By Katy Butler
NOT LONG AGO, MOST therapists who heard a story like Albert Grow’s would have thought about what his experience in Vietnam did to his relationship with his family, his community and his sense of self. Few would have given much thought to what it did to his biochemistry. That is about to change.
Grow, a policeman in Salem, New Hampshire, came back from Vietnam nearly 30 years ago on a “freezer flight” a transport plane piled with body bags. At the Boston airport, a woman called him trash and spit in his face. Not long afterward, he punched out two coworkers in a photo lab because they wore black arm bands to honor the Vietnamese dead. After a brief stay on a psychiatric ward, he burned his Marine uniform in his parents’ backyard. He avoided war movies. He didn’t go to his sister’s wedding.
Grow moved to New Hampshire and for decades lived an ordinary life: he finished college, became a husband and a father and coached Little League. Then, during the Gulf War, he watched American missiles explode on television and thought about his 14-year-old son. “I remember saying, You’re not going to do it to him. Not him,” he says. “It was like somebody took the switch I had turned off and turned it back on.”
He began to see the faces of dead young men he had long succeeded in forgetting. He would drive fast for miles, going nowhere, or rent a motel room and sit in the dark for days to keep his anger away from his wife and son. He was put on anti-depressants and anti-anxiety drugs. “I smell something and I’m back in the jungle. I have nightmares and wake up in a pool of perspiration,” he says. “I’m very jumpy, almost like I’m on alert.
“I want to learn some new coping skills,” says Grow, who is currently an inpatient at the Department of Veterans Affairs medical center at West Haven, Connecticut, a leading site for federal research on the emerging neuroscience of Post-Traumatic Stress Disorder (PTSD). “I can feel anger and rage like that, but where’s the good stuff? I love my son, but I have a very hard time saying it. I love my wife, but I isolate. I’m tired of the sleepless nights, the dreams. I wish they could do loboto-mies and get rid of it.”
It is a story that a psychologist trained in talk therapy, not neurobiology, might find comfortingly familiar at first! A good clinician might note Grow’s abandonment by his culture after living through a year of horrors; his love for his son; his profound rage against the illusions propagated about war. In the 1970s and 1980s, when men like him began pouring into vets’ centers, it was thought that rap groups, talk therapy and alcohol counseling would ultimately resolve things. But talk therapy has not done the trick, neither for veterans nor for many survivors of torture, severe childhood abuse and other trauma.
Now, research psychiatrists at the West Haven VA, Yale, Harvard, UCLA and Dartmouth are documenting what many clinicians have come, over time, to suspect: PTSD is not only an emotional response to troubling events, it is the expression of a persistent disregulation of body and brain chemistry. The research so far suggests that moments of overwhelming terror can alter brain chemistry for decades, and may kill brain cells crucial to memory.
Whether this process can be reversed is not yet known. It is clear, however, that therapists who want to treat PTSD effectively are about to venture into an unfamiliar landscape. Here, all of the signposts are in a foreign language. The metaphors have changed. Talk of fear, rage, family process and dissociation has been replaced by “dendritic atrophy,” “neuronal death” and “glucocorticoids.” For therapists whose last exposure to physiology or neuro-chemistry was a ninth-grade frog autopsy, the new territory may be unnerving. It requires an understanding of systems theory more complex and subtle than anything most family therapists bargained for. But hidden in this uncharted landscape may be ways of alleviating a form of suffering that has only recently come to light.
POST-TRAUMATIC STRESS DISORDER can mean anything from a nightmarish few months to a lifetime of misery. About 5 to 10 percent of us can expect to suffer PTSD symptoms at some point in our lives: 46 percent of women and 65 percent of men who have been raped suffer acute PTSD, as do 21 percent of women and 2 percent of men who are physically attacked. Studies suggest that chronic PTSD a condition lasting more than 6 months affects 15 percent of Vietnam combat veterans and 50 percent of Cambodian refugee youth who witnessed genocide.
People with PTSD complain of almost unbearable states of physiological arousal: a hypersensitive emotional trip-wire, an exaggerated startle response and profound distortions of memory. In paradoxical, oscillating fashion, sleeplessness and hypervigilance alternate with numbness and withdrawal; amnesia coexists with flashbacks. These wildly swinging inner states make people feel helpless they fear they’re going crazy and sense that they’re not the same person they used to be. This, in turn, can set off a cascade of negative effects, disrupting relationships and driving people to self-medicate with alcohol or drugs.
