7

The Benzo Trap

“What seemed so good about the benzodiazepines

when I was playing with them was that it seemed like

we really did have a drug that didn’t have many

problems. But in retrospect it’s difficult to put a

spanner into a wristwatch and expect that it won’t

do any harm.”

—ALEC JENNER, BRITISH PHYSICIAN WHO

CONDUCTED FIRST TRIALS OF A BENZODIAZEPINE IN

THE UK (2003)1

Fans of the cable television series Mad Men, which tells of the lives of Don Draper and other Madison Avenue advertising men in the early 1960s, may recall a scene from the last episode of season two, when a friend of Draper’s wife, Betty, says to her: “Do you want a Miltown? It’s the only thing keeping me from chewing my nails off.” That was a nice, historically accurate touch, and if the creators of Mad Men retain this period accuracy in season three and beyond, which will tell the story of the ad men and their families during the turbulent years of the mid-1960s, viewers can expect Betty Draper and her friends to reach into their purses and make sly references to “mother’s little helper.” Hoffmann-La Roche brought Valium to market in 1963, advertising it in particular to women, and from 1968 to 1981, it was the bestselling drug in the Western world. Yet, as Americans gobbled up this pill designed to keep them tranquil, something very odd happened: The number of people admitted to mental hospitals, psychiatric emergency rooms, and mental health outpatient clinics soared.

The scientific literature can explain why the two were linked.

Anxiety Before Miltown

Although anxiety is a regular part of the human psyche, our minds fashioned by evolution to worry and fret, there are some people who are more anxious than others, and the notion that such emotional distress is a diagnosable condition can be traced back to a New York nerve doctor, George Beard. In 1869, he announced that dread, worry, fatigue, and insomnia resulted from “tired nerves,” a physical illness he dubbed “neurasthenia.” The diagnosis proved to be a popular one, this illness thought to be a by-product of the industrial revolution that was sweeping America in the wake of the Civil War, and naturally the market created a variety of therapies that could restore a person’s “tired” nerves. Makers of patent medicines sold “nerve revitalizers” laced with opiates, cocaine, and alcohol. Neurologists touted the restorative powers of electricity, and this led those diagnosed with neurasthenia to buy electric belts, suspenders, and handheld massagers. Those who were wealthier could head to spas that offered “rest cures,” the patients’ nerves restored through the healing touch of soothing baths, massages, and various electric gadgets.

Sigmund Freud provided psychiatry with a rationale for treating this group of patients and, in so doing, enabled psychiatry to move out of the asylum and into the office. Born in 1856, Freud set out his shingle as a nerve doctor in Vienna in 1886, which meant that many of his patients were women suffering from neurasthenia (Beard’s disease had become popular in Europe, too). After hours of conversation with his clients, Freud became convinced that their feelings of dread and worry were psychological in origin, rather than the result of tired nerves. In 1895, he wrote about “anxiety neurosis” in women, which he theorized arose in large part from their unconscious repression of sexual desires and fantasies. Those suffering from such psychological conflicts could find relief through psychoanalysis, the patient on the couch led by the doctor into an exploration of her unconscious mind.

At this time, psychiatry was a profession for those who treated mad patients in the asylum. People with tired nerves went to see a nerve doctor or a general practitioner for help. But if anxiety arose from a psychological disorder in the brain, rather than from a frazzling of the nerves, then it made sense that psychiatrists could tend to these patients, and after Freud visited America in 1909, psychoanalytic societies began to form, with New York City the hub of this new therapy. Nationwide, only 3 percent of psychiatrists were in private practice in 1909; thirty years later, 38 percent were seeing patients in private settings.2 Moreover, Freudian theory made nearly everyone a candidate for the psychiatrist’s couch. “Neurotics,” Freud explained during his 1909 tour, “fall ill of the same complexes with which we sound people struggle.”3

Thanks to Freudian theories, psychiatric disorders were now divided into two basic categories: psychotic and neurotic. In 1952, the American Psychiatric Association published the first edition of its Diagnostic and Statistical Manual, and it described the neurotic patient in this way:

The chief characteristic of [neurotic] disorders is “anxiety,” which may be directly felt and expressed or which may be unconsciously and automatically controlled by the utilization of various psychological defense mechanisms…. In contrast to those with psychoses, patients with psychoneurotic disorder do not exhibit gross distortion or falsification of external reality (delusions, hallucinations, illusions) and they do not present gross disorganization of the personality.4

Such was the understanding of anxiety when Miltown came to market. Anxious people had their feet firmly planted in reality, and rarely was anxiety a condition that required hospitalization. In 1955, there were only 5,415 “psychoneurotic” patients in state mental hospitals.5 As Stanford psychiatrist Leo Hollister confessed after the benzodiazepines were introduced, these drugs were “designed to treat what many would regard as a ‘minor disorder.’”6 The drugs were a balm for the “walking wounded,” and thus, as we review the outcomes literature for the benzodiazepines, we should expect this patient group to function well. After all, that was the future promised by Miltown inventor Frank Berger: “Tranquilizers, by attenuating the disruptive influence of anxiety on the mind, open the way to a better and more coordinated use of the existing gifts,” he said.7

