Like my colleagues, I eagerly embraced the pharmacological revolution. In 1973 I became the first chief resident in psychopharmacology at MMHC. I may also have been the first psychiatrist in Boston to administer lithium to a manic-depressive patient. (I’d read about John Cade’s work with lithium in Australia, and I received permission from a hospital committee to try it.) On lithium a woman who had been manic every May for the past thirty-five years, and suicidally depressed every November, stopped cycling and remained stable for the three years she was under my care. I was also part of the first U.S. research team to test the antipsychotic Clozaril on chronic patients who were warehoused in the back wards of the old insane asylums.6 Some of their responses were miraculous: People who had spent much of their lives locked in their own separate, terrifying realities were now able to return to their families and communities; patients mired in darkness and despair started to respond to the beauty of human contact and the pleasures of work and play. These amazing results made us optimistic that we could finally conquer human misery.
Antipsychotic drugs were a major factor in reducing the number of people living in mental hospitals in the United States, from over 500,000 in 1955 to fewer than 100,000 in 1996.7 For people today who did not know the world before the advent of these treatments, the change is almost unimaginable. As a first-year medical student I visited Kankakee State Hospital in Illinois and saw a burly ward attendant hose down dozens of filthy, naked, incoherent patients in an unfurnished dayroom supplied with gutters for the runoff water. This memory now seems more like a nightmare than like something I witnessed with my own eyes. My first job after finishing my residency in 1974 was as the second-to-last director of a once-venerable institution, the Boston State Hospital, which had formerly housed thousands of patients and been spread over hundreds of acres with dozens of buildings, including greenhouses, gardens, and workshops—most of them by then in ruins. During my time there patients were gradually dispersed into “the community,” the blanket term for the anonymous shelters and nursing homes where most of them ended up. (Ironically, the hospital was started as an “asylum,” a word meaning “sanctuary” that gradually took on a sinister connotation. It actually did offer a sheltered community where everybody knew the patients’ names and idiosyncrasies.) In 1979, shortly after I went to work at the VA, the Boston State Hospital’s gates were permanently locked, and it became a ghost town.
During my time at Boston State I continued to work in the MMHC psychopharmacology lab, which was now focusing on another direction for research. In the 1960s scientists at the National Institutes of Health had begun to develop techniques for isolating and measuring hormones and neurotransmitters in blood and the brain. Neurotransmitters are chemical messengers that carry information from neuron to neuron, enabling us to engage effectively with the world.
Now that scientists were finding evidence that abnormal levels of norepinephrine were associated with depression, and of dopamine with schizophrenia, there was hope that we could develop drugs that target specific brain abnormalities. That hope was never fully realized, but our efforts to measure how drugs could affect mental symptoms led to another profound change in the profession. Researchers’ need for a precise and systematic way to communicate their findings resulted in the development of the so-called Research Diagnostic Criteria, to which I contributed as a lowly research assistant. These eventually became the basis for the first systematic system to diagnose psychiatric problems, the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM), which is commonly referred to as the “bible of psychiatry.” The foreword to the landmark 1980 DSM-III was appropriately modest and acknowledged that this diagnostic system was imprecise—so imprecise that it never should be used for forensic or insurance purposes.8 As we will see, that modesty was tragically short-lived.
INESCAPABLE SHOCK
Preoccupied with so many lingering questions about traumatic stress, I became intrigued with the idea that the nascent field of neuroscience could provide some answers and started to attend the meetings of the American College of Neuropsychopharmacology (ACNP). In 1984 the ACNP offered many fascinating lectures about drug development, but it was not until a few hours before my scheduled flight back to Boston that I heard a presentation by Steven Maier of the University of Colorado, who had collaborated with Martin Seligman of the University of Pennsylvania. His topic was learned helplessness in animals. Maier and Seligman had repeatedly administered painful electric shocks to dogs who were trapped in locked cages. They called this condition “inescapable shock.”9 Being a dog lover, I realized that I could never have done such research myself, but I was curious about how this cruelty would affect the animals.
After administering several courses of electric shock, the researchers opened the doors of the cages and then shocked the dogs again. A group of control dogs who had never been shocked before immediately ran away, but the dogs who had earlier been subjected to inescapable shock made no attempt to flee, even when the door was wide open—they just lay there, whimpering and defecating. The mere opportunity to escape does not necessarily make traumatized animals, or people, take the road to freedom. Like Maier and Seligman’s dogs, many traumatized people simply give up. Rather than risk experimenting with new options they stay stuck in the fear they know.
I was riveted by Maier’s account. What they had done to these poor dogs was exactly what had happened to my traumatized human patients. They, too, had been exposed to somebody (or something) who had inflicted terrible harm on them—harm they had no way of escaping. I made a rapid mental review of the patients I had treated. Almost all had in some way been trapped or immobilized, unable to take action to stave off the inevitable. Their fight/flight response had been thwarted, and the result was either extreme agitation or collapse.
