Allow me to explain the title to this piece and to a recent piece:
“Creative destruction” is a term popularized by Joseph Schumpeter in the 1940s to explain the necessary and typically heart-breaking disruption and chaos that gives rise to economic progress. Think changing times. The advent of the automobile put buggy whip manufacturers out of business. In turn, the likes of GM grew at the expense of smaller auto manufacturers. And the process continues today with GM fighting for its life in a new global economy.
It’s a never-ending cosmic dance of destruction and creation, exemplified by the Hindu diety Shiva.
A post-GM world, followers of Schumpeter would argue, promises to be a better one: Imagine a leaner and greener auto industry responsive to consumer needs and environmental realities. Yes, the transition is bound to be devastating, but indiscriminately trying to soften the pain, they would say, only leads to stagnation and decline.
In the field of psychiatry, the exemplar of creative destruction was Robert Spitzer, who boldly took on the cult of Freud and ushered in a new era of psychiatry. The ground-breaking DSM-III of 1980 and its follow-up DSM-III-R of 1987 were his great achievements. Thanks to Spitzer and his contemporaries, we seek out psychiatrists and therapists to treat our depression rather than undergo analysis to root out our neurosis.
Ironically, though, the unprecedented success of Spitzer's DSM spawned its own problems. Suddenly, we had “stakeholders” in the form of the insurance industry, the drug industry, the research establishment, not to mention psychiatry and its related professions. Oh, yes, patients too, but who listens to us?
Overnight, the DSM became entrenched, incapable of correcting even its most obvious faults, incapable of folding in new insight. Take the current DSM’s view of depression - please! - which is virtually unchanged since the DSM-III. Yes, the DSM-III version is an improvement on the DSM-II of 1968, but at least the older view recognized the complexity of the condition and its context, namely:
The DSM-II viewed depression as both separate from (in the sense of “depressive neurosis”) and as part of manic-depression (in the sense of “manic depressive illness, depressed type”) and tied into anxiety (in the form of “involuted melancholia” and as the driving force of “neurosis”) as well as embedded into personality (as in “cyclothymic personality disorder characterized by depression”).
Moreover, the DSM-II distinguished between depression seen as a result of the mysterious biology of the brain (“endogenous”) and depression seen to be caused by a reaction to events (“exogenous”).
The DSM-III replaced all that with a monolithic view of unipolar depression, separating it out from manic-depression and anxiety and personality and doing away with the endogenous-exogenous distinction. Instead, for the first time, we were treated to the famous and extraordinarily arbitrary nine-item symptom checklist.
Viewing depression as a single and non-complex entity offers the advantage of clarity in a world where clinicians and other interested parties need to be speaking the same language. The problem occurs when this simplistic view encourages equally simplistic treatments.
(Yes, the current DSM distinguishes the likes of melancholic from atypical depression and makes room for depression with psychosis and the like, but only if the full criteria is met for a depressive episode.)
In my book, "Living Well with Depression and Bipolar Disorder," I cite a 2004 article by Gordon Parker MD, PhD of the University of New South Wales in support of the proposition that this one-size-fits-all view of depression results in clinical trials that indiscriminately lump all patients together, with no regard to critical distinctions that may spell the difference between success and failure.
We know for instance that an SSRI such as Paxil gets 50 percent of patients with “major depression” 50 percent better over a period of about six weeks. This is good enough for the drug companies, who now have a license to print money, but what about the patients? Who wants a 50 percent chance of success? And who wants to be just 50 percent better?
What do we know about Paxil, anyway? Does it work better on a patient whose depression is marked by sadness? If so, is it possible to target this group of patients? Maybe then we would be seeing 80 percent of these individuals getting 80 percent better.
And try this on for size. Maybe a patient whose main feature is lack of motivation (about which the DSM has nothing to say) would benefit from something else, as would depression brought on by stress (the type of “exogenous” depression axed from the DSM-III). Maybe these drugs don’t exist. Maybe Pharma would be encouraged to develop them. As Dr Parker in a 2007 piece concludes:
Depression is a diagnosis that will remain a non-specific "catch all" until common sense brings current confusion to order. As the American journalist Ed Murrow observed in another context: "Anyone who isn't confused doesn't really understand the situation."
In other words, never mind what is convenient to the industry-professional-research establishment. To move forward, first we need to journey back to the naive and confusing DSM-II and acknowledge that the real world of depression is highly nuanced and complex. Then, maybe we could deploy our modern knowledge to develop a new and sophisticated, but no less confusing, understanding.
Instead, the DSM-5 Mood Disorders Work Group in a report from April 2009 signaled it was using the DSM-III (upon which the DSM-IV is based) as its starting point, noting that a subgroup was reviewing “whether there is sufficient data to support adding or removing symptoms” to or from the major depression checklist.
Often, the results justify working off an existing document. But no changes? With no explanation? After all we have learned since 1980? With our lives at stake?
A little creative destruction, please. Time to rip the thing up and start over.
Much more on the DSM-5 draft to come ...
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