Anatomy of an Epidemic (31 page)

Young or old woman? If you shift your eyes slightly, your perception of the image will change from one to the other. Courtesy of Exploratorium.

The old-hag picture of the psychopharmacology era arises from a more careful reading of history and a more thorough review of the science. When we reviewed the history of deinstitutionalization, we found that the discharge of chronic schizophrenia patients resulted from the enactment of Medicare and Medicaid legislation in the mid-1960s, as opposed to from Thorazine’s arrival in asylum medicine. As for the drugs, we discovered that there was no scientific breakthrough that led to the introduction of Thorazine and other first-generation psychiatric medications. Instead, scientists studying compounds for use as anesthetics and as magic bullets for infectious
diseases stumbled upon several agents that had novel
side effects
. Then, over the course of the next thirty years, researchers determined that the drugs work by perturbing the normal functioning of neuronal pathways in the brain. In response, the brain undergoes “compensatory adaptations” to cope with the drug’s mucking up of its messaging system, and this leaves the brain functioning in an “abnormal” manner. Rather than fix chemical imbalances in the brain, the drugs
create
them. We then combed through the outcomes literature, and we found that these pills
worsen
long-term outcomes, at least in the aggregate. Researchers even put together biological explanations for why the drugs had this paradoxical long-term effect.

Those are the dueling visions of the psychopharmacology era. If you think of the drugs as “anti-disease” agents and focus on short-term outcomes, the young lady springs into sight. If you think of the drugs as “chemical imbalancers” and focus on long-term outcomes, the old hag appears. You can see either image, depending on where you direct your gaze.

Just for a moment, before we examine whether we have solved the puzzle that we set forth in the opening of this book, here is a quick way to see the old-hag picture a bit more clearly. Imagine that a virus suddenly appears in our society that makes people sleep twelve, fourteen hours a day. Those infected with it move about somewhat slowly and seem emotionally disengaged. Many gain huge amounts of weight—twenty, forty, sixty, and even one hundred pounds. Often, their blood sugar levels soar, and so do their cholesterol levels. A number of those struck by the mysterious illness—including young children and teenagers—become diabetic in fairly short order. Reports of patients occasionally dying from pancreatitis appear in the medical literature. Newspapers and magazines fill their pages with accounts of this new scourge, which is dubbed metabolic dysfunction illness, and parents are in a panic
over the thought that their children might contract this horrible disease. The federal government gives hundreds of millions of dollars to scientists at the best universities to decipher the inner workings of this virus, and they report that the reason it causes such global dysfunction is that it blocks a multitude of neurotransmitter receptors in the brain—dopaminergic, serotoninergic, muscarinic, adrenergic, and histaminergic. All of those neuronal pathways in the brain are compromised. Meanwhile, MRI studies find that over a period of several years, the virus shrinks the cerebral cortex, and this shrinkage is tied to cognitive decline. A terrified public clamors for a cure.

Now such an illness has in fact hit millions of American children and adults. We have just described the effects of Eli Lilly’s best-selling antipsychotic, Zyprexa.

We began this book by raising a question: Why have we seen such a sharp increase in the number of disabled mentally ill in the United States since the “discovery” of psychotropic medications? At the very least, I think we have identified one major cause. In large part, this epidemic is iatrogenic in kind.

Now there may be a number of social factors contributing to the epidemic. Our society may be organized in a way today that leads to a great degree of stress and emotional turmoil. For instance, we may lack the close-knit neighborhoods that help people stay well. Relationships are the foundation of human happiness, or so it seems, and as Robert Putnam wrote in 2000, we spend too much time “bowling alone.” We also may watch too much television and get too little exercise, a combination that is known to be a prescription for becoming depressed. The food we eat—more processed foods and so on—might be playing a role too. And the common use of illicit drugs—marijuana, cocaine, and hallucinogens—has clearly contributed to the epidemic. Finally, once a person goes on SSI or SSDI, there is a tremendous financial disincentive to return to work.
People on disability call it the “entitlement trap.” Unless they can get a job that pays health insurance, they will lose that safety net if they go back to work, and once they start working, they may lose their rent subsidy, too.

However, in this book, we have been focusing on the role that psychiatry and its medications may be playing in this epidemic, and the evidence is quite clear. First, by greatly expanding diagnostic boundaries, psychiatry is inviting an ever-greater number of children and adults into the mental illness camp. Second, those so diagnosed are then treated with psychiatric medications that increase the likelihood they will become chronically ill. Many treated with psychotropics end up with new and more severe psychiatric symptoms, physically unwell, and cognitively impaired. That is the tragic story writ large in five decades of scientific literature.

The record of disability produced by psychiatric medications can be easily summarized. With schizophrenia, in the decade prior to the introduction of Thorazine, roughly 70 percent of people suffering a first episode of psychosis were discharged from the hospital within eighteen months, and the majority didn’t return to the hospital during fairly lengthy follow-up periods. Researchers in the post-Thorazine era reported similar results for unmedicated patients. Rappaport, Carpenter, and Mosher all found that perhaps half of those diagnosed with schizophrenia would do fairly well if they were not continuously medicated. But that is now the standard of care, and as Harrow’s study showed, only 5 percent of medicated patients recover over the long term. Today, there are an estimated 2 million adults disabled by schizophrenia in the United States, and this disability number could perhaps be halved if we adopted a paradigm of care that employed antipsychotic medications in a selective, cautious manner.

