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Mad Science: The Treatment of Mental Illness Fails to Progress [Excerpt]

Recent questions about the validity of diagnostic criteria for mental illness have raised deeper questions about the current state of psychiatry

From Madness in Civilization: A Cultural History of Insanity from the Bible to Freud, from the Madhouse to Modern Medicine, by Andrew Scull. Published by Princeton University Press in arrangement with Thames & Hudson, Ltd., London. Copyright ©2015, Andrew Scull. Reprinted by permission.

As civilized human beings, we like to console ourselves with visions of progress, illusory as that concept often proves to be. Perhaps we have not seen progress in the realms of literature and art (though some would dispute that claim), but surely science moves forward, and medicine too, insofar as it is a science rather than an art. In the developed world, at least, we now enjoy longer, and certainly more materially abundant if not culturally richer and happier lives. Except if we are mad, that is. Modern psychiatry and its potions notwithstanding, one of the more sobering realities about serious mental illness in the twenty-first century is that its sufferers not only die at a much younger age on average than the rest of us (as much as twenty-five years sooner), but also that the incidence of serious illness and mortality in this population has accelerated in recent decades. On this most basic of levels we seem to be regressing.

Psychiatry seems to be in trouble too. The neo-Kraepelinian approach it adopted when DSM III was published in 1980 at first served it well. The reliability and replicability of psychiatric diagnoses increased, and embarrassing disputes about what was wrong with a particular patient receded into the past. Freudians lost the internecine professional war decisively, and psychiatrists embraced once more a biological account of mental disorders that superficially made sense to their medical brethren, however schematic it remained. And the new approach proved extraordinarily attractive to the drug companies, who underwrote the psychiatric research enterprise, and as the years went by, increasingly influenced the very terms in which mental illness was discussed, even the categories of illness that purportedly exist in the world.


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Each successive edition of the manual, the revised third edition (III R) of 1987, the fourth edition (IV of 1994) and its ‘text revision’ (IV TR of 2000), adhered to the fundamental approach psychiatry had adopted in 1980, though new ‘illnesses’ were added on each occasion, the definitions of psychopathology were tweaked and the page count mounted. But as ‘illnesses’ proliferated in each revision, and the criteria for assigning a particular diagnosis were loosened, the very problem that had led to the invention of the new versions of the DSM recurred, and major new threats to psychiatric legitimacy surfaced.

The loosening of diagnostic criteria led to an extraordinary expansion of the numbers of people defined as mentally ill. This has been particularly evident among, but by no means confined to, the ranks of the young. ‘Juvenile bipolar disorder’, for example, increased forty-fold in just a decade, between 1994 and 2004. An autism epidemic broke out, as a formerly rare condition, seen in less than one in five hundred children at the outset of the same decade, was found in one in every ninety children only ten years later. The story for hyperactivity, subsequently relabelled ADHD is similar, with 10 per cent of male American children now taking pills daily for their ‘disease’. Among adults, one in every seventy-six Americans qualified for welfare payments based upon mental disability by 2007.

If psychiatrists’ inability to agree among themselves on a diagnosis threatened to make them a laughing-stock in the 1970s, the relabelling of a host of ordinary life events as psychiatric pathology promised more of the same. Thus, when American psychiatry embarked on still another revision of the manual in the early twenty-first century, the resulting DSM 5 was supposed to be different from its predecessors. (The change from the previous system of Roman numerals was designed to allow for continuous updating of the manual, as with software releases: DSM 5.1, 5.2 and so on.) Those put in charge of the enterprise announced that the logic that had underpinned the two previous editions was deeply flawed, and they would fix things. Drawing on the findings of neuroscience and genetics, they would move away from the symptom-based system that they now acknowledged was inadequate, and build a manual that linked mental disorders to brain function. They would also take account of the fact that mental disorder is a dimensional, not a categorical kind of thing: a matter of being more or less sane, not a black and white world with sanity in this corner and mental illness in that. It was a grand ambition. The only problem was that it was an ambition impossible to fulfill. Having thrashed about in pursuit of this chimera, those running the project were ultimately forced to concede defeat, and by 2009 they were back to tinkering with the descriptive approach.

As the work proceeded, it appeared that social anxiety disorder, oppositional defiant disorder, school phobia, narcissistic and borderline personality disorders would be joined by such things as pathological gambling, binge eating disorder, hypersexuality disorder, temper dysregulation disorder, mixed anxiety depressive disorder, minor neurocognitive disorder and attenuated psychotic symptoms syndrome. Yet we are almost as far removed as ever from understanding the aetiological roots of major psychiatric disorders, let alone these more controversial diagnoses (which many people would argue do not belong in the medical arena in the first place). Such diagnoses do, however, provide lucrative new markets for psychopharmacology’s products, which has caused some critics to question whether commercial concerns are illegitimately driving the expansion of the psychiatric universe – and these critics have had a field day by pointing to the fact that the great majority of the members of the DSM task force are recipients of drug company largesse.

In May 2013, DSM 5 finally materialized. It did not make an auspicious debut. Just before its publication, two enormously influential psychiatrists rendered their own verdicts. Steven E. Hyman, the former director of NIMH condemned the whole enterprise. It was, he pronounced, ‘totally wrong in a way [its authors] couldn’t have imagined. So in fact what they produced was an absolute scientific nightmare. Many people who get one diagnosis get five diagnoses, but they don’t have five diseases – they have one underlying condition.’ Thomas R. Insel (b. 1951), the current director of the National Institute of Mental Health issued a similar verdict. The manual, he pro- claimed, suffered from a scientific ‘lack of validity.... As long as the research community takes the D.S.M to be a bible, we’ll never make progress. People think everything has to match D.S.M. criteria, but you know what? Biology never read that book.’ NIMH, he said, would be ‘reorienting its research away from D.S.M. categories [because] patients with mental illness deserve better’.

