“I don’t think I’ve ever read a book that paints such a complex and accurate landscape of what it is like to live with the legacy of trauma as this book does, while offering a comprehensive approach to healing.” –from the foreword by Bessel van der Kolk
A pioneering researcher gives us a new understanding of stress and trauma, as well as the tools to heal and thrive
Stress is our internal response to an experience that our brain perceives as threatening or challenging. Trauma is our response to an experience in which we feel powerless or lacking agency. Until now, researchers have treated these conditions as different, but they actually lie along a continuum. Dr. Elizabeth Stanley explains the significance of this continuum, how it affects our resilience in the face of challenge, and why an event that’s stressful for one person can be traumatizing for another.
This groundbreaking book examines the cultural norms that impede resilience in America, especially our collective tendency to disconnect stress from its potentially extreme consequences and override our need to recover. It explains the science of how to direct our attention to perform under stress and recover from trauma.
With training, we can access agency, even in extreme-stress environments. In fact, any maladaptive behavior or response conditioned through stress or trauma can, with intentionality and understanding, be reconditioned and healed. The key is to use strategies that access not just the thinking brain but also the survival brain.
By directing our attention in particular ways, we can widen the window within which our thinking brain and survival brain work together cooperatively. When we use awareness to regulate our biology this way, we can access our best, uniquely human qualities: our compassion, courage, curiosity, creativity, and connection with others. By building our resilience, we can train ourselves to make wise decisions and access choice–even during times of incredible stress, uncertainty, and change.
With stories from men and women Dr. Stanley has trained in settings as varied as military bases, healthcare facilities, and Capitol Hill, as well as her own striking experiences with stress and trauma, she gives readers hands-on strategies they can use themselves, whether they want to perform under pressure or heal from traumatic experience, while at the same time pointing our understanding in a new direction.
” Widen the Window is a comprehensive overview of stress and trauma, responses to it, and tools for healing and thriving. It’s not only for those in high-intensity work, but for everyone.” –Mindful Magazine
“This high-octane book could give you back your life. When we experience dysregulation, we have to reclaim our core capacities and develop them to serve our health, performance, and quality of life. Liz Stanley expertly maps an inner adventure through training our attention and ability to stay grounded in highly stressful situations. Time to live the life that is yours to live, one hundred percent.”— Jon Kabat-Zinn, Ph.D., author of Full Catastrophe Livingand creator of mindfulness-based stress reduction (MBSR)
“Our ‘suck it up and drive on’ culture has seriously impaired both our country and ourselves. It is imperative that we find a way to heal so that we don’t just survive but thrive. Liz Stanley give us the tools we need to create a better way of being, both individually and collectively. This book is a must-read for everyone who cares about our future.” — Congressman Tim Ryan, author of Healing America
“Our frantic culture generates trauma and stress that limit our capacity to live full and healthy lives. Widen The Window is a clearly written guide into our shocked physiology and a time-tested, practical method of regaining power over it, through awareness and attention.” —Gabor Maté M.D., author of When The Body Says No: Exploring The Stress-Disease Connection and In The Realm of Hungry Ghosts
“Like all things in life, it is how we manage—not just cope—with the pressures that envelop us all. Dr. Stanley has written an exceptional book of understanding, relating to and controlling stress and trauma.” —Chuck Hagel, 24th Secretary of Defense
About the Author
Elizabeth A. Stanley, PhD, is an associate professor of security studies at Georgetown University. She is the creator of Mindfulness-Based Mind Fitness Training (MMFT)®, taught to thousands in civilian and military high-stress environments. MMFT® research has been featured on 60 Minutes, ABC Evening News, NPR, and inTime magazine and many other media outlets. An award-winning author and U.S. Army veteran with service in Asia and Europe, she holds degrees from Yale, Harvard, and MIT. She’s also is a certified practitioner of Somatic Experiencing, a body-based trauma therapy.
In the summer of 2002, I worked incessantly to complete my Ph.D. dissertation on deadline. My faculty advisors at Harvard had already set my defense date so I could begin a prestigious fellowship starting in September. Everything seemed on track for a successful start to my academic career. Well, everything except for that one minor detail I’d neglected to share with my committee: Of the ten chapters and appendixes in my dissertation, I still needed to write seven of them.
In mid-June, I finally quit my full-time job to finish it. Early one August morning, after weeks of pushing myself to write sixteen hours a day without any days off, I carried my coffee mug into my study and turned on the computer. I opened my draft, reread the paragraph I’d finished late the night before, and started writing.
I was halfway through my first sentence when I puked all over the keyboard.
After running for paper towels to clean up my mess, it quickly became apparent that my vomit was permanently lodged under some of the keys. (The space bar was especially hard hit.) No amount of wiping it up could rectify the situation.
I brushed my teeth, washed my spew-speckled arms, and found my shoes and my wallet. Outside, I threw the keyboard into the trash can and climbed into the car. I drove to a shopping center and parked. It was seven fifty in the morning. When Staples opened at eight, I was the first one in the door.
New keyboard in hand, I was back at my computer finishing that first sentence of the morning by eight thirty.
SUCK IT UP AND DRIVE ON To be clear, I didn’t have a stomach bug or food poisoning. Rather, I’d been living for years with relentless bouts of nausea and lack of appetite.
Here’s a snapshot of me-and my overscheduled, extremely compartmentalized, and rigorously well-organized life-circa 2002: I was compulsively driven to achieve. I was addicted to demanding workouts, to maintain my body’s physical prowess. I was incessantly cheerful at work, while experiencing radical mood swings and crying jags at home. My mind raced with thoughts about my never-ending to-do list and “what-if” worst-case scenarios. My body was hypervigilant and tense from projecting an external aura of self-confidence while internally bracing against when the other shoe would drop. I was severely claustrophobic and hypersensitive to crowds, traffic, loud noises, and bright lights. Between insomnia and terrible nightmares, I rarely slept.
In retrospect, I see that the message that my body transmitted to me that morning was clever, dramatic, and spot on: At that moment, I was literally sick of this (expletive here) project and I desperately needed a break.
However, I didn’t have the time to think about that right then. I had a dissertation to finish, and I was running out of time.
And so I overrode this rather extreme signal from my body and just kept writing.
I delivered my completed manuscript by deadline. I successfully defended my Ph.D. dissertation and started my fellowship on schedule that fall.
I was also an anxious, workaholic wreck.
So how did I get here? How did I end up literally puking out a Harvard Ph.D. dissertation? Why did my body present me with such an extreme signal that morning? And why was my (mostly unconscious) default response simply to ignore and override that signal and keep pushing?
In many ways, finding answers to these questions has motivated my work over the last fifteen years. Perhaps not surprising, since I’m a political scientist who teaches about international security, in 2002 I made sense of the Keyboard Incident as my body waging an insurgency against my mind’s drive to perform and succeed. Of course, inherent in this explanation is its own recommended cure: counterinsurgency. In other words, just dig in, access deep wells of willpower and determination, and power through. Otherwise, it’s just mental weakness and laziness, right?
For many decades, I considered my capacity to ignore and override my body and my emotions in this way to be a good thing-a sign of strength, self-discipline, and determination. And from one perspective, it was. But as I’ll explain in this book, from another perspective, this default strategy was actually undermining my performance and well-being.
Of course, I’m not alone in this conditioning. It’s a common way of relating to experience that many people call “suck it up and drive on” or “powering through.” Contemporary American culture in general-and warrior culture in particular-prizes this approach to life. We’ve all heard and perhaps even admire stories of people overcoming extreme adversity or simply pushing through challenges and setbacks with perseverance to succeed. And, as I’ll explain shortly, many conveniences of our modern world exist almost entirely to facilitate our suck-it-up-and-drive-on addictions. Nonetheless, although the self-determination to power through stressors in this way can be admirable-and during certain immediate life-or-death situations is absolutely critical for survival-this way of approaching life can have some dark consequences over the longer term.
