Category Archives: DSM

What’s Really Wrong with DSM-5

By Liah Greenfeld

The essence of the DSM-5 consists in the modifications it introduces in the extensive psychiatric nosology, specifically adding diagnostic categories to diseases of unknown biological origin and uncertain etiology. But the real problem lies much deeper – in the understanding of such diseases itself. It is the problem with the old, fundamental, and universally accepted diagnostic categories of thought disorder- vs. affective disorders, or schizophrenia vs. manic and unipolar depression, on which all the other diagnostic categories of mental illness of unknown etiology, new and not so new, are based. DSM-5’s approach is similar to attempting to salvage a house, falling apart because it is built on an unsound foundation, by adding to it a fresh coat of paint and new shutters.

What Mind, Modernity, Madness does, in contrast, is to dismantle the structure, establish a sound foundation, and then rebuild the house on top of it. I begin by questioning and analyzing the fundamental diagnostic categories themselves, consider them against the existing clinical, neurobiological, genetic, and epidemiological evidence, bring into the mix the never-before-considered cultural data, and on this basis propose that the two (schizophrenia and manic-depressive illness) or even three (schizophrenia, manic depression, and unipolar depression) discreet diseases are better conceptualized–and therefore treated–as the same disease, with one cause, which expresses itself differently depending on the circumstances in which this cause becomes operative. Psychiatric epidemiologists, at least, have long suspected that “the black box of culture” is an important contributing factor in these diseases. However, as the phrase indicates, they lack the means to understand or even examine its contribution. By unpacking the “black box” (and showing, specifically, how it is reflected in the logically necessary structures of the mind, such as identity, will, and thinking self), I add a missing yet essential dimension to the diagnostic tool-kit, which the DSM-5, like the previous editions, disregards.

On DSM-V and the Diagnosis of Mental Illness

Allen Frances in “Diagnosing the D.S.M.,” The New York Times

…the D.S.M. is the victim of its own success and is accorded the authority of a bible in areas well beyond its competence. It has become the arbiter of who is ill and who is not — and often the primary determinant of treatment decisions, insurance eligibility, disability payments and who gets special school services. D.S.M. drives the direction of research and the approval of new drugs. It is widely used (and misused) in the courts… Psychiatric diagnosis is simply too important to be left exclusively in the hands of psychiatrists. They will always be an essential part of the mix but should no longer be permitted to call all the shots.

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Schizophrenia and Manic-Depressive Illness: What do We Know about Biological Causes?

By David Phillipi

While the technological advancements of recent decades allow us to map the human genome and look at the brain on the molecular level, the enormous amount of data that has been amassed is virtually useless for psychiatrists trying to diagnose their sick patients because the assumed biological causes of schizophrenia and manic-depressive illness have not been found. No brain abnormalities that are specific to either illness or present in all cases have been identified. Nevertheless, the experts who study and treat schizophrenia and manic-depressive illness (MDI) keep the faith (quite literally) that a breakthrough is just around the corner.

For years, genetic research has appeared to be the most promising of the recently opened avenues, but the excitement seems unwarranted by the findings. The relatively large number of chromosomal regions which may be implicated in susceptibility for bipolar disorder means that hope of finding a specific bipolar gene or even a small number of genes must be given up. Some researchers think the way to go is to narrow the search by looking for genes associated with specific aspects of the disease. Of course, this further refinement is only possible because of the huge variation in symptoms and experiences of those who fall under the MDI/bipolar umbrella, and we are once again reminded of the difficulty of defining what this illness or group of illnesses even is. Furthermore, even the distinction between schizophrenia and MDI seems to collapse in light of the genetic linkage data. In Manic-Depressive Illness: Bipolar Disorders and Recurrent Depression (2nd Edition), Drs. Frederick Goodwin and Kay Redfield Jamison write:

While the search for predisposing genes had traditionally tended to proceed under the assumption that schizophrenia and bipolar disorder are separate disease entities with different underlying etiologies, emerging findings from many fields of psychiatric research do not fit well with this model. Most notably, the pattern of findings emerging from genetic studies shows increasing evidence for an overlap in genetic susceptibility across the traditional classification categories. (49)

Genetic studies in the schizophrenia research community lead to pretty much the same hypothesis as with bipolar: genetic susceptibility is most likely polygenic, meaning dependent on the total number of certain genes which may contribute to vulnerability. It must be noted that genetic vulnerability is a condition, not a cause of schizophrenia and bipolar – something else must be acting on this vulnerability. In one way or another, this fact is usually noted in the literature that deals with genetic data, but it is often obscured by a tone of confidence which suggests the information may be more meaningful and explanatory than it truly is.

Even when a specific gene has been well studied across illnesses, its usefulness in understanding genetic susceptibility may be extremely limited. Some studies in both schizophrenia and MDI have found an increased risk of illness for those who possess the short form of the serotonin transporter promoter gene 5-HTT. The thing is, each of us has two copies of this gene, and over two-thirds of us have one long and one short form, meaning that having the normal variant of the gene is the risk factor! If most of us possess a gene which puts us at risk for an illness which only a small minority of people have, then this particular trait is obviously not much of a causal explanation.

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