The brain-disease-drug crowd has been singing the same tired, misleading refrain for a while now. It’s in two parts.
The first consists of the seemingly courageous admission that what the psychiatric profession, pharmaceutical companies, and government agencies have been claiming is the established science behind the “brain disease,” “mental illness” conception of psychic distress…well, isn’t.* Turns out, it’s been bogus and hollow from the start. The scientific diagnoses have nothing behind them, and the so-called hypotheses at the heart of the model have now been discarded.
A few examples:
An
NPR story by Alex Spiegel from last year:
And really, it is because of the popularity of Prozac that the low-serotonin story took hold, even though, Frazer argues, the scientific research has not borne that out.
"I don't think there's any convincing body of data that anybody has ever found that depression is associated to a significant extent with a loss of serotonin," he says.
A
recent piece in Nature by David Adam:
DSM-5, like the two preceding editions, will place disorders in discrete categories such as major-depressive disorder, bipolar disorder, schizophrenia and obsessive–compulsive disorder (OCD). These categories, which have guided psychiatry since the early 1980s, are based largely on decades-old theory and subjective symptoms.
The problem is that biologists have been unable to find any genetic or neuroscientific evidence to support the breakdown of complex mental disorders into separate categories.
…Despite decades of work, the genetic, metabolic and cellular signatures of almost all mental syndromes remain largely a mystery.
Another
recent article by NIMH head Thomas Insel:
The goal of this new manual, as with all previous editions, is to provide a common language for describing psychopathology. While DSM has been described as a “Bible” for the field, it is, at best, a dictionary, creating a set of labels and defining each. The strength of each of the editions of DSM has been “reliability” – each edition has ensured that clinicians use the same terms in the same ways.** The weakness is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. In the rest of medicine, this would be equivalent to creating diagnostic systems based on the nature of chest pain or the quality of fever. Indeed, symptom-based diagnosis, once common in other areas of medicine, has been largely replaced in the past half century as we have understood that symptoms alone rarely indicate the best choice of treatment.
Steven E. Hyman, last month***:
The scientific issues facing translational psychiatry—the application of basic discoveries in neuroscience, genetics, and psychology to understanding disease and to advancing therapeutics—are daunting. The molecular and cellular underpinnings of psychiatric disorders remain unknown; there is broad disillusionment with the animal models used for decades to predict therapeutic efficacy; psychiatric diagnoses seem arbitrary and lack objective tests; and there are no validated biomarkers with which to judge the success of clinical trials.
A natural and reasonable response to the statements I’ve bolded would be to stop, step back, and consider the import of these acknowledgements. It’s being conceded that these biological disorders, as such, don’t exist. The premise for the alleged effectiveness of the drugs being prescribed to and sometimes forced upon people around the world - costing billions of dollars, causing harm, and diverting resources from potentially fruitful investigations and approaches - is invalid. The existing brain disease model is false.
In fact, reports of these facts are, regularly and repeatedly, treated as “explosive,”
only to be greeted as explosive again months or years later. It would seem astounding that people haven’t been enraged and that this hasn’t much altered the status quo. But some of the explanation (in addition to the pharmaceutical companies’ huge propagandistic capacity) for the failure of these particular articles to cause widespread uproar can be found in the way they’re framed.
First, these stories tend to minimize and distort the admissions. Spiegel’s piece, for example, is titled “When It Comes To Depression, Serotonin Isn’t The Whole Story,” and contains this passage:
Coyle is less absolute in his dismissal of the evidence on serotonin. His take is that while low serotonin probably doesn't cause depression, some abnormality in the serotonin system clearly plays a role. But most researchers have moved on, he says, and are looking at more fundamental issues like identifying the genes that might put people at risk for developing depression.
"What's being looked at are processes that are much more fundamental than just serotonin levels," he says. "We need to move beyond serotonin, and I think the field is."