In my life, my habitual reliance on suck it up and drive on not only allowed me to meet my dissertation deadline. To name just a few other examples, it also allowed me to achieve a top-5-percent ranking at a physically demanding military qualification course while still recovering from a massive injury to my Achilles tendon; run a marathon in just over four hours (in barely-above-freezing rain, of course!) seven days after accidentally impaling the claw end of a hammer one inch into my right heel; and attain basic proficiency in a new foreign language while working 120-hour weeks before my U.S. Army unit deployed to Bosnia after the 1995 Dayton Peace Accords.
At the same time, I lived for many years an awkward double life: the outward appearance of success (as our society usually defines it) and the inner sense that I was a failure, struggling secretly with symptoms and barely holding it together. As willful as I was, it would eventually take losing my eyesight and leaving a marriage to finally understand that there’s an easier way. This book is about how I healed that division in myself-and how you can do the same.
THE GOALS OF THIS BOOK In the course of my personal quest to understand my self-described mind-body insurgency and the devastating effects it was having on my life, I detoured into a parallel professional quest to understand how life adversity, prolonged stress exposure, and trauma affect us-and influence our decision making and performance. Along the way, I created a resilience training program for people working in high-stress environments, called Mindfulness-based Mind Fitness Training (MMFT), about which I’ll say much more later in the book. I also collaborated with neuroscientists and stress researchers to test MMFT’s efficacy among troops as they prepared to deploy to combat, through four research studies funded by the U.S. Department of Defense and other foundations. In addition to training and certifying others to teach MMFT, I’ve taught MMFT (pronounced “M-fit”) to hundreds of troops before their combat deployments to Iraq and Afghanistan, as well as many other military leaders, service-members, and veterans. I’ve also taught MMFT concepts and skills to thousands of individuals in other high-stress environments, including healthcare providers, intelligence agents, firefighters, police officers and other law enforcement agents, lawyers, diplomats, social workers, students, teachers and academics, inmates at a maximum-security prison, disaster relief workers, athletes, members of Congress, senior government officials, and corporate executives.
On my journey to wholeness, I engaged in many different tools and therapeutic techniques, including several kinds of therapy, yoga, meditation, and shamanic and mind training. Since late 2002, I’ve maintained a daily mindfulness practice. I’ve also completed many long, intensive periods of silent practice, including time as a Buddhist nun at a monastery in Burma. Finally, I sought several years of clinical training and supervision, culminating with certification as a Somatic Experiencing practitioner, perhaps the best known of the body-based trauma therapies.
Despite this wealth of experience, I often found that no one could explain to me, concisely and coherently, how or why particular techniques worked (or didn’t)-or why my responses to them often differed significantly from others’.
Thus, my original intention in creating MMFT-and the first goal of this book-is to share the road map that I discovered with you. I aim to share some of the core scientific and intellectual concepts that undergird MMFT. To be clear, however, this book is not the MMFT course-it covers additional topics not addressed directly in MMFT, but also by necessity it can’t replicate all of MMFT’s experiential practices. I’ll draw on recent scientific findings to explain how to train yourself to be more resilient before, during, and after stressful and traumatic events. My hope is that after finishing this book, you’ll understand your own neurobiology better and thereby make better decisions-without experiencing unnecessary anxiety and without criticizing your imperfections or choices along the way.
Part of why my journey took years is that there is no quick-fix way to achieve these transformations. Rewiring the brain and body to improve our performance and build resilience requires an integrated training regimen and consistent practice over time. Just as muscle growth and improved cardiovascular functioning require months of consistent physical exercise, the benefits that can result from mind fitness training require consistent practice over time, too. With consistent practice, we usually see some shifts relatively quickly, while others take longer to manifest. However, you can’t just achieve them from reading this book. Thus, I don’t want you to take my word for anything in this book-I want you to practice and observe these dynamics in your own life. Rewiring the brain and body is an embodied, experiential process. These are basic laws of nature; there are no shortcuts.
This book draws on a lot of evidence from high-stress occupations, such as the military, firefighters, police, medical personnel, and other first responders. That’s because much of the peer-reviewed empirical research about stress, resilience, performance, and decision making has been conducted with these groups. Likewise, at other points the book may seem a little heavy with clinical findings about people who’ve experienced abuse or trauma. Nonetheless, especially if you don’t work in a high-stress profession or don’t believe you have a history of trauma-and may not feel particularly connected to either category-I want to emphasize: If you are a human being living in today’s world, this book still pertains to you. Scientific evidence about how our minds and bodies work, and how we make decisions before, during, and after stress and trauma, applies to everyone.
However, I don’t just want this book to help you understand and manage your stress better. My second goal is to engage you in a wider reflection about the way that we, individually and collectively, approach stress and trauma. As I’ve noted, the mind-body insurgency I experienced in 2002 was an outgrowth of my conditioning-and thus, it embodied some deep familial, societal, and cultural beliefs, values, coping strategies, and habits. In this book, I hope to expose such underlying structures, which aggravate our stress and trauma and undermine our performance and well-being. These underlying structures not only affect the strategies we individually rely on to cope with our stress-or not. They also affect the way we interact in our families and relationships; nurture and educate our children; train, incentivize, and reward our employees; and organize our companies and public institutions. They even affect the way our nation interacts with the rest of the world.
Are these strategies aligned with and capable of delivering the desired results? Our culture seems to want it both ways: We want better performance, resilience, and even happiness, yet we don’t want to examine the wider blind spots that impede their development. Some of this wanting it both ways manifests in how many of us feel like we don’t have choice-that we’re powerless in the face of job stress, health problems, rapid technological change, or toxicity in the news. Yet it’s possible to change how we interact with these things, to relate to them from a more empowered stance. Ultimately, to feel like we have agency requires clear intentions, consistent practice of the skills that help us develop awareness and self-regulation, and deliberate choices about how we prioritize different aspects of our lives.
Can the bacterial community that lives in your gut actually be related to psychiatric illnesses such as schizophrenia and bipolar disorder? Research on the human microbiome and its effects on health and illness has exploded into the worlds of medicine and research. It is increasingly clear that the microorganisms in the human intestinal tract, and the genes produced by all of these microscopic living things, play critical roles in an individual’s patterns of overall wellness — far beyond helping us digest food effectively.
Microbiota and Microbiome Defined
Microbiota is the ecological community of microorganisms (mostly bacteria, but also fungi, viruses, and so on) that live in a particular location, such as your gut. Microbiomerefers collectively to the genes harbored in these microorganisms. Researchers must understand the patterns of both the organisms and the genes to help clarify the roles these microscopic creatures play in the body’s health and function. So, if you read something about the microbiome that’s about only the bacteria and not the genes, you know it is an incomplete discussion. Also, while most of the discussions are about the gut microbiota and microbiome, humans actually have colonies of microorganisms living in other areas in and on their bodies, including their skin, reproductive tract, and the mouth and throat (which are technically part of the gut but sometimes are not thought of in that way).
A study in the journal Brain, Behavior, Immunology (May 2017), entitled “The microbiome, immunity, and schizophrenia and bipolar disorder,” summarizes some of the current research looking at the microbiome as it relates to schizophrenia and bipolar disorder. The article reports that many studies in animal models have shown that the gut microbiome could affect thinking and behavior through effects on the immune system. Some human studies have shown that people with psychiatric conditions took antibiotics more frequently than people without these disorders. Humans take antibiotics to kill off unwanted bacterial infections, but these medications also kill off some of the microbiota, changing the person’s microbiome. The question that comes up then is whether these microbiome changes were related to the development of the psychiatric conditions. This article also points to studies that found different microbiota in the mouths and throats (oro-pharyngeal microbiota) of people with schizophrenia compared to those without.