With the affective disorders, the iatrogenic effects of our drug-based paradigm of care are even more apparent. Anxiety used to be viewed as a mild disorder, one that rarely required hospitalization. Today, 8 percent of the younger adults on the SSI and SSDI roles due to a psychiatric disability have anxiety as a primary diagnosis. Similarly, outcomes for major depression used to be good. In 1955, there were only thirty-eight thousand people hospitalized with depression,
and the illness could be expected to remit. Today, major depression is the leading cause of disability in the United States for people fifteen to forty-four years old. It is said to strike 15 million adults, and according to researchers at Johns Hopkins School of Public Health, 60 percent are “severely impaired.” As for bipolar disorder, an extremely rare illness has become a common one. According to the NIMH, nearly 6 million adults suffer from it today. Whereas 85 percent of those struck by it used to recover and go back to work, now only about a third of bipolar patients function this well, and over the long term those bipolar patients who reliably take their medications end up nearly as impaired as those with schizophrenia who stay on neuroleptics. The Johns Hopkins investigators concluded that 83 percent are “severely impaired.”

In sum, there were fifty-six thousand people hospitalized with anxiety and manic-depressive illness in 1955. Today, according to the NIMH, at least 40 million adults suffer from one of these affective disorders. More than 1.5 million people are on SSI or SSDI because they are disabled by anxiety, depression, or bipolar illness, and, according to the Johns Hopkins data, more than 14 million people who have these diagnoses are “severely impaired” in their ability to function in society. That is the astonishing bottom-line result produced by a medical specialty that has dramatically expanded diagnostic boundaries in the past fifty years and treated its patients with drugs that perturb normal brain function.

Moreover, the epidemic continues its march. In the eighteen months it took me to research and write this book, the Social Security Administration released its 2007 reports for its SSI and SSDI programs, and the numbers were as expected. There were 401,255 children and adults under sixty-five years old added to the SSI and SSDI rolls in 2007 because of a psychiatric disability. Imagine a large auditorium filling up
every day
with 250 children and 850 adults newly disabled by mental illness, and you get a visual sense of the horrible toll exacted by this epidemic.

Fleshing out the nature of a disease usually involves identifying all the symptoms that may develop, and then following their course over time. In the previous chapters, we mostly focused on studies that showed that psychiatric medications worsen target symptoms over the long run, and only briefly noted that the drugs may cause physical problems, emotional numbing, and cognitive impairment. This is also a form of care that leads to early death. The seriously mentally ill are now dying fifteen to twenty-five years earlier than normal, with this problem of early death having become much more pronounced in the past fifteen years.
²
They are dying from cardiovascular ailments, respiratory problems, metabolic illnesses, diabetes, kidney failure, and so forth—the physical ailments tend to pile up as people stay on antipsychotics (or drug cocktails) for years on end.
³

Here are three stories that bear witness to these various long-term risks.

Amy Upham lives in a small one-bedroom apartment in Buffalo, and as I enter the living room, she points to a table cluttered with papers. “This is me on psychiatric drugs,” she says and hands me a stack of medical documents. They tell of a drug-induced swelling of the brain, faltering kidneys, a swollen liver, a swollen gallbladder, thyroid problems, gastritis, and cognitive abnormalities. A little over five feet tall, with frizzy reddish brown hair, Amy, who is thirty years old, weighs ninety pounds. She squeezes a fold of loose skin near her elbow, the muscle underneath having wasted away. “This is like what you see with heroin users.”

Amy first took a psychiatric medication at age sixteen when she contracted Lyme disease and suffered a bout of depression. Twelve years later, she was still on antidepressants, and as she reviews that history, she identifies several instances when the drugs stirred
hypomanic episodes and worsened her obsessive-compulsive behaviors. Finally, in 2007, she decided to gradually wean herself from the two-drug combo she was taking, and at first, it went well. However, at the time, she was working for the county mental health department as an advocate for the mentally ill, and eventually someone anonymously informed her bosses that she was going off her medication. This went against what the agency preached, and it all ended with Amy out of a job and paranoid that someone was stalking her. “I had a nervous breakdown,” she says. “I went into the hospital to hide.”

This was the first time Amy had ever been hospitalized, and she was immediately put on a cocktail that included lithium. Within a few months, her endocrine system began to fail. Her menstrual cycle ceased, her thyroid went haywire, and an EEG revealed that her brain was swollen. Then her kidneys started shutting down. She had to abruptly stop taking the lithium, and that triggered a manic episode. Doctors put her on Ativan to counter the mania, but that drug stirred feelings of horrible rage and left her feeling suicidal. Months passed, and in December 2008, she checked herself into a psych hospital, where she was diagnosed with Ativan toxicity. “I’ve never seen a drug fuck up a person like Ativan fucks you up,” a nurse told her. The hospital switched her from Ativan to Klonopin and prescribed Abilify, which triggered a seizure. Next a doctor discovered something wrong with her heart, which appeared to be related to the Klonopin, and so Amy was put back on Ativan. “Now I start hallucinating for the first time in my life,” she says. “I was pacing uncontrollably and crawling out of my skin.” Other drug-related complications ensued, and on February 24, 2009, Amy moved into a shelter on the hospital grounds, her thoughts now so scattered that a nurse wondered “if early Alzheimer’s runs in the family.”

Remarkably, much of that story is documented in the sheaf of papers that Amy has given me. She spent the last four months trying to get off the Ativan, but every time she dropped to a lower dose, she suffered fits of rage and something akin to delirium. “I am feeling scared,” she says, as I hand the papers back to her. “The withdrawals are really bad and I live alone. I’m in a constant state of panic, anxiety, and I have some agoraphobia. It’s not safe.”