Maier and Seligman also found that traumatized dogs secreted much larger amounts of stress hormones than was normal. This supported what we were beginning to learn about the biological underpinnings of traumatic stress. A group of young researchers, among them Steve Southwick and John Krystal at Yale, Arieh Shalev at Hadassah Medical School in Jerusalem, Frank Putnam at the National Institute of Mental Health (NIMH), and Roger Pitman, later at Harvard, were all finding that traumatized people keep secreting large amounts of stress hormones long after the actual danger has passed, and Rachel Yehuda at Mount Sinai in New York confronted us with her seemingly paradoxical findings that the levels of the stress hormone cortisol are low in PTSD. Her discoveries only started to make sense when her research clarified that cortisol puts an end to the stress response by sending an all-safe signal, and that, in PTSD, the body’s stress hormones do, in fact, not return to baseline after the threat has passed.
Ideally our stress hormone system should provide a lightning-fast response to threat, but then quickly return us to equilibrium. In PTSD patients, however, the stress hormone system fails at this balancing act. Fight/flight/freeze signals continue after the danger is over, and, as in the case of the dogs, do not return to normal. Instead, the continued secretion of stress hormones is expressed as agitation and panic and, in the long term, wreaks havoc with their health.
I missed my plane that day because I had to talk with Steve Maier. His workshop offered clues not only about the underlying problems of my patients but also potential keys to their resolution. For example, he and Seligman had found that the only way to teach the traumatized dogs to get off the electric grids when the doors were open was to repeatedly drag them out of their cages so they could physically experience how they could get away. I wondered if we also could help my patients with their fundamental orientation that there was nothing they could do to defend themselves? Did my patients also need to have physical experiences to restore a visceral sense of control? What if they could be taught to physically move to escape a potentially threatening situation that was similar to the trauma in which they had been trapped and immobilized? As I will discuss in
the treatment part 5 of this book, that was one of the conclusions I eventually reached.
Further animal studies involving mice, rats, cats, monkeys, and elephants brought more intriguing data.10 For example, when researchers played a loud, intrusive sound, mice that had been raised in a warm nest with plenty of food scurried home immediately. But another group, raised in a noisy nest with scarce food supplies, also ran for home, even after spending time in more pleasant surroundings.11
Scared animals return home, regardless of whether home is safe or frightening. I thought about my patients with abusive families who kept going back to be hurt again. Are traumatized people condemned to seek refuge in what is familiar? If so, why, and is it possible to help them become attached to places and activities that are safe and pleasurable?12
ADDICTED TO TRAUMA: THE PAIN OF PLEASURE AND THE PLEASURE OF PAIN
One of the things that struck my colleague Mark Greenberg and me when we ran therapy groups for Vietnam combat veterans was how, despite their feelings of horror and grief, many of them seemed to come to life when they talked about their helicopter crashes and their dying comrades. (Former New York Times correspondent Chris Hedges, who covered a number of brutal conflicts, entitled his book War Is a Force That Gives Us Meaning.13) Many traumatized people seem to seek out experiences that would repel most of us,14 and patients often complain about a vague sense of emptiness and boredom when they are not angry, under duress, or involved in some dangerous activity.
My patient Julia was brutally raped at gunpoint in a hotel room at age sixteen. Shortly thereafter she got involved with a violent pimp who prostituted her. He regularly beat her up. She was repeatedly jailed for prostitution, but she always went back to her pimp. Finally her grandparents intervened and paid for an intense rehab program. After she successfully completed inpatient treatment, she started working as a receptionist and taking courses at a local college. In her sociology class she wrote a term paper about the liberating possibilities of prostitution, for which she read the memoirs of several famous prostitutes. She gradually dropped all her other courses. A brief relationship with a classmate quickly went sour—he bored her to tears, she said, and she was repelled by his boxer shorts. She then picked up an addict on the subway who first beat her up and then started to stalk her. She finally became motivated to return to treatment when she was once again severely beaten.
Freud had a term for such traumatic reenactments: “the compulsion to repeat.” He and many of his followers believed that reenactments were an unconscious attempt to get control over a painful situation and that they eventually could lead to mastery and resolution. There is no evidence for that theory—repetition leads only to further pain and self-hatred. In fact, even reliving the trauma repeatedly in therapy may reinforce preoccupation and fixation.
Mark Greenberg and I decided to learn more about attractors—the things that draw us, motivate us, and make us feel alive. Normally attractors are meant to make us feel better. So, why are so many people attracted to dangerous or painful situations? We eventually found a study that explained how activities that cause fear or pain can later become thrilling experiences.15 In the 1970s Richard Solomon of the University of Pennsylvania had shown that the body learns to adjust to all sorts of stimuli. We may get hooked on recreational drugs because they right away make us feel so good, but activities like sauna bathing, marathon running, or parachute jumping, which initially cause discomfort and even terror, can ultimately become very enjoyable. This gradual adjustment signals that a new chemical balance has been established within the body, so that marathon runners, say, get a sense of well-being and exhilaration from pushing their bodies to the limit.
At this point, just as with drug addiction, we start to crave the activity and experience withdrawal when it’s not available. In the long run people become more preoccupied with the pain of withdrawal than the activity itself. This theory could explain why some people hire someone to beat them, or burn themselves with cigarettes. or why they are only attracted to people who hurt them. Fear and aversion, in some perverse way, can be transformed into pleasure.