So in some cases the current brain-disease model isn’t really fully acknowledged to be false, as it would at first seem. To some extent, it’s presented as just a part of a larger story or a simplified, superficial, or reductionistic version of a complex explanation. This parallels
the evasive response received by Leo and Lacasse when they tried to challenge deceptive direct-to-consumer advertising of antidepressants based on the monoamine “hypothesis”:
Since 2002, the first author (JRL) has repeatedly contacted the FDA regarding these issues. The only substantive response was an E-mail received from a regulatory reviewer at the FDA: “Your concern regarding direct-to-consumer advertising raises an interesting issue regarding the validity of reductionistic statements. These statements are used in an attempt to describe the putative mechanisms of neurotransmitter action(s) to the fraction of the public that functions at no higher than a 6th grade reading level” (personal communication, 2002 April 11).
It is curious that these advertisements are rationalized as being appropriate for those with poor reading skills. If the issues surrounding antidepressants are too complex to explain accurately to the general public, one wonders why it is imperative that DTCA of antidepressants be permitted at all. However, contrary to what the FDA seems to be implying, truth and simplicity are not mutually exclusive. Consider the medical textbook, Essential Psychopharmacology, which states, “So far, there is no clear and convincing evidence that monoamine deficiency accounts for depression; that is, there is no ‘real’ monoamine deficit” [44]. Like the pharmaceutical company advertisements, this explanation is very easy to understand, yet it paints a very different picture about the serotonin hypothesis.
The attempt to characterize demonstrably false claims as merely simplifications or partial explanations after appearing to acknowledge that they’re baseless is a fairly constant feature of the sorts of admissions I’m talking about here. No evidence for continued claims like “some abnormality in the serotonin system clearly plays a role” is provided or requested.
Further, the persistent acceptance of the existing model is portrayed as desirable and beneficial. People wanted it, and it’s been socially useful even if, as it unexpectedly turns out, much to their surprise, it's not backed by science. The articles often insist on including passages attributing the tenacity of the brain-disease-drug model to the demands of the psychologically distressed public. Hyman, for example: “Even if current drugs recycle old action in the brain, the existing pharmacopeia is a great blessing to many patients and their families.” Or Spiegel:
So why are so many people still talking about low serotonin causing depression?
Frazer says it's probably because it has had, and continues to have, important cultural uses. For one, he says, by initially framing the problem as a deficiency — something that needed to be returned to normal — patients felt more comfortable taking a drug.
"If there was this biological reason for them being depressed, some deficiency that the drug was correcting," Frazer says, then taking a drug was OK. "They had a chemical imbalance and the drug was correcting that imbalance." In fact, he says, the story enables many people to come out of the closet about being depressed, which he views as a good thing.
But Delgado agrees with Frazer and says the story has some benefits. He points out that years of research have demonstrated that uncertainty itself can be harmful to people — which is why, he says, clear, simple explanations are so very important.
"When you feel that you understand it, a lot of the stress levels dramatically are reduced," he says. "So stress, hormones and a lot of biological factors change."
This is the standard narrative: the model is so popular because people want clarity and certainty, even if it’s false, and this model has provided them that. It’s also been beneficial because it’s reduced stigma. It’s not greed-driven corporations, a profession trying to gain status and money, or billions of dollars spent to market not just the drugs but the model itself that have been behind its cultural success – it was people’s need for simple solutions and the important destigmatizing function the model has served in the culture. (Really, we should all be thanking them!)
Like the model itself, these claims have an estranged relationship with the facts. The role of corporate marketing and psychiatric maneuvering (and media complicity) in pushing this model is extremely well documented, and the model is, in fact, stigmatizing. Even if this weren’t the case, as I’ve argued before,
it’s not just condescending but fundamentally unprofessional and unethical for doctors, therapists, or government officials to lie to people because they think they want to be lied to or, worse, to get them to take drugs.
But these articles and reports aren’t particularly interested in evaluating the individual and social consequences of the model’s acceptance. Their purpose, it seems, is protecting the larger brain-disease enterprise. The framing of frank admissions that the model isn’t scientifically supported in the ways I’ve described sets the stage for the second part of the refrain: the breathless, almost comically arrogant predictions about the wondrous scifi possibilities of new research. The fact that the existing model is scientifically invalid can be pushed aside. New and exciting frontiers in genetics (of course) and imaging and so on are opening up that will save the day.