The Minor Tranquilizers Fall from Grace

When Miltown first appeared, there were a number of studies published in medical journals that told—as two Harvard Medical School researchers, David Greenblatt and Richard Shader, later re-called—of how it “was almost magically effective in reducing anxiety.” But as has often been the case in psychiatry, once a successor pill appeared on the market (Librium, in 1960), the efficacy of the old drug suddenly began to fade. In their review of the Miltown literature in 1974, Greenblatt and Shader found that in twenty-six well-controlled trials, there were only five in which Miltown “was more effective than placebo” as a treatment for anxiety. Nor was there any evidence that Miltown was better than a barbiturate in calming the nerves. The initial popularity of this drug, they wrote, “illustrates how factors other than scientific evidence may determine physicians’ patterns of drug use.”8

However, Miltown’s fall from favor with the public arose from a different problem than lack of scientific efficacy. Many who tried the drug found that they became sick when they stopped taking it, and in 1964, Carl Essig, a scientist at the Addiction Research Center in Lexington, Kentucky, reported that it “could induce physical dependence in man.”9 Science News quickly announced that the happy pill could be “addictive,” and on April 30, 1965, Time all but buried Miltown. There is “a growing disillusionment with Miltown on the part of many doctors,” the magazine wrote. “Some doubt that it has any more tranquilizing effect than a dummy sugar pill…. A few physicians have reported that in some patients, Miltown may cause a true addiction, followed by withdrawal symptoms like those of narcotics users ‘kicking the habit.’”10

Publicly, the benzodiazepines mostly escaped this opprobrium during the 1960s. When Hoffmann-La Roche brought Librium to market in 1960, it claimed that its drug provided “pure anxiety relief,” and unlike Miltown and the barbiturates, was “safe, harmless and non-addicting.” That belief took hold and the FDA did little to counter it, even though very early on it started receiving letters from people who were experiencing odd and quite distressing symptoms when they tried to quit a benzodiazepine. They told of awful insomnia, anxiety more severe than they had known before, and a rash of physical symptoms—tremors, headaches, and nerves that “jangled like crazy.” As one man wrote the FDA, “I was not sleeping and in general felt horrible. Sometimes I thought I would die and other times wished I had.”11 Although the FDA held a hearing on the matter, it did not impose any legal control on benzodiazepines similar to what had been placed on amphetamines and barbiturates, and so the public’s belief that the drugs were relatively nonaddictive and harmless survived until 1975, when the U.S. Justice Department demanded that they be classified as schedule IV drugs under the Controlled Substances Act. This designation limited the number of refills a patient could obtain without a new prescription, and revealed to the public that the government had concluded that benzodiazepines were, in fact, addictive.

“Danger ahead! Valium—The Pill You Love Can Turn on You,” a Vogue headline screamed. A benzodiazepine, the magazine explained, could lead to a “far worse addiction than heroin.”12 The Valium backlash had begun, particularly in the pages of women’s magazines, and soon Ms. magazine provided readers with firstperson accounts of the horrors of withdrawing from it. “My withdrawal symptoms are a double-dose of the anxiety, irritableness, and insomnia I used to feel,” one user said. Confessed another: “I can’t begin to describe the physical and mental anguish that accompanied my withdrawal.”13 The happiness pill of the 1950s was turning into the misery pill of the 1970s, with the New York Times reporting in 1976 that “some critics go so far to say that [Valium] is doing more harm than good, or even deny that it is doing any good at all for the great majority of patients. Some cry with alarm that it is far from being as safe as it is proclaimed, that it can be hideously and dangerously addictive, and may be the direct cause of addicts’ deaths.”14 Two million Americans were said to be addicted to benzodiazepines, four times the number of heroin addicts in the country, and one of the pill takers turned out to be former first lady Betty Ford, who checked herself into an alcohol and drug rehab center in 1978. Abuse of tranquilizers, said her physician Joseph Pursch, was “the nation’s number one health problem.”15

Over the next few years, the benzodiazepines officially fell from grace. In 1979, Senator Edward Kennedy held a Senate Health Subcommittee hearing on the dangers of benzodiazepines, which he said had “produced a nightmare of dependence and addiction, both very difficult to treat and recover from.”16 After reviewing the scientific literature, the White House Office of Drug Policy and the National Institute of Drug Abuse concluded that the drugs’ sleep-promoting effects didn’t last more than two weeks, and this finding was soon seconded by the Committee on the Review of Medicines in the United Kingdom, which found that the drugs’ anti-anxiety effects didn’t last beyond four months. As such, the committee recommended that “patients receiving benzodiazepine therapy be carefully selected and monitored and that prescriptions be limited to short-term use.”17 As an editorial in the British Medical Journal put it: “Now that benzodiazepines have been shown to cause drug dependence should their use be more closely controlled—or even banned?”18

