Three Books about the Chemical Imbalance Theory of Mental Illness

I highly recommend the two-part article by Marcia Angell in recent issues of the New York Review of Books.   In June, she wrote a piece entitled ‘The Epidemic of Mental Illness:  Why?’; then in the July issue, she followed up with another piece entitled ‘The Illusions of Psychiatry.’ In these two articles, she discusses several important books that address the “epidemic” of mental illness in this country, including Robert Whitaker’s book
Anatomy of an Epidemic which I reviewed in three separate posts:  one about the theory that mental illness is caused by a chemical imbalance in the brain, another concerning the actual effects of psychiatric medications and the third addressing the entirely false belief that treating psychological disorders with such drugs is like taking insulin for diabetes.  Marcia Angell is a Senior Lecturer in Social Medicine at Harvard Medical School and a former Editor in Chief of the New England Journal of Medicine; these lengthy articles are thorough and scholarly.

The other two books under review are The Emperor’s New Drugs:  Exploding the Antidepressant Myth by Irving Kirsch and Unhinged:  The Trouble with Psychiatry — a Doctor’s Revelations About a Profession in Crisis by Daniel Carlat.  I haven’t yet read these two latter books, but here is Marcia Angell’s description of them:

“The authors emphasize different aspects of the epidemic of mental illness. Kirsch is concerned with whether antidepressants work. Whitaker, who has written an angrier book, takes on the entire spectrum of mental illness and asks whether psychoactive drugs create worse problems than they solve. Carlat, who writes more in sorrow than in anger, looks mainly at how his profession has allied itself with, and is manipulated by, the pharmaceutical industry. But despite their differences, all three are in remarkable agreement on some important matters, and they have documented their views well.”

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The Rise of Bipolar Disorder Symptoms and Treatment

If you’ve been around as long as I have, you may remember a time when the diagnostic label “Bipolar Disorder” was relatively unknown.  Although that term has been around since the 1950s, it came into common usage only in 1980 when the APA released its third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III); before then, mental health professionals discussed and wrote about Melancholia or Manic-Depressive Illness. It was considered quite rare.   As you may know, that revision to the prior version of the DSM sought to eliminate its psychoanalytic/psychodynamic bias and replace it with a supposedly more “scientific” approach, thereby embedding psychiatry within the medical model of treatment.

According to the 1969 book, Manic Depressive Illness by George Winokur of Washington University, Bipolar Disorder used to be fairly rare.  In 1955, only one person in every 13,000 was hospitalized for it.  Today, by contrast, according to the National Institute of Mental Health, Bipolar Disorder symptoms affect an astounding one in every forty adults in our country!!!  It’s also worth noting that, before psychiatric medications were introduced, the long-term outcome for those patients was fairly good.  Only 50% of the people hospitalized for a first attack of mania ever suffered a second one.  Studies have found that, in the pre-drug period, 75-80% of hospitalized patients recovered within a year and only half of them had even one more attack within the next 20 years.  Today, Bipolar Disorder is a chronic illness, with patients spending years and years on psychiatric medications.  In other words, Bipolar Disorder was comparatively rare before 1980 and the prognosis for hospitalized patients was fairly good; today it’s 325 times more common than it used to be and has become a lifelong illness.

How are we to account for this change, from a rare and acute illness to one that is pervasive and chronic?

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“Psychiatric Meds Are Like Insulin for Diabetes” (Big Lie #3)

In Part One of my discussion of Robert Whitaker’s Anatomy of an Epidemic, we learned that there is no  scientific basis for the theory that mental illness results from an imbalance in brain chemistry; Part Two showed how, in the main, patients who were never given psychiatric meds have far better outcomes than people exposed early on to such drugs.  In this third and final part, I’ll discuss what these medications actually do to your brain chemistry and why they lead to a worse prognosis in the long run.

In order to understand these processes, we need a bit of basic neurology.  I’ll try to keep it simple.  As you probably know, the brain is made up of billions of neurons; each one of these neurons is connected to many other neurons.  Messages travel along the neurons, to and from the brain, moving from one neuron to another across a tiny gap called a neural synapse or the synaptic cleft.  One neuron releases a chemical messenger  called a neurotransmitter into the synapse; the molecule then travels across that tiny gap and bonds to the next neuron on the other side, thereby delivering its message.  The message subsequently continues along this second neuron until the next synapse, and so on.  Here’s a diagram of a typical neural synapse; you can ignore most of the labels:


So the message travels down the yellow neuron, releasing neurotransmitters into the synaptic cleft.  On the other side, the green neuron has receptors (the red ovals) where the neurotransmitter bonds, thereby sending  a message which then travels down the green neuron to the next synapse, and so on.  After the message has been sent, the neurotransmitter is released from the receptor back into the synapse where one of two things occurs:  either another chemical agent, an enzyme, goes to work on the neurotransmitter and dissolves it, or the (yellow) neuron re-absorbs it for later use.