Hyman gushes:
As long as we guard against renewed self-deception about what constitutes meaningful advances, there is good reason to feel optimistic about the long-term future of translational psychiatry—despite its palpable scientific challenges. My optimism is based partly on the extraordinary vitality of neuroscience and perhaps, even more important, on the emergence of remarkable new tools and technologies to identify the genetic risk factors for psychiatric disorders, to investigate the circuitry of the human brain, and to replace current animal models that have failed to predict efficacious new drugs that act by novel mechanisms in the brain. New ideas are, of course, central to scientific progress, but new tools can open up unexpected worlds and thus undergird the formulation of truly novel hypotheses.
…Our best hope is that the genetics will unfold over the next several years, due to the efforts of large international consortia that have formed to recruit and to study patients. As genetic clues accumulate, scientists are devising new ways to investigate their neurobiological functions and dysfunctions.
…The leading approach is to take a small skin biopsy from the arms of volunteers and to transform skin fibroblasts into neural progenitors and into neurons. Genetic engineering can then be used to add risk-causing mutations to “healthy” neurons and to reverse risk mutations in patients’ neurons. But it is still early in this new field, and it is not yet possible to engineer the specific kinds of neurons implicated in schizophrenia by postmortem studies.
This barrier is likely to fall soon. Whether or not engineered neurons or human neural circuits on a chip prove to be good systems for studying gene function, researchers will make substantial efforts to turn genetic clues into ideas for therapeutics. Many researchers hope that such efforts will help attract the pharmaceutical industry back to psychiatry by demonstrating new paths to treatment development. The emerging genetic results may be the best clues we have ever had to the etiology of psychiatric disorders. If other areas of medicine can guide us, there is enormous promise in deprioritizing existing drugs and old-fashioned animal-based assays as investigative tools and instead focusing on actual disease mechanisms identified by genetics. Technology has only recently begun to make this possible.
David Adams writes,
Research could yet come to the rescue. In 2010, the US National Institute of Mental Health (NIMH) in Bethesda, Maryland, launched an initiative, called the Research Domain Criteria project, that aims to improve understanding of dimensional variables and the brain circuits involved in mental disorders. Clinical psychologist Bruce Cuthbert, who heads the project, says that it is an attempt to go “back to the drawing board” on mental illness. In place of categories, he says, “we do have to start thinking instead about how these disorders are dysregulation in normal processes”.
…All involved agree on one thing. Their role model now is not Freud or Kraepelin, but the genetic revolution taking place in oncology. Here, researchers and physicians are starting to classify and treat cancers on the basis of a tumour's detailed genetic profile rather than the part of the body in which it grows. Those in the psychiatric field say that genetics and brain imaging could do the same for diagnoses in mental health. It will take time, however, and an entire generation will probably have to receive flawed diagnoses before the science is developed enough to consign the category approach to clinical history.
“I hope I'll be able to give a patient with possible bipolar a proper clinical assessment,” Craddock says. “I'll do a blood test and look for genetic risks and send them into a brain scanner and ask them to think of something mildly unhappy to exercise their emotional system.” The results could be used to trace the underlying cause — such as a problematic chemical signal in the brain. “I'll then be able to provide lifestyle advice and treatment.” He pauses. “Actually it won't be me, because I will have retired by then.”
Here’s Insel’s description of the program:
NIMH has launched the Research Domain Criteria (RDoC) project to transform diagnosis by incorporating genetics, imaging, cognitive science, and other levels of information to lay the foundation for a new classification system. Through a series of workshops over the past 18 months, we have tried to define several major categories for a new nosology (see below). This approach began with several assumptions:
• A diagnostic approach based on the biology as well as the symptoms must not be constrained by the current DSM categories,
• Mental disorders are biological disorders involving brain circuits that implicate specific domains of cognition, emotion, or behavior,
• Each level of analysis needs to be understood across a dimension of function,
• Mapping the cognitive, circuit, and genetic aspects of mental disorders will yield new and better targets for treatment.