The ABCs of Benzodiazepines

This story of the benzodiazepines’ fall from grace might seem like ancient history, a footnote in our quest to understand why there has been such a rise in the number of disabled mentally ill in the United States over the past fifty years, except for the fact that the benzodiazepines never really went away. Although the number of prescriptions for benzodiazepines dropped after they were classified as schedule IV drugs, from 103 million in 1975 to 71 million in 1980, the following year Upjohn brought Xanax to market, and this helped stabilize sales of benzodiazepines.19Psychiatrists continued to prescribe benzodiazepines to many of their nervous patients, and in 2002, Stephen Stahl, a well-known psychopharmacologist at the University of California in San Diego, confessed to psychiatry’s dirty little secret in an article titled “Don’t Ask, Don’t Tell, But Benzodiazepines Are Still the Leading Treatments for Anxiety Disorders.”20 Since that time, the prescribing of benzodiazepines in the United States has increased, from 69 million prescriptions in 2002 to 83 million in 2007, which isn’t all that far below the number written at the height of the Valium craze in 1973.21

So, given that benzodiazepines have been widely used for fifty years, we need to look at what science has to tell about these drugs, and whether their use may be contributing in some way to the increase in the number of disabled mentally ill in the United States.

Short-term efficacy

As anyone who has taken a benzodiazepine can attest, it acts rapidly, and if a person hasn’t become habituated to the drug, it will numb his or her emotional distress. As such, a benzodiazepine has an obvious utility in helping people through a situational crisis. The writer Andrea Tone, in her book The Age of Anxiety, relates how a benzodiazepine enabled her to get on an airplane after she somewhat mysteriously developed a fear of flying. But as clinical trials revealed, that immediate efficacy quickly begins to fade and pretty much disappears by the end of four to six weeks.

In 1978, Kenneth Solomon at Albany Medical College in New York reviewed seventy-eight double-blind trials of benzodiazepines and determined that the drugs had proved to be significantly better than a placebo in only forty-four of them. At best, the collective results could be said to “hint at therapeutic efficacy,” he wrote.22 Five years later, Arthur Shapiro at Mt. Sinai School of Medicine in New York City fleshed out this efficacy picture a bit more, reporting that in a trial of 224 anxious patients, Valium proved superior to a placebo for the first week, but then this advantage began to lessen. Based on the patients’ self-assessment of their symptoms, by the end of the second week there was no difference between the drug and a placebo, and by the end of six weeks, the placebo group was faring slightly better. “It is unlikely in our opinion that carefully controlled studies would consistently show significant benzodiazepine therapeutic antianxiety effects,” Shapiro wrote.23

That picture of the short-term efficacy of benzodiazepines has not markedly changed since then. The drugs show clear efficacy for the first week, and then their advantage over a placebo abates. But, as British investigators noted in 1991, this brief period of efficacy comes at a fairly high cost. “Both psychomotor and cognitive functioning may be impaired, and amnesia is a common effect of all benzodiazepines,” they said.24 In 2007, researchers in Spain looked at whether these adverse events negated the small “efficacy benefit” provided by the drugs, and found that the drop-out rates in clinical trials, a measure often used to assess the overall “effectiveness” of a drug, were the same for benzodiazepine and placebo patients. “This systematic review did not find convincing evidence of the short-term effectiveness of the benzodiazepines in the treatment of generalized anxiety disorder,” they reported.25

Malcolm Lader, a psychiatrist at the Institute of Psychiatry in London who is one of the world’s leading experts on benzodiazepines, explained the importance of this finding in an interview: “Effectiveness is a measure of what it’s like in real practice.”26

Withdrawal syndromes

Although the first report of benzodiazepine dependence appeared in the scientific literature in 1961, when Leo Hollister at Stanford University reported that patients withdrawing from Librium were experiencing odd symptoms, it wasn’t until the Justice Department classified benzodiazepines as schedule IV drugs that researchers began investigating the problem with any vigor. In 1976, physicians Barry Maletzky and James Kotter jump-started this inquiry, reporting that when their patients stopped taking Valium, many complained of “extreme anxiety.”27 Two years later, physicians at Pennsylvania State University announced that patients withdrawing from benzodiazepines often experienced “an increase in anxiety above baseline levels … a condition that we term ‘rebound anxiety.’”28 In Britain, Lader reported similar findings. “Anxiety rose sharply during withdrawal, and to a point of panic in several patients. Patients commonly experienced bodily symptoms of anxiety, such as a choking feeling, dry mouth, hot and cold, legs like jelly, etc.”29

Rebound Anxiety with Valium

In this 1985 study by British investigators, the patients treated with Valium did not fare better than the placebo patients during the first six weeks. The Valium patients were then withdrawn from the drug and their anxiety symptoms soared, to a much higher level than the symptoms in placebo patients. Source: Power, K. “Controlled study of withdrawal symptoms and rebound anxiety after six week course of diazepam for generalised anxiety.” British Medical Journal 290 (1985): 1246–48.

