Updates on the Epidemic


Here’s a rundown of a hodgepodge of studies that I’ve come across recently that relate to themes I wrote about in Anatomy of an Epidemic. (Two of the studies were published prior to 2010, but it was only recently that I discovered them.)

1) Antidepressants are depressogenic over the long term

In a 2008 study by Dutch investigators, “Continuation and Maintenance Use of Antidepressants in Recurrent Depression,” 172 adults who had recovered from a bout of “recurrent depression,” were then followed for two years. The relapse rates for patients during that followup period, according to antidepressant use, was as follows:

    Continual antidepressant use: 60.4%.

    Intermittent antidepressant use: 63.4%.

    No antidepressant use: 26%.

As in the many longer-term studies I cited in Anatomy of an Epidemic, those who stayed on antidepressants in this study were much more likely to become depressed again.

2) Antipsychotics increase a person’s biological vulnerability to psychosis

During the 1970s, researchers learned that antipsychotics blocked a particular subtype of dopamine receptor, known as the D2 receptor. In response to that blockade, the brain increases the density of its D2 receptors. This, reasoned two Canadian physicians, Guy Chouinard and Barry Jones, makes a person “supersensitive” to dopamine, and thus more biologically vulnerable to psychosis.

Chouinard and Jones reasoned that this was why so many schizophrenia patients relapsed when they tried to go off an antipsychotic, and also why schizophrenia patients who stayed on the medications long-term nevertheless worsened. Many patients develop “tardive psychosis” over the long-term, and when this happens, Chouinard and Jones reported, the “illness appears worse” than ever before.

When Chouinard and Jones raised this hypothesis in the late 1970s and early 1980s, it caused a brief fury, and then was largely forgotten. This hypothesis, which in fact was supported by clinical findings, suggested that antipsychotics worsened psychotic symptoms over the long term, and that understanding clearly imperiled the story that psychiatric had told to the public, which was that people diagnosed with schizophrenia needed to be on antipsychotics all their lives.

However, in 2005, Philip Seeman at the University of Toronto revived it with a report that in animal models of psychosis, all of the various psychotic triggers—such as amphetamines, angel dust, genetic mutations, or brain lesions—caused an increase in D2 receptors that have a “HIGH affinity” for dopamine, and that so did antipsychotics, including the newer atypicals like Zyprexa. In other words, antipsychotics caused the very biological abnormality identified as the “common pathway” in animal models of psychosis.

Then, in 2007—and this is the study I recently came across—Seeman and his colleagues reported that this dopamine supersensitivity was why “ongoing antipsychotic treatment leads to treatment failure over time.”

Here’s how they determined this. When rats are given amphetamines, which up dopamine levels in the brain, they show increased locomotion. An antipsychotic—at first—blocks  this amphetamine-induced locomotion in rats, and that is because the drug blocks dopamine receptors (and thus counter the effects of an amphetamine.) But over time, the antipsychotic induced a notable increase in D2 receptors in the rat brain, and more than a doubling of D2 receptors with a high affinity for dopamine, Seeman reported. The rats had become “supersensitive” to dopamine, and after this happened,  when they were given amphetamines, the antipsychotic no longer blocked the amphetamine-induced locomotion.

This, Seeman reported, explained why “antipsychotics so often fail” over time . . . our results suggest that an antipsychotic-induced increase in dopamine sensitivity might predispose certain individuals to psychotic relapse.”

In other words, their study animal confirmed the  “dopamine supersensitivity” hypothesis advanced by Chouinard and Jones 30 years. Antipsychotics increase a person’s biological vulnerability to psychosis over time, and this leads many to become chronically ill.

3) Acknowledgement that chemical imbalances do not underlie mental disorders

As I wrote in Anatomy of an Epidemic, the chemical imbalance theory of mental disorders arose in the 1960s and 1970s, but researchers subsequently failed to find that people diagnosed with depression actually had low levels of serotonin, or that people diagnosed with schizophrenia had overactive dopamine systems. Still, the psychiatric profession, pharmaceutical companies, and NAMI continued to promote the chemical imbalance story, such that a study published in 2010 found that 87% of Americans thought that schizophrenia was due to a “chemical imbalance,” and 80% thought that depression was due to one as well.

In an article published in November in the American Journal of Psychiatry, Eric Nestler and Vaishnav reviewed the chemical imbalance theory of depression. They wrote:

“After more than a decade of PET studies (positioned aptly to quantitatively measure receptor and transporter numbers and occupancy), monamine depletion studies (which transiently and experimentally reduce brain monamine levels), and 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.”

In a similar vein, Nestler and Stephen Hyman, who is a former director of the National Institute of Mental Health, in their 2009 text Molecular Neuropharmacology, reviewed the chemical imbalance theory of schizophrenia. They wrote:

“It must be emphasized that neurotransmitter related-hypotheses that attempt to explain the etiology of schizophrenia are based solely on pharmacological evidence, and thus are likely to be incomplete or misleading. Although pharmacologic manipulations of neurotransmitter systems may exacerbate or ameliorate psychotic symptoms, aberrations in these systems do not necessarily underlie psychotic disorders.”

Once again, we see in these quotes admissions by leaders in the field that there is no actual evidence that people diagnosed with mental disorders actually suffer from chemical imbalances. And yet the vast majority of Americans believe that they do.

4) The Epidemic in Children Grows

The widespread prescribing of psychiatric medications to American children and youth began in the early 1990s. In Anatomy of An Epidemic, I reported on how the use of stimulants and antidepressants has “created” many juvenile bipolar patients. Now comes more evidence of this epidemic.

In a poster presentation at the 2010 annual meeting of the American Academy of Child and Adolescent Psychiary, Joseph Blader reported that psychiatric hospitalizations for children five to 13 years old nearly doubled from 1996 to 2007. Psychiatric hospitalizations for adolescents, 14 to 19 years old, rose 42% during this period.

The prescribing of psychiatric medications to children and adolescents jumps, and sure enough, the number of psychiatric hospitalizations for American youth soars.


Dec 5, 2010


Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.