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“Psychiatric Medications Have Led to Dramatic Improvements in Mental Health Outcomes” (Big Lie No. 2)

In continuing my discussion of Robert Whitaker’s Anatomy of an Epidemic from my last post, I begin with the results of a study on the use of anti-psychotic medication for treating schizophrenia; it is one of many such studies discussed by Whitaker which report very similar outcomes.  This study was funded by the National Institute of Mental Health (NIMH) and conducted at NIMH’s clinical research facility in Bethesda, Maryland.  According to Whitaker:

“[T]hose treated without drugs were discharged sooner that the drug-treated patients, and only 35 percent of the non-medicated group relapsed within a year after discharge, compared to 45 percent of the medicated group.  The off-drug patients also suffered less from depression, blunted emotions, and retarded movements.”  The investigators reported that, over the long term, the medicated patients were “less able to cope with subsequent life stresses.”

Study after study shows that, in the short term, anti-psychotics do reduce unrealistic thinking, anxiety, suspiciousness and auditory hallucinations, but in the long-term, they make those continuing on medication much more prone to relapse and re-hospitalization than non-medicated patients or patients given a placebo.   “Schizophrenic patients discharged on medications were returning to psychiatric emergency rooms in such droves that hospital staff dubbed it the ‘revolving door syndrome.’  Even when patients reliably took their medications, relapse was common, and researchers observed that ‘relapse is greater in severity during drug administration than when no drugs were given.'”

In other words, schizophrenic patients who received no medication had much better long-term results than those treated with anti-psychotic drugs.  This jibes with both (1) a historical comparison between long-term outcomes for schizophrenic patients prior and subsequent to the introduction of anti-psychotics; and (2) a comparison between long-term outcomes for schizophrenics treated with anti-psychotics in the developed world versus those in poor countries treated without them (much better).  Study after study bears this out.

In short-term usage, psychiatric medications for psychotic disorders have value in stabilizing patients and reducing the severity of their symptoms, but long-term usage makes those people more prone to relapse and “may prolong the social dependency of many discharged patients.”   And here is the tricky part:  If patients are withdrawn from their medications, they do poorly, then do better once they have been put back on those drugs.  For this reason, it appears to be proof that the drugs “work”; but do they only “work” in the sense that they ameliorate a problem created by placing the patient on those very drugs in the first place?  In study after study, it is patients given no medication whatsoever who have the best outcomes.

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“You Have a Chemical Imbalance in Your Brain” (Big Lie No. 1)


My colleague Jeff Kaye PhD recommended that I read Robert Whitaker’s The Making of an Epidemic (pictured above) for insight into the scientific evidence concerning the effects of psychiatric medication. I read the entire book in one day and feel it is the most important work I’ve read in years. This and the following two posts will summarize Whitaker’s most important findings but I recommend that you read this book if you’re at all interested in or concerned about these drugs and what they actually do.  Although some sections of the book discuss neurological processes and there’s a fair amount of statistical data to support his arguments, you don’t need to be a psychologist or a physician to understand the material. For me, the experience was like reading a well-written legal thriller: I found it riveting.   As a clinician, I’ve always doubted the effectiveness claims associated with Prozac and the other so-called “anti-depressants”, viewing them as propaganda that drives profits for Big Pharma, as I’ve discussed elsewhere.  The full truth is far more disturbing.

Whitaker began as a newspaper reporter, then co-founded his own publishing company that reported on the business aspects of clinical testing for new drugs; his readers worked at pharmaceutical companies, medical schools and private medical practices, so he did not come to his subject area with an ax to grind.  He began his research for Anatomy when he discovered that as a whole, schizophrenic patients in poor countries, only 16 percent of whom were regularly given antipsychotic medication, had much better long-term outcomes than patients in developed countries who received such drugs. He set out to understand this puzzle, not to launch a crusade.  Before writing his book, he “believed that psychiatric researchers were discovering the biological causes of mental illness and that this knowledge had led to the development of a new generation of psychiatric drugs that helped ‘balance’ brain chemistry.” Many of you may believe the very same thing — not surprising, since it’s the story that has been given to us by the medical profession and regularly repeated in the media.

After painstaking research, Whitaker found that there is absolutely no scientific evidence to support the theory that mental illness is a result of an imbalance in brain chemistry. Let me repeat that: there is absolutely no scientific evidence to support the theory that mental illness is a result of an imbalance in brain chemistry.  As an example, let’s take the best known theory, that depression is caused by low serotonin levels in the neural synapses.  An entire class of drugs — the “selective serotonin reuptake inhibitors” (SSRIs) inhibits the removal of serotonin from those synapses and thus ( in theory) restores normal serotonin levels.  So, if this theory is true, depressed people should have below-normal levels of 5-HIAA (serotonin is matabolized into 5-HIAA) in their cerebrospinal fluid.

Study after study has failed to find any significant difference in the 5-HIAA levels of depressed and non-depressed patients.   No correlation has been found between 5-HIAA levels and severity of depressive symptoms.  Whitaker is thorough and devastating on this particular point, exposing flawed research designs and statistical analysis in the very few studies that purport to show even a very small link between serotonin levels and depressive symptoms.  Furthermore, no correlation has been found between levels of 5-HIAA in cerebrospinal fluid and degree of response to anti-depressants.  This widely accepted theory has absolutely no basis in fact:

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