Patients withdrawing from benzodiazepines, it seemed, were becoming more anxious than they had ever been. Over the course of the next decade, Lader and other British physicians (most notably Heather Ashton, a doctor at the University of Newcastle upon Tyne who ran a withdrawal clinic) continued to investigate this problem, and they compiled a long list of symptoms that could bedevil those quitting a benzodiazepine. In addition to rebound anxiety, patients could experience insomnia, seizures, tremors, headaches, blurred vision, a ringing in the ears, extreme sensitivity to noise, a feeling that insects were crawling over them, nightmares, hallucinations, extreme depression, depersonalization, and derealization (a sense that the external world is unreal). Withdrawal, one patient told Heather Ashton, was like “living death … I thought I had gone mad.”

“These findings show very clearly that benzodiazepine withdrawal is a severe illness,” Ashton wrote. “The patients were usually frightened, often in intense pain, and genuinely prostrated…. Through no fault of their own, the patients suffered considerable physical as well as mental distress.”30

Not all people withdrawn from benzodiazepines suffer in this way. The risk of suffering withdrawal symptoms varies according to how long a person has been on the drug, the potency of the benzodiazepine, and the speed of the drug-tapering process. A majority of patients who’ve taken a benzodiazepine for a relatively short time, such as a month or two, may be able to withdraw from it with little difficulty. However, some people experience withdrawal symptoms after taking a benzodiazepine for only a few weeks, and it can take a longtime user a year or longer to taper from the drug. More over, a small percentage of people suffer a “protracted withdrawal syndrome,” their anxiety remaining at elevated levels “for many months after benzodiazepine withdrawal,” Ashton observed.31 Depression may deepen, and the odd perceptual symptoms—the depersonalization, the derealization, the sensation of insects crawling on the skin—can haunt a person for an extended period. Most alarming, a small percentage of long-term users never fully recover. “It is very worrying,” Lader said, in an interview. “Somehow there has been a change [in the brain]. I cannot say that everybody is going to recover back to normality when they come off long-term usage.”

The biology of benzodiazepine withdrawal

In 1977, researchers discovered that benzodiazepines affect a neurotransmitter in the brain known as GABA. Unlike dopamine and serotonin, which transmit an “excitatory” message telling a neuron to fire, GABA (gamma-aminobutyric acid) inhibits neuronal activity. A neuron receiving the GABA message either fires at a slower rate or stops firing for a period of time. A majority of neurons in the brain have GABA receptors, which means that this neurotransmitter acts as the brain’s brake on neuronal activity. A benzodiazepine binds to the GABA receptor and, in so doing, amplifies GABA’s inhibitory effects. It pushes down on the GABA brake, so to speak, and as a result, it suppresses central nervous system activity.

In response, the brain decreases its output of GABA and decreases the density of its GABA receptors. It is trying to “restore normal GABA transmission,” British scientists explained in 1982.32 However, as a result of these adaptive changes, the brain’s braking system is now in a physiologically impaired state. Its braking fluid is low (GABA output), and its brake pads are worn (GABA receptors). As a result, when the benzodiazepine is withdrawn, the brain is no longer able to properly inhibit neuronal activity, and its neurons may begin firing at a helter-skelter pace. This overactivity, Heather Ashton concluded, may “account for many of the effects of withdrawal.”33 The anxiety, the insomnia, the sensation of insects crawling across the skin, the paranoia, the derealization, the seizures—all of these vexing symptoms may arise from neuronal hyperactivity.

If a person gradually tapers off from a benzodiazepine, the GABA system may slowly revert to normal, and thus withdrawal symptoms may be mild. However, the fact that some long-term users suffer “protracted symptoms” is probably “due to the failure of the [GABA] receptors to revert to their normal state,” Ashton said.34 Long-term benzodiazepine use, she explained, may “give rise not only to slowly reversible functional changes in the central nervous system, but may also occasionally cause structural neuronal damage.”35 In such cases, the GABA brake never again functions like it should.

Long-term effects

Once researchers in the United States and the United Kingdom determined that benzodiazepines did not provide any durable relief from anxiety, an obvious question arose: Do these drugs, when taken on a continual basis, worsen the very symptom they are supposed to treat? In 1991, Karl Rickels at the University of Pennsylvania School of Medicine reported on a group of anxious patients who had tried to quit benzodiazepines three years earlier, and he found that those who had successfully gotten off the drugs were doing “significantly” better than those who had failed to do so.36 A few years later, he was back with a new study: When long-term users withdrew from benzodiazepines, they “became more alert, more relaxed, and less anxious, and this change was accompanied by improved psychomotor functions.”37 Those who stayed on the benzodiazepines were more emotionally distressed than those who got off.

