the biological basis of conditions that warrant that exploration. I’m arguing against the global point they’re making, not all the specifics. The rest of this book lays out a plan to explore other ways to classify mental illness, chasing the biology and the responses to biological treatment.  They say very little about revising<\/font><\/strong><\/em> the DSM. Their focus was on changing<\/font><\/strong><\/em> it. And that continued in a series of expensive and extensive symposia over the next several years: <\/div>\n