Mental Illness on the rise

SS: Your research also shows that there is a real increase in people who have a severe mental disorder. Now, this seems counterintuitive, but is it true that you believe much of this increase is caused by the overuse of some of the new generations of psychiatric drugs?
RW: Yes, exactly. I looked at the number of the so-called severely disabled mentally ill -- people who aren't working or who are somehow dysfunctional because of mental illness. So I wanted to chart through history the percentage of the population who are considered the disabled mentally ill.

Now, by 1903, we see that roughly 1 out of every 500 people in the United States is hospitalized for mental illness. By 1955, at the start of the modern era of psychiatric drugs, roughly one out of every 300 people was disabled by mental illness. Now, let's go to 1987, the end of the first generation of antipsychotic drugs; and from 1987 forward we get the modern psychiatric drugs. From 1955 to 1987, during this first era of psychiatric drugs -- the antipsychotic drugs Thorazine and Haldol and the tricyclic antidepressants (such as Elavil and Anafranil) -- we saw the number of disabled mentally ill increase four-fold, to the point where roughly one out of every 75 persons are deemed disabled mentally ill.

Now, there was a shift in how we cared for the disabled mentally ill between 1955 and 1987. In 1955, we were hospitalizing them. Then, by 1987, we had gone through social change, and we were now placing people in shelters, nursing homes, and some sort of community care, and gave them either SSI or SSDI payments for mental disability. In 1987, we started getting these supposedly better, second-generation psychiatric drugs like Prozac and the other selective serotonin re-uptake inhibitor (SSRI) antidepressants. Shortly after that, we get the new, atypical antipsychotic drugs like Zyprexa (olanzapine), Clozaril and Risperdal.

What's happened since 1987? Well, the disability rate has continued to increase until it's now one in every 50 Americans. Think about that: One in every 50 Americans disabled by mental illness today. And it's still increasing. The number of mentally disabled people in the United States has been increasing at the rate of 150,000 people per year since 1987. That's an increase every day over the last 17 years of 410 people per day newly disabled by mental illness.

SS: So that leads to the obvious question. If psychiatry has introduced these so-called wonder drugs like Prozac and Zoloft and Zyprexa, why is the incidence of mental illness going up dramatically?
RW: That's exactly it. This is a scientific question. We have a form of care where we're using these drugs in an ever more expansive manner, and supposedly we have better drugs and they're the cornerstone of our care, so we should see decreasing disability rates. That's what your expectation would be.

Instead, from 1987 until the present, we saw an increase in the number of mentally disabled people from 3.3 million people to 5.7 million people in the United States. In that time, our spending on psychiatric drugs increased to an amazing degree. Combined spending on antipsychotic drugs and antidepressants jumped from around $500 million in 1986 to nearly $20 billion in 2004. So we raise the question: Is the use of these drugs somehow actually fueling this increase in the number of the disabled mentally ill?

When you look at the research literature, you find a clear pattern of outcomes with all these drugs -- you see it with the antipsychotics, the antidepressants, the anti-anxiety drugs and the stimulants like Ritalin used to treat ADHD. All these drugs may curb a target symptom slightly more effectively than a placebo does for a short period of time, say six weeks. An antidepressant may ameliorate the symptoms of depression better than a placebo over the short term.

What you find with every class of these psychiatric drugs is a worsening of the target symptom of depression or psychosis or anxiety over the long term, compared to placebo-treated patients. So even on the target symptoms, there's greater chronicity and greater severity of symptoms. And you see a fairly significant percentage of patients where new and more severe psychiatric symptoms are triggered by the drug itself.

SS: New psychiatric symptoms created by the very drugs people are told will help them recover?
RW: Absolutely. The most obvious case is with the antidepressants. A certain percentage of people placed on the SSRIs because they have some form of depression will suffer either a manic or psychotic attack -- drug-induced. This is well recognized. So now, instead of just dealing with depression, they're dealing with mania or psychotic symptoms. And once they have a drug-induced manic episode, what happens? They go to an emergency room, and at that point they're newly diagnosed. They're now said to be bipolar and they're given an antipsychotic to go along with the antidepressant; and, at that point, they're moving down the path to chronic disability.