Others told of similar long-term results. Canadian investigators found that benzodiazepine usage led to a fourfold increase in depressive symptoms.38 In England, Ashton observed that those who stay on the drugs tend to became more ill: “Many patients find that anxiety symptoms gradually increase over the years despite continuous benzodiazepine use, and panic attacks and agoraphobia may appear for the first time.”39 These studies and observations told of a very problematic long-term course, and in 2007, French researchers surveyed 4,425 long-term benzodiazepine users and found that 75 percent were “markedly ill to extremely ill … a great majority of the patients had significant symptomatology, in particular major depressive episodes and generalized anxiety disorder, often with marked severity and disability.”40

In addition to causing emotional distress, long-term benzodiazepine usage also leads to cognitive impairment. Early on, researchers recognized that memory problems were associated with short-term use, and this led David Knott, a physician at the University of Tennessee, to warn in 1976 that “I am very convinced that Valium, Librium and other drugs of that class cause damage to the brain. I have seen damage to the cerebral cortex that I believe is due to the use of these drugs, and I am beginning to wonder if the damage is permanent.”41 Over the next twenty-five years, reports of cognitive impairment in long-term benzodiazepine users regularly appeared in scientific journals. These studies told of people who were having trouble focusing, remembering things, learning new material, and solving problems. However, the patients “are not aware of their reduced ability,” Lader wrote, evidence that their self-insight was impaired as well.42 In 2004, a group of Australian scientists, after reviewing the relevant literature, concluded that “long-term benzodiazepine users were consistently more impaired than controls across all cognitive categories,” with these deficits “moderate to large” in magnitude. The studies showed the “higher the intake, dose and period of use [of a benzodiazepine], the greater the risk of impairment.”43

Increased anxiety, increased depression, and cognitive impairment—all of these factors contribute to a decline in a person’s ability to function in society. In 1983, the World Health Organization noted a “striking deterioration in personal care and social interactions” in long-term benzodiazepine users.44 Another investigator reported that they end up with poor coping skills.45 In a study funded by Hoffmann-La Roche, the manufacturer of Valium, University of Michigan investigators determined that taking this drug was “associated with poor quality of life, poor performance in work and personal life, low social support, perceived lack of internal control, poor perceived health and high levels of stress.”46 Ashton determined that long-term use led to “malaise, ill-health, and elevated scores for neuroticism.”47 Benzodiazepines, she said, contribute to “job loss, unemployment, and loss of work through illness.”48

Such is the history told about benzodiazepines in the scientific literature. Moreover, it is a story easily traced, as Dr. Stevan Gressitt, who today is the medical director for Adult Mental Health Services in Maine, can attest. In 2002, he helped form the Maine Benzo Study Group, which was comprised of physicians and other health-care professionals, and it concluded that “there is no evidence supporting the long-term use of benzodiazepines for any mental health condition.” Benzodiazepines, Gressitt and his colleagues wrote, may “aggra vate” both “medical and mental health problems.” In an interview, I asked Dr. Gressitt whether those “problems” included increased anxiety, cognitive impairment, and functional decline. Was his understanding of the scientific literature, I wondered, the same as mine?

“Your words I don’t contradict or argue with,” he replied.49

Geraldine, Hal, and Jill

The scientific literature reveals that benzodiazepines—much as the neuroleptics do—act like a trap. The drugs ameliorate anxiety for a short period of time, and thus they can provide a distressed person much needed relief. However, they work by perturbing a neurotransmitter system, and in response, the brain undergoes compensatory adaptations, and as a result of this change, the person becomes vulnerable to relapse upon drug withdrawal. That difficulty in turn may lead some to take the drugs indefinitely, and these patients are likely to become more anxious, more depressed, and cognitively impaired.

Here are the stories of three people who fell into the trap.

Geraldine Burns, a thin woman with dark red hair, still lives in the house she grew up in. She tells me her story while we sit in her kitchen, her elderly mother darting in and out.

Born in 1955, Geraldine was one of six children, and theirs was a happy family. Her father was Irish, her mother Lebanese, and their Boston neighborhood was known as “Little Lebanon,” a place where everybody definitely knew your name. Aunts, uncles, and other relatives lived nearby. At age eighteen, Geraldine started dating a boy who lived down the block, Joe Burns. “I’ve been with him ever since,” she says, and for a time their life unfolded just as Geraldine had hoped. She had a job that she enjoyed in human resources at a rehabilitation center, she and Joe had a healthy son (Garrett) in 1984, and they basked in their close-knit neighborhood. Geraldine—outgoing and energetic—was the constant hostess for gatherings of family and friends. “I loved my life,” she says. “I loved working, I loved my family, and I loved this neighborhood. I was the one who organized the reunion of my grammar school. I still had friends from kindergarten. I couldn’t have been more normal.”

However, in March 1988, Geraldine gave birth to a daughter, Liana, and she felt physically unwell afterward. “I kept telling the doctors and nurses that I felt like I weighed a thousand pounds,” she says, and after a doctor ruled out an infection, he figured she must be anxious and prescribed Ativan. Geraldine came home from the hospital with a prescription for that benzodiazepine, and although it helped for a short while, months later she still felt something wasn’t right and so she went to see a psychiatrist. “She immediately tells me I have a chemical imbalance,” Geraldine recalls. “She says that I should keep taking the Ativan and assures me that it is harmless and nonaddictive. She tells me that I will have to take this drug for the rest of my life. Later, when I questioned her about this, she explained it this way: ‘If you were a diabetic you would have to take insulin for the rest of your life, wouldn’t you?’”

