By Robert Whitaker
August 13, 2022
Source: Mad in America
Photo / Image Source: Unsplash,
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The Trail of Fraud
As is well-known, the low-serotonin theory of depression had its roots in findings, dating back to the 1960s, that the first generation of antidepressants, tricyclics and monoamine oxidase inhibitors, both prevented the usual removal of neurotransmitters known as monoamines from the synaptic cleft between neurons. This led researchers in the 1965 to hypothesize that a deficit in monamines could be a cause of depression.
Once this hypothesis was floated, researchers then sought to determine whether if patients with depression actually suffered from a monamine deficiency. It’s a history of one negative finding after another.
As early as 1974, researchers concluded that all such studies up to that time indicated that “the depletion of brain norepinephrine, dopamine, or serotonin is in itself not sufficient to account for the development of the clinical syndrome of depression.” This was the first round of findings, and after that there was speculation that a monoamine deficit might be present in a subset of depressed patients (as opposed to being a pathology common to all such patients.) In 1984, the NIMH conducted a study to investigate that possibility. Once more, the bottom-line findings were negative, which led the NIMH researchers to conclude that “elevations or decrements in the functioning of serotonergic systems per are not likely to be associated with depression.”
At that point, the hypothesis had been around for nearly two decades and found to be wanting. In the research community, there was a sense that the hypothesis had always presented an overly reductive picture of how the brain functioned, and thus it wasn’t a surprise that research had failed to support the hypothesis. Even so, after that 1984 report, investigators continued to study whether depressed patients suffered from low serotonin, with this research quickening after Prozac arrived on the market in 1988. Many different investigative methods were tried, but once again, the results were negative... They wrote:
“The monoamine hypothesis, which was first proposed in 1965, holds that monoamines such as norepinephrine and 5-HT [serotonin] are deficient in depression and that the action of antidepressants depends on increasing the synaptic availability of these monoamines.
The monoamine hypothesis was based on observations that that antidepressants block reuptake inhibition of norepinephrine, 5-HT, and/or dopamine. However, inferring neurotransmitter pathophysiology from an observed action of a class of medications on neurotransmitter availability is similar to concluding that because aspirin causes gastrointestinal bleeding, headaches are caused by too much blood and the therapeutic action of aspirin in headaches involves blood loss. Additional experience has not confirmed the monoamine depletion hypothesis.”1
Other experts in the field echoed this point in the next few years, psychiatrist Stephen Stahl wrote that “there is no clear and convincing evidence that monamine deficiency accounts for depression; that is, there is no ‘real’ monoamine deficit.”2
More such confessions appeared in the research literature, and finally, in a 2010 paper, Eric Nestler, famous for his work on the biology of mental disorders, detailed how the many types of inquiries into the low-serotonin theory had all come to the same conclusion:
“After more than a decade of PET studies (positioned aptly to quantitatively measure receptor and transporter numbers and occupancy), monoamine depletion studies (which transiently and experimentally reduce brain monoamine levels), as well as genetic association analyses examining polymorphisms in monoaminergic genes, there is little evidence to implicate true deficits in serotonergic, noradrenergic, or dopaminergic neurotransmission in the pathophysiology of depression. This is not surprising, as there is no a priori reason that the mechanism of action of a treatment is the opposite of disease pathophysiology.”
This is the research history that psychiatrists today, when asked to comment about Moncrieff’s paper, are referring to when they state, “there is nothing new here.” They are right. The theory was abandoned long ago. In a 2011 blog, Ronald Pies, editor of Psychiatric Times, put it this way: “In truth, the ‘chemical imbalance’ notion was always a kind of urban legend—never a theory seriously propounded by well-informed psychiatrists.”
The argument could be made that while the biology of depression remained unknown, one hypothesis was that it was due to low serotonin, and that there were still efforts to see if that might be true. However, after that date, the APA, the pharmaceutical companies, and the academic psychiatrists that populated the scientific advisory councils had an obligation to inform the public that the low-serotonin theory had not panned out. If instead these three groups informed the public that depressed patients suffered from a chemical imbalance that could be fixed by a drug, they were knowingly telling the public a lie, and thus, by informed consent standards, they were abetting medical malpractice and the medical battery of patients.
And it’s easy to document that is exactly what the APA, the pharmaceutical companies, and the scientific advisory boards did.
The APA’s Promotion of the Chemical Imbalance Story
The APA’s promotion of the chemical imbalance theory of mental disorders can be traced back to 1980, when it published the third edition of its Diagnostic and Statistical Manual. That publication is regularly characterized as a transformative moment for American psychiatry, as this was when the APA adopted a “disease” model for diagnosing and treating psychiatric disorders.
There were no scientific findings that spurred this transformation. The scientific impulse that was present arose from the failure of DSM II: the diagnoses in that edition were understood to “lack reliability and validity.” That led a team of researchers at Washington University in St. Louis to advocate that psychiatry should start fresh: it could develop categories for grouping patients with like symptoms, with the hope that subsequent research would “validate” the groupings as real diseases. DSM II would be abandoned, and new categories would be drawn up for research purposes.
However, during the 1970s, APA leaders spoke of how, in the face of various criticisms, psychiatry was fighting for its survival. Its diagnostic manual was understood to lack validity; psychologists and counselors were offering talk therapies that appeared to be as effective as psychoanalysis; One Flew Over the Cuckoo’s Nest depicted staff in mental hospitals as the truly crazy ones; and an “antipsychiatry” movement described psychiatry as an agency of social control.
How can such practices impact your health? Why? What is your experience?
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