Six weeks after being raped in Des Moines, Iowa, Nancy Ziegenmayer was so afraid at night that her husband had to escort her from the bedroom to the bathroom. In California, a computer-graphics artist injured while driving on a rain-swept freeway jumped at unexpected noises for months afterward, raged at her husband over trivial things and was too frightened to ride her bike. A New Haven woman who had never told anyone about being raped at 12 by her father appeared at a psychiatric emergency room at the age of 18, overwhelmed by panic attacks. At the first snowfall of the year, a retired Chicago policeman who survived the merciless winter slaughter in Belgium during the Battle of the Bulge becomes unusually quiet and withdrawn; he once told his daughter that he sees blood on the snow.
For more than 100 years, doctors and therapists have wondered whether such symptoms were neurophysiologi-cal, emotional or merely a sign of borderline personality disorder or weak character. In the 1860s, doctors described frequent coronary troubles in Civil War veterans as “soldier’s heart.” Victims of World War I “shell-shock” were thought to be suffering from the physical impact of repeated bombardments. During World War II, “traumatic neurosis” and “battle fatigue” were sometimes explained in symbolic or psychoanalytic terms, as the expression of a conflict between the id’s drive to survive and the superego’s sense of patriotic obligation.
The syndrome got a new name after Vietnam, and entered the DSM lexicon in 1980 as Post-Traumatic Stress Disorder. Naming it was one thing, but understanding its mechanics much less, treating it effectively was something else again.
For decades, clinicians have listened and speculated about what was going on inside their clients’ brains and nervous systems. But they were Kremlin-watchers, trying to map the contents of a black box they could not open. Now the box is opening, thanks to new findings from endocrinology, animal behavior, neurochemistry and computerized brain-imaging devices like Magnetic Resonance Imaging (MRI) and Positron Emission Tomography (PET). It is clear that PTSD is more than a symbolic and existential crisis of meaning and human betrayal.
“Victims of devastating trauma may never be the same, biologically,” says Dennis Charney, head of the clinical neuroscience division of the National Center for PTSD at the West Haven VA “It does not matter if it was the incessant terror of combat, torture or repeated abuse in childhood, or a one-time experience, like being trapped in a hurricane or almost dying in an auto accident,” he told The New York Times. “All uncontrollable stress can have the same biological impact.” Boris Pasternak put it another way in Doctor Zhivago: “Our nervous system isn’t just a fiction,” he wrote. “It’s a part of our physical body, and our soul exists in space and is inside us, like the teeth in our mouth. It can’t be forever violated with impunity.”
THE BIOLOGICAL PART OF THE PTSD story is summarized in a dauntingly technical 1995 book called Neurobiological and Clinical Consequences of Stress (Lippincott-Raven), written mostly by research psychiatrists funded by the Veterans Administration and the congressionally mandated National Center for PTSD. Their informed speculation is that the body responds to extreme stress by releasing a cascade of cortisol, adrenaline and other hormones that can damage brain cells, impair memory and set in motion a long-lasting and worsening disregulation of the body’s complex biochemistry. “The system gets overtaxed and starts flailing,” says Harvard trauma researcher Bessel van der Kolk, coauthor of the forthcoming Traumatic Stress (Guilford Press). “It’s a breakdown of the normal stress response.”
Disregulation of the Flight-or-Fight Response
The neurochemical response to extreme stress illustrates the saying that you can have too much of a good thing. Just as a single Martini can stimulate singing and laughter, while a fifth of Jack Daniels brings on depression, brain chemicals can help or harm, depending on the dose. Anyone who has felt the senses quicken and the mind clear in the face of danger knows the benefits of the “adrenaline rush.” Raised levels of epinephrine and norepinephrine (the two primary fight-or-flight hormones, also known as adrenaline and noradrenaline) increase the brain’s alertness, enhance memory and quicken the heartbeat. People can do extraordinary things, like lift a car that is crushing a loved one or push a baby carriage out of the path of a speeding train.
When stress becomes overwhelming, too much epinephrine and norepinephrine induce confusion and impair learning and memory. At a fatal car crash, one person may display self-possession, while another may “run around like a chicken with its head cut off,” or appear “scared out of his wits.” At high enough levels in maze-running laboratory rats, the fight-or-flight hormones induce amnesia.