Babies are born with “sterile” guts; they don’t have any gut microbiota. But in the birth process, microorganisms colonize the baby’s mouth and intestine, starting off their process of building a microbiome that eventually looks like an adult’s. Many researchers are exploring how the developing microbiome might affect the developing brain and nervous system. While it seems clear that there are effects, the exact processes mediating the effects and what exactly gets changed or affected remains very unclear. While the immune system is thought to be one pathway, other mechanisms are also being investigated.
Many other areas of research show promising results when looking at the microbiota, microbiome, and illness. Autism researchers are looking at the “gut-microbiome-brain” connection, and there are strong indicators that the microbiota and microbiome have some relationship to autism. Obesity — not a mental illness but of concern to so many people living with mental illness — has been shown to have some very interesting connections to the microbiota in mouse studies. Changing the patterns of bacteria in mouse guts can transform the mouse from lean to obese and vice versa without changing diets. A study from China last month in the World Journal of Gastroenterologyreports a case of a 20-year-old with Crohn’s disease and seizures. They treated her with fecal microbiota transplantation — giving her the gut microbiota of a healthy person — and her gastrointestinal symptoms and seizures improved significantly.
The potential benefits to understanding how the microbiota and microbiome interact with the brain and central nervous system could be enormous. Understanding microorganism mechanisms that increase the likelihood of mental illness such as bipolar disorder or neurodevelopmental condition like autism would make room to build new interventions that target those mechanisms. The research in these areas is still in early stages, and there is much more to do, but this is an intriguing and promising story in the quest to understand and treat disorders of the brain.
Scientists discover a brain process that explains why some fear-related memories may not be accessible to traumatized patients. TraumaAndDissociation, CC by 2.0
While some victims of trauma too easily remember what causes their pain, other victims suffer tremendous anxiety for no apparent reason whenever they’re in some innocuous-seeming place — a room in their grandparents’ house, for example. Some mysterious event clearly happened there, yet no memory exists. In a new study (conducted on mice), scientists discovered a brain process that explains why some fear-related memories may not be available.
“Distinct neurobiological mechanisms can explain why some trauma victims go on to remember and re-experience their trauma, whereas [other victims] develop dissociative amnesia (an inability to consciously access a stored memory),” Dr. Jelena Radulovic, principal investigator and a professor at Northwestern University Feinberg School of Medicine, toldMedical Daily in an email.
Scientists have long understood that there’s more than one pathway through the brain to the storage closet of memory. Now, Radulovic and her colleagues track a unique trail directly related to trauma. In fact, the microRNA-GABA pathway they describe in their new study may also indicate how susceptible each of us is to developing amnesia after a traumatic event.
They discovered this pathway by exploring a special phenomenon of learning.
What Influences Memory?
Learning is a state-dependent process, which means that when we learn something new in a particular situation or state of consciousness, we’re able to remember it best when we place ourselves back in the original circumstance or state of mind. Students, then, who learn information in one room will get higher scores if they are tested in the same room. Not only place, but time of day as well as common drugs also influence memory abilities. If students learn something while drinking coffee, for instance, they will remember it best when they return to their original caffeinated state.
Based on this phenomenon, various researchers have used drugs to try and access hidden memories. But while some pharmaceuticals may return the brain to the state of consciousness that occurred during encoding — the first step in memory storage — they haven’t done well in excavating traumatic memories. A drug targeting different processes in the brain, then, would be necessary for fear-based recall.
So, Radulovic and her colleagues focused on two amino acids in the brain: glutamate and GABA. These work in tandem to control levels of excitation and inhibition in the brain, and, under normal conditions, remain balanced. Hyper-arousal, however, which occurs when we are terrified, causes glutamate to surge.
Glutamate, is known as the excitable amino acid; it’s also the primary chemical that helps store memories across distributed brain networks. GABA, on the other hand, is calming and partly works by blocking glutamate and its excitable actions. Synaptic GABA receptors, in particular, will balance glutamate receptors in the presence of stress. Yet, extra-synaptic GABA receptors also exist. These work independently, responding to levels of a variety of neurochemicals, including sex hormones and micro RNAs.
Between the drugs amobarbital and diazepam, only amobarbital, which binds to all GABA receptors is able to stimulate memory recall — diazepam is ineffective, due to the fact it only binds to synaptic GABA receptors. Knowing this, Radulovic and her colleagues hypothesized the ability to remember stressful experiences might be mediated by the extra-synaptic GABA receptors.
For its experiment, the research team injected the mice with gaboxadol, a drug that stimulates extra-synaptic GABA receptors. Next, they placed the mice in a box and gave them an electric shock. When the mice returned to the same box the next day, they moved about freely and without fear. Clearly, the rodents did not remember the electric shock.
Then, the scientists injected the mice with the drug once again and returned them to the box. This time, the rodents froze in anticipation of another shock.
Rerouting Painful Memories
When extra-synaptic GABA receptors were activated by a drug, the researchers said, the brain used completely different molecular pathways and neuronal circuits to store the memory. The brain rerouted the memory so that it couldn’t be accessed. The researchers say their findings imply that in response to trauma, some people will not activate the glutamate system but instead the extra-synaptic GABA system.
This system is regulated by a small microRNA: miR-33. Some patients with psychiatric illnesses have different levels of miR-33 compared to healthy individuals.
The power of any memory lies, to a large extent, in the amount of processors within the cells creating a pathway through the brain, explained Dr. Vladimir Jovasevic, lead study author and a former postdoc in Radulovic’s lab.
“The role of microRNAs is to fine-tune the amount of the processors, so they can function at optimal level,” said Jovasevic, and “miR-33 sets the optimal amount of processors involved in state-dependent learning.” But when levels of miR-33 change, this “results in an increased predisposition to psychiatric disorders caused by improper processing of state-dependent memories.”
Evidence from the new study, Radulovic and Jovasevic said, may lead to new treatments for patients with psychiatric disorders who cannot recover unless they gain conscious access to the memory of what caused their trauma.
Source: Jovasevic V, Corcoran KA, Leaderbrand K, et al. GABAergic mechanisms regulated by miR-33 encode state-dependent fear. Nature Neuroscience. 2015.
In my mid-20s, at the beginning of my training as a clinical psychologist, I was placed on a psychiatric day treatment ward in one of the poorer parts of Boston. One day, the experienced therapist with whom I led a men’s group was sick, and I was called on to do the group by myself. A ball of nerves, I decided to ask the men about their ancestry (with the helpful presence of a globe in the room) rather than risk silence. I briefly spoke of my Russian and Eastern European great-grandparents to set the tone and then spoke with each man in turn. After a few minutes of this exercise, there was a pause. A fellow from across the room looked at me and said softly, “You think you’re better than us, don’t you? You think this could never happen to you.”
I was stunned. Somehow I stammered a denial, but of course he was right. Perhaps I didn’t think I was better than them, but I certainly thought I was different from them. Like most of us in Western societies, I had grown up believing that psychiatric disorders were illnesses—diseases like any other—and there had been nothing in my training until then to convince me otherwise.
But learning about trauma, dissociation, and attachment in the ensuing decades has changed my mind. And I am not the only one.
PARADIGMS IN CONFLICT
Over the past several decades, the study of schizophrenia and the study of the dissociative disorders have been dominated by opposing paradigms. For schizophrenia, the assumption of a genetic basis and biological causation has reigned supreme. Adverse childhood experiences are viewed as irrelevant at best and adult stressful or traumatic experiences as only “releasing” underlying disease mechanisms. Symptoms are considered meaningless—unrelated to a person’s life circumstances—and psychotherapeutic approaches, when used at all, are limited to supporting medical interventions. In diagnosing schizophrenia for clinical or research purposes, posttraumatic and dissociative disorders are rarely considered or ruled out; indeed, in adherents to this paradigm, posttraumatic disorders are frequently disdained, discredited, or simply ignored.