A few months earlier, in a private conversation that he must have realized would become public, Insel had voiced an even more heretical thought. His psychiatric colleagues, he said dismissively, ‘actually believe [that the diseases they diagnose using the DSM] are real. But there’s no reality. These are just constructs. There is no reality to schizophrenia or depression...we might have to stop using terms like depression and schizophrenia, because they are getting in our way, confusing things.  Insel is keen to replace descriptive psychiatry with a diagnostic system built upon biological foundations. But in the present state of our knowledge, that formula is an idle fantasy. Much as psychiatry (and many of those who suffer from mental disorders) might wish it otherwise, madness remains an enigma, a mystery we seemingly cannot solve. Its depredations remain something we can at best palliate. Over the past half century, the expansion of neuroscience has been remarkable, and its discoveries legion. Unfortunately, none of them have proved of much clinical use to date in the treatment of mental illness. Nor have neuroscientists as yet uncovered the aetiological roots of madness. In recent decades, new imaging technologies have flourished. Functional Magnetic Resonance Imaging (fMRI) has been employed, its digital read-outs transformed by modern electronic alchemy into pictures of the brain that light up in technicolour. Surely these marvels of modern science will at last reveal the germ of madness?

Not yet, and not likely for some time to come. Despite important advances in our understanding, we are very far indeed from being able to connect even very simple human actions to the underlying structure and functioning of people’s brains. We are decades away, after all, from successfully mapping the brain of the fruit fly, let alone successfully tackling the infinitely more complex task of unravelling the billions upon billions of connections that make up our own brains.

Some enthusiasts for neuroscience make much of the fact that particular regions of the brain show heightened levels of activity on fMRIs when people, for example, are making choices, or telling lies. Even the philosophical idealist Bishop Berkeley would not be surprised by that. When I move, speak, think, experience an emotion, presumably this is correlated with physical changes in my brain, but such correlations prove nothing about the causal processes, any more than the existence of a particular sequence of events demonstrates that some early event in the sequence ineluctably caused a later event. Post hoc ergo propter hoc (‘after this, therefore because of this’) is an elementary logical fallacy. What fMRIs are crudely measuring is the flow of blood in the brain, and demonstrating heightened activity of this sort is a far cry from giving us privileged insights into the contents of people’s thoughts, not to mention the instability and ambiguity of the results when experiments are replicated.

Like the poor folks waiting for Godot (who, as it happens, were quite possibly waiting for a madman), we are still waiting for those mysterious and long-rumored neuropathological causes of mental illness to surface. It has been a long wait, and on more than one level a misguided one, I think, if the expectation is that the ultimate explanation of madness lies here and only here.

Why is that? It makes no sense to regard the brain (as biological reductionists do) as an asocial or a pre-social organ, because in important respects its very structure and functioning are a product of the social environment. For the most remarkable feature of the human brain is how deeply and profoundly sensitive it is to psychosocial and sensory inputs. What this means, as the neuroscientist Bruce Wexler (b. 1947) puts it, is that ‘our biology is social in such a fundamental and thorough manner that to speak of a relation between the two suggests an unwarranted distinction’.

To an extent unprecedented in any other part of the animal kingdom, humans’ brains continue to develop post-natally, and the environmental elements that most powerfully affect the structure and functioning of these brains are themselves a human creation. Human beings exhibit a remarkable neuroplasticity, at least through adolescence, and we must thus bear in mind the critical importance of non-biological factors in transforming the neural structures we are born with, thereby creating the mature brain. The very shape of the brain, the neural connections that develop and that constitute the physical underpinnings of our emotions and cognition, are profoundly influenced by social stimulation, and by the cultural and especially the familial environment within which these developments take place. It is in these settings that the brain’s structure and organization are fine-tuned. Quite simply, to quote Bruce Wexler again, ‘human nature...allows and requires environmental input for normal development’– and, one can immediately add, abnormal development. And that development continues for a very long time, with increases in connectivity and changes in brain organization, especially in the parietal and frontal lobes, taking place well into the third decade of life. Freud’s speculations about how the early psychosocial environment was connected to psychopathology may no longer seem remotely plausible to most of us, but the fundamental notion that some of the roots of madness need to be sought outside our bodies is surely not misplaced.

The metaphysical wager that much of Western medicine embraced centuries ago, that madness had its roots in the body, has in most respects yet to pay off. Perhaps, I have suggested, it never will entirely. It is hard to imagine, at least for the most severe forms of mental aberration, that biology will not prove to play an important role in their genesis. But will madness, that most solitary of afflictions and most social of maladies, be reducible at last to biology and nothing but biology? There one must have serious doubts. The social and the cultural dimensions of mental disorders, so indispensable a part of the story of madness in civilization over the centuries, are unlikely to melt away, or prove to be nothing more than epiphenomenal features of so universal a feature of human existence. Madness indeed has its meanings, elusive and evanescent as our attempts to capture them have been. It remains a fundamental puzzle, a reproach to reason, inescapably part and parcel of civilization itself.