The negative effects of too much epinephrine and norepinephrine are both immediate and delayed. Although the underlying brain chemistry is not understood, repeated adrenaline rushes seem to progressively sensitize brain chemistry, provoking ever-greater floods of adrenaline at lower thresholds. Laboratory animals who have been previously shocked release even more norepinephrine when shocked again. The same increasing vulnerability probably occurs in humans, as the old proverb, “once bitten, twice shy,” suggests: a 1993 west Haven study of 66 veterans found that those with childhood histories of physical or sexual abuse were significantly more likely to develop PTSD after combat in Vietnam.
Emotional reactivity is a hallmark of PTSD. Years after trauma, its sufferers startle at the slightest surprise and remain easily frazzled. The fight-or-flight response is disregulated; the nervous system is always on alert. A 1987 study of the urine of PTSD veterans found chronically elevated levels of epinephrine and norepinephrine. Heightened norepinephrine levels were also reported recently by National Institutes of Health researcher Frank Putnam in an ongoing longitudinal study of 80 sexually abused girls aged 7 to 14.
The hyperactive fight-or-flight response can also be activated by specific reminders of trauma: a tape of machine-gun fire, for instance, will provoke sweating, heart-pounding and rising blood pressure in combat veterans with PTSD, but not in matched controls. This mildly disturbing event, it seems, is “read” by the PTSD-affected brain and nervous system as life-threatening, even when the rational mind knows otherwise. Sometimes, one cannot talk oneself out of fear.
Floods of epinephrine and norepinephrine not only increase and accompany emotional and neurobiological arousal, they also can trigger the seizure-like cinematic relivings of trauma known as flashbacks in previously traumatized people. In 1990, researchers at West Haven VA injected 15 veterans suffering from PTSD with yohimbine, a psychoactive drug from the bark of a South American tree that stimulates secretions of norepinephrine. Nontrauma-tized people usually feel a little heart-pounding under the influence of yohimbine; but nine of the vets suffered panic attacks and six had fullblown flashbacks. One veteran given the drug told researchers he could see a helicopter go down in a bright flash and a trail of smoke. “When we started doing these studies not quite 10 years ago, some people thought symptoms like flashbacks were completely the products of mentation that they were just psychological phenomena, and didn’t have any basis in the physiology of the brain,” says Yale professor and West Haven VA research psychiatrist John Krystal. “Now, it’s obvious that’s not so.”
The experiment suggests a link between flashbacks and high brain levels of norepinephrine, because yohimbine temporarily disables alpha-2 receptors brain-cell structures that act as tiny governors, slowing and calibrating the release of epinephrine to the brain. Other research has shown that PTSD patients, for reasons not yet understood, have 40 percent fewer of these alpha-2 receptors than normal controls.
The research suggests that the brain chemistry of traumatized people may have changed, so that arousing events even those dissimilar from the original trauma can provoke flashbacks. The result is a vicious circle: arousing the fight-or-flight response can trigger flashbacks, and flashbacks can further intensify the fight-or-flight response.
Other hormonal systems especially those involving cortisol and brain opiates continue to function abnormally years after trauma. A 1992 study by Roger Pitman, van der Kolk and others found that veterans with PTSD who watched a 15-minute video of combat scenes from Platoon registered a 30-percent drop in pain sensitivity; their brains released natural opiates with the pain-killing equivalent of eight milligrams of morphine. This over-activation of a natural anesthetic response, in the face of something rationally known not to be dangerous, may partly explain the numbness reported by some people with PTSD.
Damage to Brain Structure
The most disturbing recent neuro-science suggests that trauma may do long-lasting damage to the hippocampus, a seahorse-shaped structure deep in the brain. Much about the hippocampus remains mysterious, but it is crucial to short-term memory and may play a role in the sorting and storing of long-term memories, a process that takes about a month. (H.M., a famous patient whose hippocampus was removed in the 1950s to mitigate his epilepsy, could remember his past prior to his surgery, but accumulated no additional memories, forgetting new faces or names after a few minutes.)