In contrast, the overriding paradigm for the study of dissociative disorders has focused almost exclusively on life events—traumatic or otherwise—that are assumed to be meaningfully related to the symptoms a person experiences. A wide range of psychotherapeutic approaches to treatment are supported and advocated, whereas most medical interventions are viewed as anathema. At the same time, many trauma-oriented clinicians and researchers think of schizophrenia only as something dissociative disorders are not—but are often confused with; schizophrenia’s validity as a biologically based entity is rarely questioned.
Consider how these two paradigms deal with auditory verbal hallucinations. To persons adhering to the dominant biological paradigm (or “medical model”), voices are psychotic symptoms to be treated with medications or coped with using distraction techniques. As Colin Ross (2008Ross, C. A.2008. “Dissociative schizophrenia”. In Psychosis, trauma and dissociation: Emerging perspectives on severe psychopathology, Edited by: Moskowitz, A., Schäfer, I. and Dorahy, M. J.281–294. London, , England: Wiley.[Google Scholar]) put it, from this perspective the notion of talking with someone’s voices would be as absurd as “asking a patient’s knee a question” (p. 284). In contrast, in a trauma/dissociation paradigm, voices are split-off parts of the personality that are ignored at one’s own peril—acknowledging and engaging these disowned parts, though often challenging, is typically advocated. The schizophrenia field views voices as biologically generated indications of a brain disorder, whereas the dissociation field views them as psychological indications of unresolved trauma or loss. Two more disparate perspectives cannot be imagined. Currently, these fields eye each other with considerable suspicion and, to a large extent, do not speak the same language or experience the world in the same way.
EUGEN BLEULER: THE MARRIAGE OF DISSOCIATION AND SCHIZOPHRENIA
But it was not always this way. When Eugen Bleuler published his Dementia Praecox oder Gruppe der Schizophrenien (Dementia Praecox or the Group of Schizophrenias) 100 years ago, the construct of schizophrenia was infused with dissociative concepts (Moskowitz, 2008Moskowitz, A.2008. “Association and dissociation in the historical concept of schizophrenia”. In Psychosis, trauma and dissociation: Emerging perspectives on severe psychopathology, Edited by: Moskowitz, A., Schäfer, I. and Dorahy, M. J.35–49. London, , England: Wiley.[Google Scholar]; Moskowitz & Heim, 2011Moskowitz, A. and Heim, G.in press. “Affect, dissociation, psychosis: Essential components of the historical concept of schizophrenia”. In Psychosis and emotion: The role of emotions in understanding psychosis, therapy and recovery, Edited by: Gumley, A., Gilham, A., Taylor, K. and Schwannauer, M.London, , England: Routledge.[Google Scholar]). While insisting on an organic basis for the disorder, Bleuler recognized the symptoms his patients described as meaningfully related to their life experiences and used hypnotherapy and psychotherapy in his clinical work. He justified changing the name of the disorder largely on the basis that the “splitting” of the “different psychic functions” was central to its pathology (Bleuler, 1911/1950Bleuler, E.1950. Dementia praecox or the group of schizophrenias, Edited by: Zinkin, J.New York, NY: International Universities Press. Original work published 1911[Google Scholar], p. 8). Bleuler’s 1911Moskowitz, A. and Heim, G.2011. Eugen Bleuler’s Dementia praecox or the group of schizophrenias (1911): A centenary appreciation and reconsideration. Schizophrenia Bulletin, 37(3): 471–479.[Google Scholar]“definition” of schizophrenia reads almost as a calling card for dissociative disorders:
If the disease is marked, the personality loses its unity; at different times different psychic complexes seem to represent the personality … one set of complexes dominates the personality for a time, while other groups of ideas or drives are “split off” and seem either partly or completely impotent. (p. 9)
The profoundly dissociative nature of Bleuler’s concept of schizophrenia has been ignored for many decades but should be apparent to any unbiased reader, as has been recognized by Colin Ross (2004Ross, C. A.2004. Schizophrenia: Innovations in diagnosis and treatment, New York, NY: Haworth Press.[Google Scholar]) and myself (Moskowitz, 2008Moskowitz, A.2008. “Association and dissociation in the historical concept of schizophrenia”. In Psychosis, trauma and dissociation: Emerging perspectives on severe psychopathology, Edited by: Moskowitz, A., Schäfer, I. and Dorahy, M. J.35–49. London, , England: Wiley.[Google Scholar]; Moskowitz & Heim, in press).
However, Bleuler’s ideas about schizophrenia have little currency in today’s nosological world; all but the name has been jettisoned, and even that has been retained with considerable squeamishness—requiring constant vigilance against its interpretation as “split personality.” Instead, the architects of our current diagnostic system harked back to Bleuler’s predecessor, Emil Kraepelin, for inspiration.
EMIL KRAEPELIN, TAXONOMIES, AND GENERAL PARESIS
Despite Kraepelin’s experimental psychology pedigree (he studied with Wilhelm Wundt early in his career), his ideas on Dementia Praecox were far less informed by psychology than those of Bleuler (who used Jung’s word association experiments to aid his understanding), and he saw concepts of dissociation as irrelevant to diagnostic conceptualization. Rather, Kraepelin’s approach to parsing mental disorders was strongly influenced by biological classifications, such as Linnæus’s taxonomy of plants and the system developed by his own esteemed older brother, the biologist Karl Kraepelin (Weber & Engstrom, 1997Weber, M. M. and Engstrom, E. J.1997. Kraepelin’s “diagnostic cards”: The confluence of clinical research and preconceived categories. History of Psychiatry, 8: 375–385.[Google Scholar]). In addition, the model on which Kraepelin based his concept of Dementia Praecox was General Paresis of the Insane—sometimes called Dementia Paralytica. General Paresis was a terminal condition that combined psychotic symptoms with paralysis and ultimately death and was widespread in Europe during the early part of the 19th century. The triumphant linking of its symptoms with a brain disorder caused by late-stage syphilitic infections in the mid-19th century clearly provided Kraepelin with a template or paradigm—a “model disease entity”—for mental disorders in general and dementia praecox in particular (Jablensky, 1995Jablensky, A.1995. Kraepelin’s legacy: Paradigm or pitfall for modern psychiatry?. European Archives of Psychiatry and Clinical Neuroscience, 245: 186–188.[Google Scholar], p. 186).
THE NEO-KRAEPELINIAN PARADIGM OF MENTAL DISORDERS
The example of General Paresis, mental disorders were brain disorders but that any classification of psychopathology was best pursued through identifying brain pathology, not only drove Kraepelin’s typology but also still underpins that of the current diagnostic systems influenced by his thinking—the Diagnostic and Statistical Manual of Mental Disorders(3rd ed. [DSM–III]), the International Classification of Diseases–9, and their related progeny (Jablensky, 2007Jablensky, A.2007. Living in a Kraepelinian world: Kraepelin’s impact on modern psychiatry. History of Psychiatry, 18: 381–388.[Google Scholar]). For the past three or four decades, the classification of mental disorders has been dominated by this approach, which came out of a group of primarily American psychiatrists self-identified as neo-Kraepelinian (frequently referred to as a movement or even a revolution).
As the neo-Kraepelinians set about revising the psychiatric diagnostic system in the 1970s, and reached their goal with the 1980 publication of the DSM–III, they were ostensibly creating an atheoretical system with improved reliability over its precursors. But in reality, they were clearly motivated by the belief that these conditions were medical disorders like any other; indeed, in a publication from that time, two prominent researchers spoke of “coveting” for schizophrenia the solid genetic grounding of “pellagra, paresis, tuberculosis, polio, and PKU [phenylketonuria]” (Gottesman & Shields, 1973Gottesman, I. I. and Shields, J.1973. Genetic theorizing and schizophrenia. British Journal of Psychiatry, 122: 15–30.[Google Scholar], p. 15).