SS: Modern psychiatry claims that these psychiatric drugs correct pathological brain chemistry. Is there any evidence to back up their claim that abnormal brain chemistry is the culprit in schizophrenia and depression?
RW: This is the key thing everyone needs to understand. It really is the answer that unlocks this mystery of why the drugs would have this long-term problematic effect. Start with schizophrenia. They hypothesize that these drugs work by correcting an imbalance of the neurotransmitter dopamine in the brain.

The theory was that people with schizophrenia had overactive dopamine systems; and these drugs, by blocking dopamine in the brain, fixed that chemical imbalance. Therefore, you get the metaphor that they're like insulin is for diabetes; they're fixing an abnormality. With the antidepressants, the theory was that people with depression had too low levels of serotonin; the drugs upped the levels of serotonin in the brain and therefore they're balancing the brain chemistry.

First of all, those theories never arose from investigations into what was actually happening to people. Rather, they would find out that antipsychotics blocked dopamine and so they theorized that people had overactive dopamine systems. Same with the antidepressants. They found that antidepressants upped the levels of serotonin; therefore, they theorized that people with depression must have low levels of serotonin.

But here is the thing that one wishes all of America would know and wishes psychiatry would come clean on: They've never been able to find that people with schizophrenia have overactive dopamine systems. They've never been able to find that people with depression have underactive serotonin systems. They've never found consistently that any of these disorders are associated with any chemical imbalance in the brain. The story that people with mental disorders have known chemical imbalances -- that's a lie. We don't know that at all. It's just something that they say to help sell the drugs and help sell the biological model of mental disorders.

But the kicker is this. We do know, in fact, that these drugs perturb how these chemical messengers work in the brain. The real paradigm is: People diagnosed with mental disorders have no known problem with their neurotransmitter systems; and these drugs perturb the normal function of neurotransmitters.

SS: So rather than fixing a chemical imbalance, these widely prescribed drugs distort the brain chemistry and make it pathological.
RW: Absolutely. Stephen Hyman, a well-known neuroscientist and the former director of the National Institute of Mental Health, wrote a paper in 1996 that looked at how psychiatric drugs affect the brain. He wrote that all these drugs create perturbations in neurotransmitter functions. And he notes that the brain, in response to this drug from the outside, alters its normal functions and goes through a series of compensatory adaptations.

In other words, it tries to adapt to the fact that an antipsychotic drug is blocking normal dopamine functions. Or in the case of antidepressants, it tries to compensate for the fact that you're blocking a normal reuptake of serotonin. The way it does this is to adapt in the opposite way. So, if you're blocking dopamine in the brain, the brain tries to put out more dopamine and it actually increases the number of dopamine receptors. So a person placed on antipsychotic drugs will end up with an abnormally high number of dopamine receptors in the brain.

If you give someone an antidepressant, and that tries to keep serotonin levels too high in the brain, it does exactly the opposite. It stops producing as much serotonin as it normally does and it reduces the number of serotonin receptors in the brain. So someone who is on an antidepressant, after a time ends up with an abnormally low level of serotonin receptors in the brain. And here's what Hyman concluded about this: After these changes happened, the patient's brain is functioning in a way that is "qualitatively as well as quantitatively different from the normal state." So what Stephen Hyman, former head of the NIMH, has done is present a paradigm for how these drugs affect the brain that shows that they're inducing a pathological state.

SS: So the paradox is there's no evidence for modern psychiatry's claim that there is any pathological biochemical imbalance in the brain that causes mental illness, but if you treat people with these new wonder drugs, that is what creates a pathological imbalance?
RW: Yes, these drugs disrupt normal brain chemistry. That's the real paradox here. And the real tragedy is, that even as we peddle these drugs as chemical balancers, chemical fixers, in truth we're doing precisely the opposite. We're taking a brain that has no known abnormal brain chemistry, and by placing people on the drugs, we're perturbing that normal chemistry. Here's how Barry Jacobs, a Princeton neuroscientist, describes what happens to a person given an SSRI antidepressant. "These drugs," he said, "alter the level of synaptic transmission beyond the physiologic range achieved under normal environmental biological conditions. Thus, any behavioral or physiologic change produced under these conditions might more appropriately be considered pathologic rather than reflective of the normal biological role of serotonin."

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