Three 1995 studies found significant reductions in the size of the hippocampus in traumatized people, compared to nontraumatized controls. The studies used Magnetic Resonance Imaging, (MRI), a relatively new diagnostic device that produces precise, three-dimensional blueprints of the architecture of the brain. At the West Haven VA, J. Douglas Bremner and Dennis Charney found a 13-percent reduction in left hippocampal volume in 12 male and 5 female survivors of severe childhood abuse with PTSD, compared with carefully matched controls. Their similar study of 26 veterans with PTSD found an 8-percent decrease in right hippocampal volume compared with matched controls. Meanwhile, Murray Stein of the University of California at San Diego measured hippocampal volume in 43 women recruited at a women’s health clinic; the 22 with histories of prolonged childhood sexual abuse had hippocampi 5 percent smaller than the 21 nonabused women. Those with the smallest hippocampi, Stein says, displayed the most symptoms of PTSD and dissociation the tendency to “space out,” feel detached from one’s body and have unpredictable lapses in memory.
Nobody knows exactly how trauma damages the hippocampus, or whether people with small hippocampi are simply more prone to develop PTSD. But if damage is done, the prime biochemical suspect is cortisol (also known as hydrocortisone), a hormone secreted by the adrenal glands just above the kidneys, which circulates at high levels in the bloodstream and brain for hours and sometimes days after extreme stress. Moderate levels of cortisol help the body to release glucose into the bloodstream and reduce inflammation. In animals, moderate to high levels of cortisol are toxic to some brain cells in the hippocampus: autopsies of monkeys who died from the stress of prolonged laboratory overcrowding revealed high cortisol levels and hippocampal shrinkage. Animal researchers have found a link between high cortisol levels over a period of weeks and the withering of dendrites the feathery branches that allow brain cells to form communication pathways and associational networks with hundreds of thousands of their neighbors. If cortisol levels stay high for months, it can cause irreversible brain-cell death. This suggests that a single, horrific car wreck may do less damage than a decade of child abuse or a year in Vietnam. A loss of neurons and dendrites could explain, Bremner speculates, why many trauma survivors suffer from dissociation a failure to integrate fragments of memory into a coherent personal history or sense of self.
Raised cortisol levels were also found in the sexually abused girls first studied by Putnam in 1988, but the levels are declining over time. Studies of Vietnam veterans and of women who reported a previous experience of rape when reporting to an emergency room after a sexual assault found unusually low levels of cortisol. This research suggests that the body may over-reduce cortisol levels after prolonged stress. Paradoxically, low cortisol levels are associated with brain-cell death in an innermost section of the hippocampus called the dentate gyrus, a region thought to contribute to the creation and recall of long-term memories. This suggests that biochemically induced physical damage, not psychological defenses, may explain some memory loss in trauma survivors; it challenges both the Freudian speculation of a mental mechanism called repression and the assertion that traumatic amnesia is nothing more than ordinary forgetting. Even though the sexual abuse survivors and PTSD veterans studied showed unusually small hippocampi decades after trauma, research suggests that the brain can bounce back from short-term stress. “Dendritic atrophy in rats is totally reversible,” says Stanford University animal neuroscience researcher Robert Sapolsky, author of Why Zebras Don’t Get Ulcers. “Stop the stress and the dendrites grow back, and in subsequent weeks, things go back to normal. Parsimony would suggest that if this [hipppocampal damage] happens in humans which we don’t know for sure yet the same thing probably occurs.”
Changes in Memory
Clinicians often informally note memory lapses, amnesia and fragmentary memories in Vietnam veterans and adults severely abused as children. In the ideological war over recovered memory, these reports are sometimes dismissed as therapeutic folklore. But the latest research suggests that trauma affects even short-term memory of simple facts. In 1993, Bremner ran a battery of neuropsychological tests with 47 sexual abuse survivors and combat veterans with PTSD and found significant deficits in verbal recall and other forms of short-term memory, compared with matched, nontraumatized controls.
“The assumption is that people who have been exposed to extreme stress have normal memory,” says Bremner. “But the evidence is that they don’t. Some of them can’t remember the grocery list. Their memory deficits can be as extreme as those in people who have severe epilepsy and have had parts of their hippocampus removed.”