A fundamental task for the neo-Kraepelinians was to shore up the distinction between schizophrenia and manic depression, a distinction that had been blurred by Bleuler’s broad category. They accomplished this primarily by strongly emphasizing specific psychotic symptoms in the diagnostic criteria for schizophrenia (particular auditory hallucinations and delusions proposed by Kurt Schneider—so-called first rank symptoms) and by undermining the validity of the schizoaffective disorder category in a number of ways (Moskowitz & Heim, in press-a). The Kraepelinian dichotomy of schizophrenia and bipolar disorder has been explicitly seen as providing the foundation for a biologically based nosology; indeed, challenges to the clear differentiation of schizophrenia and bipolar disorder are often viewed as undermining the validity of the entire diagnostic system (Kendell, 1987Kendell, R. E.1987. Diagnosis and classification of functional psychoses. British Medical Bulletin, 43: 499–513.[Google Scholar]). In addition, the neo-Kraepelinians have articulated a number of more general assumptions, including (a) that mental disorders are discrete from one another and from “normality” and (b) that advances in understanding mental disorders will come primarily from focusing on neurobiology (Klerman, 1978Klerman, G. L.1978. “The evolution of a scientific nosology”. In Schizophrenia: science and practice, Edited by: Shersow, J. C.91–121. Cambridge, MA: Harvard University Press.[Google Scholar]). This level of domination over research and practice (for example, DSM–IV diagnoses are required for insurance payments and frequently for journal article acceptance) clearly constitutes what Thomas Kuhn termed a scientific paradigm.
PARADIGMS AND SCIENTIFIC REVOLUTIONS
According to Kuhn (1970Kuhn, T. S.1970. The structure of scientific revolutions, 2nd, Chicago, IL: University of Chicago Press.[Google Scholar]), in The Structure of Scientific Revolutions, the idea that science advances in a linear fashion with knowledge continually accruing so that “reality” or “truth” is more and more closely approximated over time is a myth. Rather, he argued, a field advances under the influence of a dominant paradigm, meaning both a particular past scientific achievement held up as a model or exemplar (as in the case of General Paresis and psychopathology) and the generally accepted beliefs and attitudes of a particular scientific community. A paradigm exerts an organizing influence on a field and guides research, determining to a large extent what types of research questions are considered legitimate and what sorts of answers are considered acceptable.
Kuhn (1970Kuhn, T. S.1970. The structure of scientific revolutions, 2nd, Chicago, IL: University of Chicago Press.[Google Scholar]) argued that paradigms change and a scientific revolution ensues when three conditions are met: (a) a period of crisis develops in which the paradigm fails to adequately answer questions considered fundamental; (b) serious “anomalies” occur in which phenomena not clearly compatible with the paradigm are observed; and, importantly (c) a suitable alternative paradigm that explains many of the previous findings and at least some of the observed anomalies comes to light. Kuhn saw scientific revolutions as taking time to resolve; he argued that changing such strongly held beliefs involved a process of persuasion and fundamental reorganization not unlike that of religious conversion: “Conversions will occur a few at a time until, after the last holdouts have died, the whole profession will again be practicing under a single, but now different paradigm” (Kuhn, 1970Kuhn, T. S.1970. The structure of scientific revolutions, 2nd, Chicago, IL: University of Chicago Press.[Google Scholar], p. 152).
Since the publication of the DSM–III in 1980, the ascendance of the neo-Kraepelinianparadigm in the psychiatric world has been paramount. It has driven our view of schizophrenia and marginalized acceptance of the dissociative disorders and posttraumatic stress disorder (PTSD). However, this paradigm is now under threat from many quarters—from within its ranks as well as from outside—and there is good reason to view it as a paradigm in crisis.
FAILURES OF THE NEO-KRAEPELINIAN PARADIGM
Evidence for fundamental tenets of the neo-Kraepelinian paradigm—that there are clear genetic or biological bases for schizophrenia and other mental disorders and that mental disorders are discrete from one another and from normal experiences—have not been supported.
Comorbidity of diagnoses, incompatible with viewing diagnoses as discrete categories, is rampant in the DSM–IV system and typically viewed as a major problem. Psychotic symptoms are now recognized as common to many disorders other than schizophrenia, and their presence in a significant portion of the community with no diagnosed mental disorder firmly suggests that the line between “normality” and “pathology” is not hard and fast (Van Os, Linscott, Myin-Germeys, Delespaul, & Krabbendam, 2008Van Os, J., Linscott, R. J., Myin-Germeys, I., Delespaul, P. and Krabbendam, L.2008. A systematic review and meta-analysis of the psychosis continuum: Evidence for a psychosis proneness—persistence—impairment model of psychotic disorder. Psychological Medicine, 39: 179–195.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]). In addition, evidence for the validity of schizoaffective disorder, a fundamental challenge to the Kraepelinian dichotomy, has accumulated over the years. The demonstrated existence of persons with prominent schizophrenic and affective symptoms undermines the core distinction between schizophrenia and bipolar disorder and provides an argument for viewing even severe psychopathology as a dimension or series of dimensions instead of as categories. Finally, the abject failure of genetic-based research to find any strong link with schizophrenia or bipolar disorder provides a further anomaly for the neo-Kraepelinianparadigm to explain or attempt to ignore (if anything, the genetic evidence points to a “shared neurobiology across the two disorders,” Thaker, 2008Thaker, G.2008. Psychosis endophenotypes in schizophrenia and bipolar disorder. Schizophrenia Bulletin, 34: 720–721.[Google Scholar], p. 720).
All of this is taking its toll on the medical model. As the neo-Kraepelinian edifice begins to crumble, adherents resort to stronger and stronger biological language, as though words such as neuropsychiatry and endophenotypes have the power to restore its once shining façade. The emphasis on endophenotypes is particularly telling, as this concept involves exploring putative underlying biological variables that may have only an indirectrelationship to the signs and symptoms of mental disorders. For example, a recent large-scale twin and family study focused on apparent genetic impairments in memory and intelligence as conveying liability for schizophrenia (Toulopoulou et al., 2010Toulopoulou, T., Goldberg, T. E., Mesa, I. R., Picchioni, M., Rijsdijk, F., Stahl, D.and … Murray, R. M.2010. Impaired intellect and memory: A missing link between genetic risk and schizophrenia?. Archives of General Psychiatry, 67: 905–913.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]). The strong emphasis on endophenotypes, arising from a failure to find clear connections between genetic makeup and psychiatric diagnoses or symptoms, suggests that the neo-Kraepelinianstalwarts have beaten a strategic retreat; at the same time that psychological approaches to treating and understanding psychiatric symptoms, including delusions and hallucinations, have made great strides, the dominant paradigm has given up the traditional territory of mental disorders—the signs and symptoms that people suffer from and that treatments target.
So, the neo-Kraepelinian, categorical, medically based diagnostic system clearly seems to be in a state of crisis. But, as Kuhn has noted, a discipline such as psychopathology will not loosen its grip on a paradigm unless a suitable alternative is available to take its place. What is the evidence that one is appearing?