…[P]atients and families should welcome this change as a first step towards "precision medicine,” the movement that has transformed cancer diagnosis and treatment. [my emphasis]
Aside from drawing needed funds away from useful investigations into the social causes of psychological distress and the interventions it can lead to, and aside from its potential – given psychiatry’s history – of leading to dreadfully harmful “therapies,” this is simply a terrible approach to science. That should be obvious.
You shouldn’t base your approach on a scientifically unfounded assumption, expecting that future discoveries will retroactively show that assumption to have been warranted.
But of most interest here is the relationship of this futuristic speculation to the existing brain-disease-drug model. The aim appears to be the implicit suggestion that future discoveries will somehow, in some vague and unarticulated sense, rescue or validate it. Of course, that’s fundamentally not how science works – science is based on the evidence we actually have
now, not on the expectation of some hypothetical evidence that could appear in the future. The evidence we have, as they acknowledge, is that
the current biopsychiatric model is not supported by or consistent with scientific knowledge.
And they recognize that what they’re talking about is in essence a fresh, clean start. Adams writes that the new research program’s advances will “be too late for the
DSM.” Spiegel, although he claims they’re making some (unspecified) progress, makes clear that “Researchers don't really know what causes depression.” Insel notes that “RDoC, for now, is a research framework, not a clinical tool. This is a decade-long project that is just beginning.” They talk about a new drawing board, scrapping the existing diagnostic categories, and “deprioritizing” existing drugs.
But at the same time they also seem to want to leave in place the current brain-disease framework, and to imply that research of the future will somehow vindicate it. But this is scientifically irrational. The odds, in particular, that genetics or imaging research over the next several decades will find something that supports the use of the current psychiatric drugs would have to be infinitesimal. And even if it were to happen, that wouldn’t justify their use
now, with the evidence we have
now. But these articles tend to obscure this. The second part of the refrain – the cheerful expectation for future research - serves rhetorically to minimize the very real, very serious problems with current practices that these articles are supposedly acknowledging.
The pharmaceutical companies have to walk a fine line. On the one hand, it’s about patents. They have to promote a model founding the efficacy and safety of their psychiatric drugs for as long as those continue to be patented and profitable; after they’ve exhausted all of their many means of extending the life of a patent for a drug, they have no reason to care. (Indeed, they’re happy to acknowledge the ineffectiveness of an off-patent drug if they’re trying to push a new one.) On the other hand, both they and the psychiatric-government-academic complex that has built up around these drugs need to sustain the model itself – both for the sales of other drugs (including any in the immediate pipeline) and for their future funding, sales, and status. These sorts of articles do that work.
Greg Benson at Mad in America criticizes some of Insel’s article, but also says: “That said, I appreciate what I think is commendable intellectual honesty on the part of Thomas Insel. Insel argues the historic failure of validity in trying to understand ‘mental disorders’ as medical conditions.” It would be more commendable, I think, if he didn’t
repeatedly give these honest (if partial) admissions the same sort of spin. The spin isn’t going to stop on its own. The best that the supporters of science and social justice can do is to keep publicizing these admissions of the failure of the biopsychiatric model, becoming more aware of the techniques through which these are spun, and putting forward the real picture.**** I hope I’ve contributed a bit to that here.
* Note that I am not providing these quotations as primary evidence of the invalidity of the brain-disease model. That evidence is abundant, and I have linked to sources
here many times.
**
Well,…
*** Hyman’s article also points to the use of nonhuman animals in psychiatric research. The Catch-22 for advocates of this research is clear: if these animals are being used as models because they’re recognized (however dubious the
specific assumptions being made) as sharing the capacity to become depressed, distressed, helpless, afraid, and so on, it’s hard for researchers to claim that the experiments aren’t cruel.
**** As
Richard Bentall does here.