Another study, published in May in The Archives of General Psychiatry, suggests that some memories of trauma are very different from “ordinary forgetting and remembering.” Harvard research psychiatrists Scott Rauch, Roger Pitman and Bessel van der Kolk stimulated flashbacks in eight combat veterans and sexual abuse survivors with PTSD by playing a tape of their most horrific memory. Then they recorded brain activity using Positron Emission Tomography (PET). The PET scan traced the brain’s metabolism of radioactively tagged oxygen to create a living show, a moving picture of activity in the brain. The researchers found that during flashbacks, areas of the brain’s cortex involved in sensory memory were relatively active, while Broca’s area known to play a role in the verbal articulation of experience was relatively quiescent. When the subjects were asked to recall something mundane, like making a bed, the opposite pattern pertained: Broca’s area was more active and the visual areas relatively quiet. The PET scans suggest, says van der Kolk, that trauma survivors remember their past horrors in a state of “speechless terror.” When they don’t describe them to therapists, they may not merely be shy, shameful or withholding: their brains may literally be unable to put their shocking experiences into words.
Researchers have also chemically induced the state of “dissociation” the tendency of some traumatized people to space out, suffer memory lapses and experience distortions in body image, including the sensation of being out of their bodies. In 1994, Yale/West Haven VA researchers injected normal volunteers with ketamine hydrochloride, a psychoactive drug that selectively disables a brain-cell receptor concentrated in the hippocampus. The volunteers experienced a wide range of dissociative symptoms, including having out-of-body experiences, feeling that their arms were like toothpicks and sensing gaps in time or having time stand still.
THESE EXPERIMENTS HAVE PRO-duced little more than hints: what is now known about the brain is dauntingly reminiscent of a 16th-century European conception of Africa: boats have landed and a few search parties have returned with stories of fertile river valleys and mysterious, unclimbed peaks, but few coordinates have been precisely plotted. Only since the mid-1980s have the PET scan and the MRI allowed researchers to peer directly into the brain’s glimmering, wet-wired sponge of neurochemicals and electromagnetic fields and get a glimpse of its 100 billion branching neurons at work. Researchers have measured the hippocampus, but have only the sketchiest idea of what it does. Far more is unknown than is known.
If the clinical neuroscience of traumatic damage is in its infancy, the neuroscience of psychological healing is still in the womb. Researchers have shown that the smell of jasmine can subtly alter brain function, as can the tug of a baby’s mouth on a mother’s nipple. Holding hands lowers cortisol levels in both apes and humans. While undergoing cardiac catheterization, those who talked to their doctors about their fears had lower cortisol levels than those who toughed it out.
Therapy can alter PET scans as well: the February 1996 issue of The Archives of General Psychiatry shows “before” and “after” PET scans of nine patients with obsessive-compulsive disorder, treated successfully with cognitive-behavioral techniques, which are like a science-fiction version of a Glamour magazine makeover.
In the meantime, neuroscience offers only the vaguest hints to therapists struggling with emotionally volatile, impulsive and chronically terrified or rage-ful people with PTSD. Years of sleeplessness, flashbacks and intrusive thoughts have taken their toll on marriages, jobs and self-image, and this negative outer cascade needs repair as much as or more than the inner neurophysiological cascade. Successful therapy remains a carefully timed and finely sewn patchwork of interventions at the biological, individual, family and social levels. What works, and what doesn’t, is still less informed by PET scans than by clinical observation, guesswork and common sense.
Different stages of PTSD call for different responses. Immediately after a trauma, reassuring therapy or perhaps even massage may be critical to help lower cortisol levels the way hand-holding can. Later, sufferers and their families can be taught that flashbacks and other alarming symptoms are natural responses to extreme stress. David Foy, a cognitive-behavioral psychologist at Pepperdine University, says early therapy can challenge beliefs that tragedy could have been avoided or that the victim was to blame. “If people don’t label themselves as abnormal, some will naturally recover if they give themselves six weeks to settle down again biologically,” he says. This is the rationale behind “critical incident debriefing,” now routine for disaster workers, police officers and children affected by schoolyard shootings and other sudden tragedies.
Clinicians are far more hopeful when treating people in the first six months after a trauma. For reasons not yet fully understood, chronic PTSD often seems intractable. Treating it is a process of incremental victories. The first step, as the new neuroscience research strongly suggests, is not to dig into the trauma but to restabilize clients neurobiologically, using such simple techniques as stress reduction, meditation, hard exercise, regular meals and a decent sleeping schedule. No medication is a magic bullet, but many therapists report good results with Prozac.
“I can’t imagine working without it,” says Bessel van der Kolk. “The very first patient I tried it with, in the late ’80s, was a very bulimic incest victim. After four days, she came in and said, ‘Food is food. When I am hungry, I eat, and when I’m not, I do other things.’ Such medications can aid therapy by helping clients tolerate the negative emotions that talking about trauma can arouse.”
Meditation can also help people tolerate and contain unpleasant emotional states, rather than impulsively express them or try to avoid them. At the stress-reduction clinic at the University of Massachusetts Medical Center in Worcester, Massachusetts, mindfulness meditation is taught to about 900 people a year, about 10 percent of whom suffer from PTSD due to combat, child sexual abuse or repeated car accidents. “We see a real change in the response pattern, and that manifests physiologically, but it’s all anecdotal,” says Ferris Urbanowsky, director of training. “We had a vet here recently who, if his wife tried to wake him from a nap and touched him, would go for her throat. After he began meditating, he found over time that the same reaction just did not occur anymore.” Other victims report success with yoga, t’ai chi, massage and body work and other forms of moving meditation.
Meditation is no magic bullet: Vietnam veteran Claude Thomas, now an ordained Zen Buddhist monk, is still plagued by sleeplessness and flashbacks, despite years of meditation. “They haven’t gone away, but my relationship to them has changed,” says Thomas. “They don’t control my life in the same way. Being able to breathe, to slow down, buys me some time. I invite myself to just hold these feelings, to just sit with them, and when they start to come, I recognize them much sooner.”
One of the most vexing unanswered questions is how much if any reliving of trauma is necessary for healing. Too hasty and too vigorous digging can have disastrous results: one study found that alcoholic veterans who had achieved sobriety were more likely than controls to return to heavy drinking if they underwent exposure therapy, which requires repeatedly remembering traumatic memories. Incest clients have been known to arrive at sessions, pour out accounts of horrific childhood molestation and then go home to drink, attempt suicide or mutilate themselves. Yet, some level of emotional arousal may be required for healing. The favored behavioral treatments for veterans with PTSD exposure, flooding and systematic desensitization all require remembering traumatic events repeatedly until the conditioned response to them is extinguished. The handful of outcome studies of PTSD therapy suggests that exposure works when paired with some form of new learning, such as an understanding that one was not to blame for the tragedy or that the world is not always as dangerous as it was then. Many veterans, however, find exposure therapy so aversive that they drop out of treatment.
Neuroscience has no answers to such quandaries so far. Therapists trying to familiarize themselves with the new paradigm without throwing out the intuitive wisdom of the old will find themselves caught between vocabularies and metaphors. The bridge between the symbolic and the neurological worlds is only half-built. Many of the psychiatrists conducting the leading-edge neuroscience research are also clinicians, and even for them the language of neurology goes only so far.
When asked about the clinical implications of their work, talk of hippocam-pal volume and glucocorticoid levels and biological substrates falls away, and the terminology of the clinical world returns. Neuroscientists with psychodynamic training speak with great conviction about the healing value of putting experience into a personal narrative. Cognitive-behavioral psychologists talk with equal conviction about the virtues of exposure and correcting misapprehensions. They fall back on what they knew before the black box of the brain began to open; sometimes, they seem a little like Wile E. Coyote suddenly realizing that he has walked off a cliff and is sauntering along in midair.
But perhaps that’s inevitable. People live in many worlds and use many languages to describe their places in them. PTSD, like everything else in life, is multifactorial, and will demand multiple interventions even after the biological part of the story is fully told. Given the complexity of the interplay of hormonal systems involved, its unlikely that a single magic bullet biochemical or psychosocial will ever eliminate PTSD. In the meantime, PTSD treatment will remain an extreme example of a universal human struggle: to master social, familial, biological and practical givens while recognizing that the neurobiolog-cal inner cascade and the outer social cascade continually inform and impinge upon each other. Perhaps the new neuroscience will encourage PTSD sufferers to treat themselves with more compassion, to understand how much lies outside conscious mental control and to develop an observer self that may help them take a breath before they fly off the handle.
Although the neuroscience of PTSD is daunting and somewhat depressing, it will plot directions for future research and clinical work. At the very least, it maps out two challenges for working psychotherapists. The first is to give more weight to the body’s physiology and to have an open mind about the contributions of a new, more sophisticated version of biological psychiatry. The second is to continue to explore the pure power of human contact to heal disregulated brain chemistry.
“We already know to what degree matter can alter mind,” is the way van der Kolk puts it. “The great challenge now is to use psychological tools to re-regulate people’s biological systems to show to what degree mind can alter matter.”
©2006 Katy Butler. All Rights Reserved. Not to be reprinted without permission.