THE EMERGING TRAUMA/DISSOCIATION PARADIGM
In recent years, evidence has accumulated that traumatizing events are strongly linked to psychopathology in general and psychotic symptoms in particular. Kenneth Kendler, a prominent psychiatric geneticist, concluded from a carefully designed large-scale twin study that childhood sexual abuse was “causally related” to the development of psychiatric and substance abuse disorders (Kendler et al., 2000Kendler, K. S., Bulik, C. M., Silberg, J., Hettema, J. M., Myers, J. and Prescott, C. A.2000. Childhood sexual abuse and adult psychiatric and substance use disorders in women: An epidemiological and cotwin control analysis. Archives of General Psychiatry, 57: 953–959.[Crossref], [PubMed], [Web of Science ®], [Google Scholar], p. 953). In a subsequent commentary, he noted that the more than threefold increase in major depression attributable to severe sexual abuse was “much greater” than the odds ratios associated with any gene putatively linked to schizophrenia or bipolar disorder (Kendler, 2006Kendler, K. S.2006. Reflections on the relationship between psychiatric genetics and psychiatric nosology. American Journal of Psychiatry, 163: 1138–1146.[Crossref], [PubMed], [Web of Science ®], [Google Scholar], p. 1140); he soberly concluded, “The project to ground our messy psychiatric categories in genes … may be in fundamental trouble” (Kendler, 2006Kendler, K. S.2006. Reflections on the relationship between psychiatric genetics and psychiatric nosology. American Journal of Psychiatry, 163: 1138–1146.[Crossref], [PubMed], [Web of Science ®], [Google Scholar], p. 1145). Psychotic symptoms in particular appear to be strongly linked to trauma, both adult trauma (particularly when associated with PTSD; e.g., Scott, Chant, Andrews, Martin, & McGrath, 2007Scott, J., Chant, D., Andrews, G., Martin, G. and McGrath, J.2007. Association between trauma exposure and delusional experiences in a large community-based sample. British Journal of Psychiatry, 190: 339–343.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]) and childhood interpersonal traumas (including in longitudinal studies such as Arseneault et al., 2011Arseneault, L., Cannon, M., Fisher, H. L., Polanczyk, G., Moffitt, T. E. and Caspi, A.2011. Childhood trauma and children’s emerging psychotic symptoms: A genetically sensitive longitudinal cohort study. American Journal of Psychiatry, 168: 65–72.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]). These studies are becoming increasingly well designed, typically controlling for many potentially confounding variables, even apparently genetic ones. Furthermore, psychological trauma has been strongly linked to the development of delusions and hallucinations (Moskowitz, Read, Farrelly, Rudegeair, & Williams, 2009Moskowitz, A., Read, J., Farrelly, S., Rudegeair, T. and Williams, O.2009. “Are psychotic symptoms traumatic in origin and dissociative in kind?”. In Dissociation and the dissociative disorders: DSM–V and beyond, Edited by: Dell, P. and ’Neil, J. O. 521–533. New York, NY: Routledge.[Google Scholar]), and dissociation has been found to consistently and powerfully predict auditory hallucinations (but not delusions) in a range of populations (Moskowitz & Corstens, 2007Moskowitz, A. and Corstens, D.2007. “Auditory hallucinations: Psychotic symptom or dissociative experience?”. In Trauma and serious mental illness, Edited by: Gold, S. N. and Elhai, J. D.35–63. Binghamton, NY: Haworth Press.[Google Scholar]; several recently published studies have supported this relationship). Finally, brain changes long assumed to indicate a core genetic or biological neurodevelopmental disturbance in schizophrenia have been linked with chronic stressful or traumatic childhood experiences (Read, Perry, Moskowitz, & Connolly, 2001Read, J., Perry, B., Moskowitz, A. and Connolly, J.2001. The contribution of early traumatic events to schizophrenia in some patients: A traumagenic neurodevelopmental model. Psychiatry: Interpersonal and Biological Processes, 64: 319–345.[Taylor & Francis Online], [Web of Science ®], [Google Scholar]; Teicher et al., 2003Teicher, M. H., Andersen, S. L., Polcari, A., Anderson, C. M., Navalta, C. P. and Kim, D. M.2003. The neurobiological consequences of early stress and childhood maltreatment. Neuroscience and Biobehavioral Reviews, 27: 33–44.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]). And these trauma-based brain changes are entirely consistent with emerging evolutionary-based explanations for psychotic symptoms (Grace, 2010Grace, A. A.2010. Ventral hippocampus, interneurons, and schizophrenia: A new understanding of the pathophysiology of schizophrenia and its implications for treatment and prevention. Current Directions in Psychological Science, 19: 232–237.[Google Scholar]; Moskowitz, 2004Moskowitz, A.2004. “Scared stiff”: Catatonia as an evolutionary-based fear response. Psychological Review, 111: 984–1002.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]).
IS THERE A SCIENTIFIC REVOLUTION IN THE HOUSE?
The failures of the current dominant medically based neo-Kraepelinian paradigm, coupled with the successes of an alternative paradigm focusing on adverse life experiences (including attachment disturbances) and dissociation, could herald the approach of a scientific revolution. Evidence that this may be occurring includes the increased willingness of prominent medical journals such as the American Journal of Psychiatry and Archives of General Psychiatry to publish studies supportive of this view (e.g., Arseneault et al., 2011Arseneault, L., Cannon, M., Fisher, H. L., Polanczyk, G., Moffitt, T. E. and Caspi, A.2011. Childhood trauma and children’s emerging psychotic symptoms: A genetically sensitive longitudinal cohort study. American Journal of Psychiatry, 168: 65–72.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]; Kendler et al., 2000Kendler, K. S., Bulik, C. M., Silberg, J., Hettema, J. M., Myers, J. and Prescott, C. A.2000. Childhood sexual abuse and adult psychiatric and substance use disorders in women: An epidemiological and cotwin control analysis. Archives of General Psychiatry, 57: 953–959.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]; Scott et al., 2007Scott, J., Chant, D., Andrews, G., Martin, G. and McGrath, J.2007. Association between trauma exposure and delusional experiences in a large community-based sample. British Journal of Psychiatry, 190: 339–343.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]). As more and more psychiatrists are shifting paradigms, it must be recognized that many medically trained individuals within the trauma and dissociative disorders field have long championed this perspective (of course, there are psychologists and other non-physicians who continue to firmly embrace the “medical model” as well, but these paradigms to a large extent do map onto disciplinary distinctions and tensions).
Should a new paradigm emerge, it will be a genuine biopsychosocial one, recognizing that genetics plays a role in psychopathology, likely in providing vulnerability to certain broad forms of mental disorders or to mental disorders in general. It will also recognize that life experiences from gestation on play a major role not only in the expression of psychiatric symptoms but also in the expression of the genes that underlie vulnerability to mental disorders. This new paradigm must also recognize some form of dimension or dimensions across apparently different types of mental disorders (evaporating the comorbidity “problem”) and between pathology and so-called normality. It will require recognition of the extent and severity of childhood trauma, a reality that has long faced considerable resistance from adherents to the medical model. Finally, the presence of dissociative conditions, with the corollary that such individuals are radically different at different times, must be taken into account not only clinically but also in the design of research—something to which the current paradigm has been blind.
The DSM–5 committees appear to have some awareness of these challenges. Dimensional perspectives are being considered for personality disorders and possibly as an axis alongside other categories. What is striking is that the schizophrenia committee is recommending the elimination of the (currently pathognomic) first rank symptoms (voices conversing or commenting, delusions involving intrusions or withdrawals of thoughts or behavior), belatedly recognizing that they have “no unique diagnostic specificity” for schizophrenia (American Psychiatric Association, 2011American Psychiatric Association. (2011). Schizophrenia.http://www.dsm5.org/ProposedRevisions/Pages/proposedrevision.aspx?rid=411# (http://www.dsm5.org/ProposedRevisions/Pages/proposedrevision.aspx?rid=411#)[Google Scholar]). This is obviously welcome news (an early indication of a paradigm shift?), as the association of these clearly dissociative symptoms with schizophrenia has led to substantial misdiagnosis of dissociative identity disorder patients. But it also reminds us of the enigma that practically every attempt to define schizophrenia, from Bleuler to the present day, has invariably called forth dissociative identity disorder. That the paradigmatic biological disorder can be so easily confused with the paradigmatic environmental disorder should already be shaking the rafters of this house (but of course, as the dominant paradigm does not recognize dissociative identity disorder, it does not recognize this enigma!). The explanation for this puzzle should help us to understand the nature of schizophrenia—until then, we can firmly state that whatever schizophrenia is, it is not psychotic symptoms and certainly not auditory hallucinations. Unfortunately, the DSM–5 schizophrenia committee has not gone this far and continues to emphasize psychotic symptoms, even as the head of that committee, William Carpenter, warns against this approach (“Psychotic experience is to the diagnosis of mental illness as fever is to the diagnosis of infection—important, but non-decisive in differential diagnosis,” Fischer & Carpenter, 2009Fischer, B. A. and Carpenter, W. T.2009. Will the Kraepelinian dichotomy survive DSM–V?. Neuropsychopharmacology, 34: 2081–2087.[Crossref], [PubMed], [Web of Science ®], [Google Scholar], p. 2081).