Soon her psychiatrist added an antidepressant to the Ativan, and as Geraldine struggled to take care of her daughter that first year, her emotions seemed numbed, her mind fogged. “I was in a daze half the time. My mother would call and I would tell her something, and she would say, ‘You told me that last night.’ And I’d say, ‘I did?’” Worse, as the months wore on, she found herself becoming ever more anxious, so much so that she started staying inside her house. Going back to her job in human resources at the rehabilitation center was now out of the question. At one point, after she stopped taking Ativan for a day or two, she had a “massive panic attack.” The federal government agreed that she was disabled by “anxiety” and thus eligible for a monthly SSDI payment. “Me, who was the most social person on the planet, is not able to go out,” Geraldine says, shaking her head in disbelief. “I wouldn’t go out unless my husband would take me.”

Over the next eight years, Geraldine cycled through an endless combination of anti-anxiety and antidepressant medications. None worked. The anxiety and panic remained, and she suffered from a medley of side effects—rashes, sexual dysfunction, weight gain, tachycardia (from the panic attacks), and excessive menstrual bleeding, the last leading to a hysterectomy. “All of the women I’ve known who were on Ativan long-term ended up having a hysterectomy, every single one of us,” she says, with evident bitterness. At last, in October 1996, she went to a new physician, who, after reviewing her medical history, identified a likely culprit. “He told me, ‘You are on one of the most addictive drugs known,’ and I thought, ‘Thank God.’ I was in tears. It was the drugs all along. I had been made iatrogenically ill.”

Geraldine spent two nightmarish years withdrawing from Ativan and the other psychiatric drugs she had been taking. Horrible smells came from her body, her muscles twitched, she lost weight, and at one point, she couldn’t sleep for weeks. “It was like hell opened up and swallowed me in,” she says. Although she did kick the habit, it took several more years for her to feel better physically, and she still suffers from a great deal of anxiety. The gregarious, socially-at-ease person she had always been before that fateful day in March 1988 when she was prescribed Ativan has never returned. “Am I back to my old self? No,” she whispers. “I mourn who I used to be. We all mourn. I am still so afraid of so many things.”

Three days before I was to meet with Hal Flugman, who lives in South Florida, he called to say that his anxiety had flared up again, and the thought of leaving his house to talk to me was too stressful. “I am not feeling right,” he said. “I’m over-breathing, I have these terrible gastrointestinal problems. I think I have to get my Klonopin dose upped…. This is what is happening to me.”

Hal, whom I’d interviewed by phone a few months earlier, first became anxious when he was thirteen years old. Overweight and small, he didn’t get along well with his classmates in middle school. “I had panic attacks, and a slight fear of being around people,” he recalls. For the next five years, he went to counseling, but he was not prescribed a medication. “I was living with it, dealing with it,” he says, but then one night at a rock concert, the panic hit so hard that he had to call his family and beg that they come get him. The following day a doctor gave him a prescription for Klonopin.

“I remember saying to the doctor, ‘Am I going to become addicted and have a really hard time coming off?’ I was worried about the side effects, too. But the doctor said that the side effects would go away in a couple of weeks, and didn’t that beat living with these unbearable panic attacks? I said, ‘Well, of course.’ And I knew from the first pill that this was going to solve my anxiety problem. It absolutely worked for me. I felt great.”

Hal’s life since then is a story of addiction. Shortly after going on the drug, he moved to San Francisco to pursue a career as a musician, and for a time it went well—he even got to hang out with Carlos Santana, the great guitarist. But his music career failed to take off, and today he thinks that the Klonopin was partly to blame, for it stifled his ambition and didn’t help his finger dexterity, either. Eventually, he fell into a deep depression—“I felt like a zombie,” he says—and at age twenty-nine he returned to Florida to live with his parents. At that point, he was diagnosed with bipolar illness, the government agreeing that he was so disabled by mental illness that he was eligible to receive SSI. The years slid by, his mother passed away, and then, in 2001, he began taking higher doses of Klonopin, as otherwise his depression would become unbearable. His doctor told him he was abusing the drug and sent him to a detox facility, where, over a period of ten days, he was withdrawn from the benzodiazepine he had been taking for sixteen years.

“What happened next was absolutely the worst thing in my life,” he says. “I could give you a list of symptoms, but that wouldn’t do justice to what I was going through mentally. Month after month I got worse and worse. I couldn’t sleep, and the symptoms—the most debilitating one was this feeling that I was dead. I felt that my brain was ripped out of my head, like I wasn’t even a living thing. I had depersonalization, my skin felt weird, my body felt weird. I didn’t even want to get into the shower. Even room-temperature water felt strange on my skin. If I put on mildly hot water, it felt like it was burning right through me. I couldn’t digest food right, I couldn’t go to the bathroom for weeks at a time, I couldn’t urinate right … I was in a constant state of panic attacks, and this doctor is telling me it’s all in my mind, that he won’t write me a script, and that withdrawal symptoms can last a maximum of thirty days. I was cracking up, going insane.”