Solomon hypothesized that endorphins—the morphinelike chemicals that the brain secretes in response to stress—play a role in the paradoxical addictions he described. I thought of his theory again when my library habit led me to a paper titled “Pain in Men Wounded in Battle,” published in 1946. Having observed that 75 percent of severely wounded soldiers on the Italian front did not request morphine, a surgeon by the name of Henry K. Beecher speculated that “strong emotions can block pain.”16
Were Beecher’s observations relevant to people with PTSD? Mark Greenberg, Roger Pitman, Scott Orr, and I decided to ask eight Vietnam combat veterans if they would be willing to take a standard pain test while they watched scenes from a number of movies. The first clip we showed was from Oliver Stone’s graphically violent Platoon (1986), and while it ran we measured how long the veterans could keep their right hands in a bucket of ice water. We then repeated this process with a peaceful (and long-forgotten) movie clip. Seven of the eight veterans kept their hands in the painfully cold water 30 percent longer during Platoon. We then calculated that the amount of analgesia produced by watching fifteen minutes of a combat movie was equivalent to that produced by being injected with eight milligrams of morphine, about the same dose a person would receive in an emergency room for crushing chest pain.
We concluded that Beecher’s speculation that “strong emotions can block pain” was the result of the release of morphinelike substances manufactured in the brain. This suggested that for many traumatized people, reexposure to stress might provide a similar relief from anxiety.17 It was an interesting experiment, but it did not fully explain why Julia kept going back to her violent pimp.
SOOTHING THE BRAIN
The 1985 ACNP meeting was, if possible, even more thought provoking than the previous year’s session. Kings College professor Jeffrey Gray gave a talk about the amygdala, a cluster of brain cells that determines whether a sound, image, or body sensation is perceived as a threat. Gray’s data showed that the sensitivity of the amygdala depended, at least in part, on the amount of the neurotransmitter serotonin in that part of the brain. Animals with low serotonin levels were hyperreactive to stressful stimuli (like loud sounds), while higher levels of serotonin dampened their fear system, making them less likely to become aggressive or frozen in response to potential threats.18
That struck me as an important finding: My patients were always blowing up in response to small provocations and felt devastated by the slightest rejection. I became fascinated by the possible role of serotonin in PTSD. Other researchers had shown that dominant male monkeys had much higher levels of brain serotonin than lower-ranking animals but that their serotonin levels dropped when they were prevented from maintaining eye contact with the monkeys they had once lorded over. In contrast, low-ranking monkeys who were given serotonin supplements emerged from the pack to assume leadership.19 The social environment interacts with brain chemistry. Manipulating a monkey into a lower position in the dominance hierarchy made his serotonin drop, while chemically enhancing serotonin elevated the rank of former subordinates.
The implications for traumatized people were obvious. Like Gray’s low-serotonin animals, they were hyperreactive, and their ability to cope socially was often compromised. If we could find ways to increase brain serotonin levels, perhaps we could address both problems simultaneously. At that same 1985 meeting I learned that drug companies were developing two new products to do precisely that, but since neither was yet available, I experimented briefly with the health-food-store supplement L-tryptophan, which is a chemical precursor of serotonin in the body. (The results were disappointing.) One of the drugs under investigation never made it to the market. The other was fluoxetine, which, under the brand name Prozac, became one of the most successful psychoactive drugs ever created.
On Monday, February 8, 1988, Proza
c was released by the drug company Eli Lilly. The first patient I saw that day was a young woman with a horrendous history of childhood abuse who was now struggling with bulimia—she basically spent much of her life bingeing and purging. I gave her a prescription for this brand-new drug, and when she returned on Thursday she said, “I’ve had a very different last few days: I ate when I was hungry, and the rest of the time I did my schoolwork.” This was one of the most dramatic statements I had ever heard in my office.
On Friday I saw another patient to whom I’d given Prozac the previous Monday. She was a chronically depressed mother of two school-aged children, preoccupied with her failures as a mother and wife and overwhelmed by demands from the parents who had badly mistreated her as a child. After four days on Prozac she asked me if she could skip her appointment the following Monday, which was Presidents’ Day. “After all,” she explained, “I’ve never taken my kids skiing—my husband always does—and they are off that day. It would really be nice for them to have some good memories of us having fun together.”
This was a patient who had always struggled merely to get through the day. After her appointment I called someone I knew at Eli Lilly and said, “You have a drug that helps people to be in the present, instead of being locked in the past.” Lilly later gave me a small grant to study the effects of Prozac on PTSD in sixty-four people—twenty-two women and forty-two men—the first study of the effects of this new class of drugs on PTSD. Our Trauma Clinic team enrolled thirty-three nonveterans and my collaborators, former colleagues at the VA, enrolled thirty-one combat veterans. For eight weeks half of each group received Prozac and the other half a placebo. The study was blinded: Neither we nor the patients knew which substance they were taking, so that our preconceptions could not skew our assessments.
The Body Keeps the Score Page 5