If a new paradigm does emerge, we can be sure that Kraepelin’s paradigmatic disease entity—General Paresis of the Insane—will be replaced. Perhaps it may not be possible to find a new exemplar for mental disorders in general, but PTSD would seem a worthwhile candidate for at least some of them—those clearly linked to trauma and characterized by dissociation (as, for example, has been proposed by Van der Hart, Nijenhuis, & Steele, 2006Van der Hart, O., Nijenhuis, E. and Steele, K.2006. The haunted self: Structural dissociation and the treatment of chronic traumatization, New York, NY: Norton.[Google Scholar], in their structural dissociation model). And the possibility that schizophrenia, or at least some form of psychotic disorder, could fit this model should not be rejected outright. Even Bleuler, the progenitor of schizophrenia, despite his commitment to an organic etiology, seemed to recognize this. A growing appreciation of this possibility could, quite literally, trigger a scientific revolution in our view of mental disorders altogether.
The stronger the affects, the less pronounced the dissociative tendencies need to be in order to produce the emotional desolation. Thus, in many cases of severe disease, we find that only quite ordinary everyday conflicts of life have caused the marked mental impairment; but in milder cases, the acute episodes may have been released by powerful affects. And not infrequently, after a careful analysis, we had to pose the question whether we are not merely dealing with the effect of a particularly powerful psychological trauma on a very sensitive person, rather than with a disease in the narrow sense of the word. (Bleuler, 1911/1950Bleuler, E.1950. Dementia praecox or the group of schizophrenias, Edited by: Zinkin, J.New York, NY: International Universities Press. Original work published 1911[Google Scholar], p. 300; Sünje Matthiesen, translation)
Lost connections by Johann Hari is simply the best book I’ve ever read. It asks all the right questions and it also provides many possible answers. I hope this will be a book that ultimately will change our society and the way we think about mental illness. Working as a psychologist myself, it felt like somebody finally provided solutions that will work in therapy and possibly change.
From the New York Times bestselling author of Chasing the Scream: The First and Last Days of the War on Drugs, a startling challenge to our thinking about depression and anxiety.
Award-winning journalist Johann Hari suffered from depression since he was a child and started taking antidepressants when he was a teenager. He was told—like his entire generation—that his problem was caused by a chemical imbalance in his brain. As an adult, trained in the social sciences, he began to investigate this question—and he learned that almost everything we have been told about depression and anxiety is wrong.Across the world, Hari discovered social scientists who were uncovering the real causes—and they are mostly not in our brains, but in the way we live today. Hari’s journey took him from the people living in the tunnels beneath Las Vegas, to an Amish community in Indiana, to an uprising in Berlin—all showing in vivid and dramatic detail these new insights. They lead to solutions radically different from the ones we have been offered up until now.
Just as Chasing the Scream transformed the global debate about addiction, with over twenty million views for his TED talk and the animation based on it, Lost Connections will lead us to a very different debate about depression and anxiety—one that shows how, together, we can change
When I was 15, I took the bus from Stavanger to Bergen after saying goodbye to my boyfriend. The last thing I wanted, was to talk with anyone. I struggled to keep my tears back and wanted to have time to think about everything we did and he said (like a typical teenager). But to my horror, an old woman sat next to me and I knew immediately that she was a talker. Little did I know that this would be one of the very conversations I remember from that year. We talked about everything, and soon started on a philosophical journey together. I told her about my boyfriend, and how hard it was to live so far apart from him (over 10 hours with a car or bus). She responded by saying how healthy it is to meet people who live in a different place than where you grew up. Because they probably see the world a little bit different than you, and that means you might end up learning something new.
This woman was so wise, and I learnt something new too: By opening up to all kinds off people, even strangers, you might change the way you think and see the world. I was reminded of this event when I listened to “an organized mind” by Daniel Levitin in my car. He described a study where the researchers asked people if they thought they would prefer sitting alone or talk with a stranger on the bus. They were quite sure about what they would like the most, but it seems like we don`t always know how much we crave connections with others. The study is described below, and I hope you enjoy it as much as me. Maybe the next time you`r filled with dread, hoping that somebody won`t disturb you on a bus, plane or train, you might look at the commute as an opportunity instead of fear.
Talking to the stranger in seat 4B on a cross-country flight is often considered one of the torments of air travel, to be avoided at all costs. But new research suggests people are deeply wrong about the misery of striking up conversations on public transit.
Contrary to expectations, people are happier after a conversation with a stranger, the study revealed.
“At least in some cases, people don’t seem to be social enough for their own well-being,” said study researcher Nicholas Epley, a professor of behavioral science at the University of Chicago Booth School of Business. “They think that sitting in solitude will be more pleasant than engaging in conversation, when, in fact, the opposite is true.” [7 Thoughts That Are Bad For You]
Talking to strangers
Epley, author of the book “Mindwise: How We Understand What Others Think, Feel, Believe and Want” (Knopf, 2014), studies social connection. Humans are social animals, he said, to the extent that having more and stronger friends and family connections is linked with a healthier life.
But in waiting rooms, trains, planes and other public spots, people fail to show their social stripes, Epley told Live Science. During his own commute in Chicago, he sees “highly social animals getting on the train every morning and being remarkably anti-social … They might as well be sitting next to a rock.”
Perhaps people know that interacting with a stranger is likely to be less pleasant than sitting in silence, so they choose the latter, Epley said.
Or maybe, just maybe, everybody is wrong about talking to strangers. Maybe it’s actually fun.
To find out which is true, Epley and his colleagues recruited real-life commuters at Chicago train stations. They also conducted a series of experiments with bus riders. In some of these experiments, they simply asked people to imagine striking up a conversation on the bus or train. Would it be pleasant? Would they feel happy afterward?
By and large, people said “no,” it wouldn’t be pleasant, and that such an interaction wouldn’t result in a happiness boost. In addition, people guessed, on average, that fewer than half of strangers would be interested in chatting. They expected to be rebuffed.
In other experiments, the researchers actually asked the commuters to go through with the conversations. At random, some participants were assigned to start a conversation. Others were asked to sit silently, and a third group was told to go about their normal commute routine (which involved silence for some and speaking to a friend for others). The participants were given sealed surveys to complete and mail in after their commute.
The results? People had a more pleasant time when they talked to a stranger versus when they stayed silent. Incredibly, the findings held even when the researchers controlled for personality traits, like extraversion and introversion.
Does the finding that talking to strangers makes people happier make you more likely to strike up conversations in public more often?
No way. You couldn’t pay me enough.
Maybe. I can see the upsides.
Definitely. I’d like to meet new people.
No – but only because I already chat with strangers.
“Everyone seems happier and has a more pleasant interaction when they connect versus sit in isolation,” Epley said.
Perhaps even more surprising, their conversation partners seemed to welcome the connection, too.
“Nobody was rejected in any of our studies, as far as I can tell,” Epley said. “Everybody who tried to talk to somebody was able to.”