This went on for ten months. He found Geraldine Burns on the Internet, as she had started a benzodiazepine support group, and she would console him for hours at a time. Ten, twenty times a night he would call his sister Susan, screaming that he was going to kill himself. He desperately sought to get a new prescription for Klonopin, but the doctors he saw didn’t believe that his torment was related to benzodiazepine withdrawal. Instead, they figured that he had abused the drug in the past and so they refused to put him back on it. “They don’t understand that the drug changes the whole biology of your brain, and that your brain doesn’t work right anymore,” Hal says. Finally, his sister found a physician who agreed to write him a script, and “within hours, the nightmare was over. Every single side effect, every single withdrawal problem I had been going through was gone. Completely. Like magic. I was jumping up and down I was so excited.”

Hal has never tried going off Klonopin again. His brain adapted to the drug, he says, and now it can’t adapt back. “Klonopin ruined my life. It takes away your drive, and in the morning, you don’t want to get out of bed, because you feel so groggy. I don’t even know what it’s like to feel normal. This is my world. Things don’t get me as excited as most people because I’m in a constant state of sedation. It should never have been prescribed for long-term use.”

Susan sees it much the same way. “My sister and I have talked at length about how our brother is very good-looking, and how when he is acting normal, you would not know there is anything wrong,” she says. “He is adorable, charming; he carries on conversations. He could have been with a nice woman and had a family. But now? He has no friends. None whatsoever. He stays at home most of the time, except when he has to go to the store. He is trapped. He can’t get off Klonopin. I feel terrible for him, and I feel terrible for my dad, who when he dies will never have seen his son do well. It kills us that he could have had a life.”

If a picture is worth a thousand words, the photos that Jill, an Ohio woman in her mid-thirties, sends me tell her story in a very succinct fashion. There is the “before” photo in which she is smiling and looking confidently into the camera, posed like a model in a fashionable black dress. One hand is posed gracefully on her hip, a pearl necklace adds a touch of elegance, and she is a bit dolled up—the makeup and styled black hair tell of a woman who presents herself carefully to the world. And then there is the “after” photo, her eyes hollowed out and bloodshot, her face taut and drawn, her hair thinned—she looks like a somewhat crazed methamphetamine addict who is now getting her photo taken following an arrest.

We first spoke on the phone in July of 2008, three months after she had taken her last dose of a benzodiazepine, a drug she had been on for thirteen years. Here’s how she starts her story: “My head is feeling crushed. It’s like horses are kicking my skull.”

Jill, who asked that I not use her last name, grew up in an affluent suburb of Columbus, Ohio, where she attended private schools and excelled in multiple ways. She sang competitively, won school awards for her art, and was a top student. Petite and pretty, she was asked by a representative of the Miss Ohio pageant to enter that competition. “I was a vibrant, creative, fun person,” she says. However, she did occasionally struggle with anxiety and depression, and during her sophomore year at Ohio State University a psychiatrist put her on an antidepressant. Unfortunately, that drug seemed to increase her anxiety, and so eventually the psychiatrist added Klonopin to the mix. “He said it was a gentle little pill used to help old ladies sleep. He said that it wasn’t addictive and that if I wanted to stop, at most I’d experience a few nights of bad sleep. But he said I would probably need to take it for life, just like a diabetic needs insulin.”

For the next ten years, Jill functioned okay. She graduated summa cum laude from Ohio State University in 1996, earned a master’s degree in counseling, and after various adventures, in 2002 she began teaching fourth grade in a public school. However, throughout this period, her anxiety returned again and again, and each time it did, her psychiatrist upped her dose of Klonopin. And as the dose increased, her ability to function declined. “I would wonder, What is wrong with me? Why am I becoming so withdrawn? Why am I losing interest in everything? I was getting sicker and sicker.” Then, in late 2004, the anxiety, panic, and depression returned worse than ever, and new symptoms—obsessions and suicidal ideation—appeared too. She was told this meant she was “bipolar” and she was prescribed an antipsychotic, Abilify. “That’s when I flipped out. My anxiety went through the roof, it was like being injected with stimulants, and I was teaching one day and I started crying in class. I couldn’t take it anymore, and I was hospitalized in a psychiatric ward.”

Now came the drug merry-go-round. During the next two years, Jill was put on Lamictal, Lexapro, Seroquel, Neurontin, lithium, Wellbutrin, and other drugs she can’t remember, with Klonopin always part of the cocktail. This treatment caused her eyes to swell, her skin to break into rashes, and her eyebrows and hair to fall out. “My poor brain was being treated like a mixing bowl,” she says. Only when she asked doctors whether the cocktail might be making her sick, “they would say, ‘We have tried the drugs and they are not helping, and so the problem is you.’” Indeed, since the drugs weren’t working, her psychiatrists gave her electroshock, which took its toll on her memory.

Growing ever more desperate, toward the end of 2006 Jill concluded that “it was the drugs that were making me sick.” She began withdrawing from the medications one by one, and although she was able to get off the antidepressants and antipsychotics, every time she tried tapering off Klonopin she suffered a long list of torments: hallucinations, horrible anxiety, vertigo, painful muscle spasms, perceptual distortions, and derealization, just to name a few. Finally, in the spring of 2008, she adopted a new strategy: She would get off by progressively switching to less potent benzodiazepines. Klonopin was replaced by Valium, the Valium by Librium, and then, in April 2008, she withdrew from Librium. She was now drug free, yet three months later, when I spoke to her on the phone, she was still in withdrawal torment. “What I’ve been through … the trauma,” she says, breaking into tears. “I feel dizzy all the time. It is like the floor is tilting one way and I am spinning the other way. It is horrific. I have had hallucinations, I have to wear sunglasses in the house, sometimes I scream from the pain.”

At the end of our interview, I asked her to think back to what her life had been like before she was put on a benzodiazepine, and once more she began to cry.

“My anxiety then was like a mild case of asthma, and today it’s like I have end-stage lung disease. I’m terrified that I’m not going to make it. I’m so, so scared.”

• • •

Those interviews provide a snapshot of three lives, and several months later I spoke to each of the subjects again to see if anything had changed. Geraldine was doing much the same. Hal had become much more distraught. The Klonopin no longer seemed to be working, his anxiety had returned with a vengeance, and he felt physically sick. “I’ve come to accept this is my life,” he said, his voice filled with what seemed like bottomless despair. There was, however, an encouraging postscript to Jill’s story. Not long after our phone interview, her withdrawal symptoms began to abate, and in early 2009, she had this to report: The hallucinations, the vertigo, the seizures, the hair loss, and the blurry vision had all disappeared. The muscle spasms, the tinnitus, and the hypersensitivity to light and noise had become less severe. The feeling that her head was “packed in cement” had lessened.

“I have a few good days now, and my bad days are not all that bad anymore,” she says. “I think I can see the light at the end of the tunnel. There is no doubt I am going to be better. I am going to move to Boston, and although I’ll have to start from scratch, I know it will be okay. I now value life like nobody else I know. I enjoy being able to walk in a straight line again, and being able to see again, and even having a normal heartbeat. My hair is beginning to come back. I am getting better; I am just waiting for the cement to completely leave my brain.”

The Disability Numbers

At least to a degree, we can track the toll that the anti-anxiety drugs have taken over the past fifty years. As was noted at the beginning of this chapter, once the Miltown craze erupted, the number of people turning up at mental hospitals, outpatient centers, and residential facilities for the mentally ill began to sharply rise. The U.S. Department of Health and Human Services dubs this number “patient care episodes,” and it soared from 1.66 million in 1955 to 6.86 million in 1975, when Valiumania was near its peak.50 On a per-capita basis, that was an increase from 1,028 patient-care episodes per 100,000 people to 3,182 per 100,000, a threefold jump in twenty years. While many factors may have contributed to that increase (the emotional struggles that some Vietnam veterans experienced is one possibility that comes to mind, and illicit drug use is a second), Valiumania was clearly a major one. In the late 1970s, Betty Ford’s physician, Joseph Pursch, concluded that benzodiazepines were the “nation’s number one health problem,” and that was because he knew they were driving people to detox centers, emergency rooms, and psychiatric wards.

As the personal stories of Geraldine, Hal, and Jill attest, benzodiazepines continue to be a pathway to disability for many. These three are part of the surge of people with an “affective disorder” who have swelled the SSI and SSDI rolls in the past twenty years. Although the Social Security Administration doesn’t detail the number of disabled mentally ill who have anxiety as a primary diagnosis, a 2006 report by the U.S. General Accountability Office provides a proxy for estimating that number. It noted that 8 percent of the younger adults (eighteen to twenty-six years old) on the SSI and SSDI rolls were disabled by anxiety, and if that percentage holds true for all ages, then there were more than 300,000 adults in the United States who received government support in 2006 due to an anxiety disorder.51 That is roughly sixty times the number of psychoneurotics hospitalized in 1955.

Although it was thirty years ago that governmental review panels in the United States and the United Kingdom concluded that the benzodiazepines shouldn’t be prescribed long-term, with dozens of studies subsequently confirming the wisdom of that advice, the prescribing of benzodiazepines for continual use goes on. Indeed, a 2005 study of anxious patients in the New England area found that more than half regularly took a benzodiazepine, and many bipolar patients now take a benzodiazepine as part of a drug cocktail.52 The scientific evidence simply doesn’t seem to affect the prescribing habits of many doctors. “The lesson has either never been learned, or it has passed people by,” Malcolm Lader said.53

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