In another study, the researchers set up participants in a waiting room, so they could test the happiness of both the conversation starter and their target. Again, everyone was happier after chatting — even the person who hadn’t started the conversation. Pairs of strangers deep in conversation also reported that the wait seemed shorter.
Nerve cells communicate through short, fleeting pulses of electrical activity. Yet some memories stored in the brain can persist for decades. Research into how the nervous system bridges these two radically different time scales has been going on for decades, and a number of different ideas have picked up some experimental support.
For instance, based on their past activity, nerve cells can dictate which partners they make contact with or increase or decrease the strength of those connections—in essence, rewiring the brain as it develops and processes experiences. In addition, individual cells can make long-term changes in the genes that are active, locking specific behaviors in place. In a paper released by Nature Neuroscience, scientists have looked at the changes in gene expression associated with memories of positive associations and found that they are held in place by chemical modifications of the cells’ DNA.
These chemical modifications fall under the broad (and somewhat poorly defined) category of epigenetic changes. Genetic changes involve alterations of the DNA sequence itself. Epigenetic changes, in contrast, alter how that DNA is processed within cells. They can be inherited as the cell divides and matures and, in rare cases, they’re passed on to the next generation. In some cases, epigenetic changes simply involve how the DNA is packaged inside a cell, which controls how accessible it is to the enzymes that transcribe it for use in making proteins. But in other cases, the DNA itself is chemically modified. That changes how various proteins interact with it.
The most common of these chemical modifications is called methylation, where a single carbon atom is attached at a specific location on one of the DNA bases. A number of studies suggest that methylation changes accompany the formation of long-term memories, so the researchers decided to test this in a well characterized experimental system that dates back to Pavlov: teaching a mouse to associate a sound with having a sugary treat appear in its cage. (Controls included playing the tone in a way that it wasn’t associated with treats and simply providing the tone.)
It only takes mice three tries before they start sniffing around the locations where the treat appears, and by five iterations, the behavior is pretty much locked-in. Past work in other systems has identified areas of the brain that are involved in this process, as well as some of the genes that are required. So, the authors started looking at how these changes came about when the association between the tone and a treat was being formed.
The researchers were able to confirm that the genes identified in past studies were involved in the formation of associative memories, and changes in the gene activity were detectable by the third trial just as behavior started to change. They were also able to detect significant changes in the DNA methylation that occurred at the same time, although only at a specific subset of the areas known to be methylated in that area of the chromosome. They were even able to show that the enzymes responsible for modifying the DNA appeared at these sites at around the time of the third trial.
All of that indicates that methylation changes are associated with the learning process, but it doesn’t get at the issue of cause and effect. So, the team injected a chemical that blocks DNA methylation into the area of the brain that’s involved with this form of associative memory, and they found that it would leave existing memories intact while blocking the formation of new ones. The effect was also specific to injections in this area of the brain. Injecting the drug into a different area, one that is involved in forming the associations involved in addiction, did not affect this particular form of memory.
Overall, the study adds another example to the growing list of cases where epigenetic changes seem to be involved in the process of locking memories into place. This doesn’t mean that the memories are permanent, as there are enzymes that can eliminate methylation as well. Still, it should help maintain the status of the memories for long periods of time—far longer than a brief burst of activity.
But it’s important to note that this sort of methylation is very context dependent: it’s specific to a subset of cells in a single area of the brain. Different methylation patterns—or even the same methylation pattern in a different set of cells—will probably encode something very different.
“There is perhaps no psychological skill more fundamental than resisting impulse. It is the root of all emotional self-control, since all emotions, by their very nature, led to one or another impulse to act.”Daniel Goleman
It soars through you like a wave. The impulse to do something you will regret later. The urge is so irresistible, that you feel there is no other way. You just have to do it. Have another drink, although it is way beyond bedtime. A cigarette after managing to not smoke for three days. The ice-cream dripping with chocolate sause that you kept in the fridge. Just in case you get visitors. We know these impulses so well, and despair when we cannot do anything to stop them. Walter Mischel found in his famous Marshmallow experiment, that children who managed to postpone having a marshmallow and get two later if they waited, had better results at school and success later in life. Unbelievable, isn`t it? That just one experiment like this, can predict what happens years later? For some this might even lead to a feeling of despair: Especially if you struggle time and time again with resisting those impulses. Is it really impossible to stop the urge when it threatens to take over? Sometimes it honestly is. When you are stressed, have too many things to think about, have no time to think through what you do during a day or feel tired, you might slip on some of your promises to yourself. Studies show that choosing and resisting alternatives, drains mental energy. In the evening you might be so exhausted that willpower simply vanishes. BUT: We can trick our gratification searching brain. First: Prepare for the fight. Do not keep what you are trying to avoid, around you. Don`t buy that chocolate bar. To avoid doing so when you are stressed, plan to go shopping when you are not hungry. Shop everything you need so you don`t need to pop into the store later. If you feel bad from not having your usual way of regulating those difficult emotions or cravings, find alternative positive activities. Talk to yourself a LOT: I am strong. I can do this. I am actually doing it already by trying to resist. Good work! And if you manage to resist the impulse, for just one or ten minutes, be sure to tell yourself what accomplishment it is. Because you have just rode on the wave instead of letting it sweep you away. Even without a surf-board. Because who actually learn how to resist impulses? If we haven`t had good role models, like many of us haven`t (especially today when everything happened two minutes ago), how could we have learnt to resist? Luckily, the marshmallow experiment showed that if the experimenter learnt the children how to resist impulses, for example by distracting them (having interesting toys in the room, asking them to close their eyes) they managed to do so in the future too. Every time you find creative ways to resist your urges, your willpower grows. It is hard work, and sometimes it feels like it`s all for nothing. But just think about how happy people who have really tried to change, often are. Why might that be? I think you already have the answer: Because it is immensely gratifying to doing what we know in our hearts are right.
But, we have to balance resistance with acceptance. Sometimes we push the brakes to often, leading to us stopping impulses that are healthy and bring life to us.
From the blog feed your soul: My concern, however, is the squashing of the other impulses, the ones that guide us to life-enhancing decisions. The impulse to express a truth even if it is unpopular. The impulse to say no, when social mores would have us say yes. The impulse to radically change a life that looks perfectly fine from the outside but feels like death on the inside. I am afraid that we will begin to live only in extremes, much like the stratification of our socioeconomic classes. We become like the addict, powerless over any whim or desire, or we become the ascetic who deems any impulse evil, and the control over our desires the mark of superiority.
Is it possible to live in the middle ground, where our impulses can go through a highly developed discernment filter and we honor all ways?
I love those thoughts from the blog. And in my opinion, it is possible to find that balance. But first we must learn the skills to stop impulses first, and then we must learn to let go. Finding the balance can`t be done if we lack the knowledge and experience necessary to either resist or let go. So if you want to resist more, can it harm to try?
An encounter at a party changed Gay Hendricks forever. A stranger asked him to imagine himself on his deathbed and to consider this question:
“Was your life a complete success?” If not, then “What would be the things you’d wish had happened that would have made it a success?” Hendricks said his deepest wish was for a loving, lasting relationship with a woman. The stranger said, “turn that wish into a goal, and put it in the present tense.” On the spot, Hendricks came up with this goal, “I enjoy a happy marriage with a woman I adore and who adores me. I enjoy a lifelong blossoming of passion and creativity with her.” This goal helped him create his marriage to Kathlyn, the date he’d taken to the party, and during the past 27 years they’ve become well-known relationship experts and co-authors of 9 books together. This short, focused book shows readers how to discover their own five wishes for a fulfilled life.
Five wishes is a wonderful book. Books CAN change lives, and this one did that for me. Today I sat down to think about what my five wishes are. I am still not completely sure what they should be, but I am starting to get an idea: