Category Archives: Mental Health

“Which of the me’s is me?” An Unquiet Mind. A Memoir of Moods and Madness – Kay Redfield Jamison.

Kay Jamison’s story is not of someone who has succeeded despite having a severe disorder, but of someone whose particular triumphs are a consequence of her disorder. She would not have observed what she has if she had not experienced what she did. The fact that she has endured such battles helps her to understand them in others.

“The disease that has, on several occasions, nearly killed me does kill tens of thousands of people every year: most are young, most die unnecessarily, and many are among the most imaginative and gifted that we as a society have. The major clinical problem in treating manic-depressive illness is not that there are not effective medications, there are, but that patients so often refuse to take them. Freedom from the control imposed by medication loses its meaning when the only alternatives are death and insanity.”

Her remarkable achievements are a beacon of hope to those who imagine that they cannot survive their condition, much less thrive with it.

I doubt sometimes whether a quiet & unagitated life would have suited me, yet I sometimes long for it. – Byron.

For centuries, the prevailing wisdom had been that having a mental illness would prevent a doctor from providing competent care, would indicate a vulnerability that would undermine the requisite aura of medical authority, and would kill any patient’s trust. In the face of this intense stigmatization, many bright and compassionate people with mental illness avoided the field of medicine, and many physicians with mental illness lived in secrecy. Kay Redfield Jamison herself led a closeted life for many years, even as she coauthored the standard medical textbook on bipolar illness. She suffered from the anguish inherent in her illness and from the pain that comes of living a lie.

With the publication of An Unquiet Mind, she left that lie behind, revealing her condition not only to her immediate colleagues and patients, but also to the world, and becoming the first clinician ever to describe travails with bipolar illness in a memoir. It was an act of extraordinary courage, a grand risk taking infused with a touch of manic exuberance, and it broke through a firewall of prejudice. You can have bipolar illness and be a brilliant clinician; you can have bipolar illness and be a leading authority on the condition, informed by your experiences rather than blinded by them. You can have bipolar illness and still have a joyful, fruitful, and dignified life.

Kay Jamison’s story is not of someone who has succeeded despite having a severe disorder, but of someone whose particular triumphs are a consequence of her disorder. Ovid said, “The wounded doctor heals best” and Jamison’s open hearted declarations have been a salve for the wounded psyches of untold thousands of people; her unquiet mind has often soothed the minds of others. Her discernments come from a rare combination of observation and experience: she would not have observed what she has if she had not experienced what she did. The fact that she has endured such battles helps her to understand them in others, and her frankness about them offers an antidote to the pervasive shame that Cloisters so many mentally ill people in fretful isolation.

Her remarkable achievements are a beacon of hope to those who imagine that they cannot survive their condition, much less thrive with it. Those who address mental illnesses tend to do so with either rigor or empathy; Jamison attains a rare marriage of the two. Just as her clinical work has been strengthened by her personal experience, her personal experience has been informed by her academic insights.

It is different to go through manic and depressive episodes when you know everything there is to know about your condition than it is to go through them in ignorance, constantly ambushed by the apparently inexplicable.

Like many people with mental illness, Jamison has had to reckon with the impossibility of separating her personality from her condition. “Which of the me’s is me?” she asks rhetorically in these pages. She kept up a nearly willful self-ignorance for years before she succumbed to knowledge; she resisted remedy at first because she feared she might lose some of her essential self to it. It took repeated descents and ascents into torment to instigate a kind of acquiescence. She has become glad of that surrender; it has saved a life that turns out to be well worth living. As this book bleached away her erstwhile denial, it has mediated her readers’ denial, too. As a professor of psychiatry at Johns Hopkins University and in her frequent lectures around the globe, Kay Jamison has taught a younger generation of doctors how to make sense of their patients: not merely how to treat them, but how to help them.

Though An Unquiet Mind does not provide diagnostic criteria or propose specific courses of treatment, it remains very much a book about medicine, with a touchingly fond portrait of science. Jamison expresses enormous gratitude to the doctors who have treated her and to the researchers who established the modes of treatment that have kept her alive. She engages medicine’s resonant clarities, and she tolerates the relative primitivism of our understanding of the brain.

Appreciating the biology of her illness and the mechanisms of its therapies allowed her to achieve a truce with her bipolar illness, and science informed her choice to speak openly about her skirmishes with it. That peace has not entirely precluded further episodes, but it makes them easier to tolerate when they come. Equally, it has given her the courage to stay on medication and the resilience to sustain other forms of self-care.

You can feel in Jamison’s writing a bracing honesty unmarred by self-pity. It seems clear Jamison is not by nature an exhibitionist, and making so much of her private life into public property cannot have been easy for her. On every page, you sense the resolve it has required. Her book differs from much confessional writing in that, although she describes certain experiences in agonizing detail, she maintains a vocabulary of discretion. An Unquiet Mind may have been intended as a book about an illness, not about a life, but it is both. There is satisfaction in making your affliction useful to other people; it redeems what seemed in the instance to be useless experiences. That insistence on making something good out of something bad is the vital force in her writing.

I met Kay Jamison in 1995, shortly after the publication of An Unquiet Mind, when I had first decided to write about depression. I contacted her to request an interview, and she suggested we have lunch; she then invited me to my first serious scientific conference, a suicide symposium she had organized, attended by the leading figures in the field. Her kindness to me in the early stages of my research points to a personal generosity that mirrors the brave generosity of her books. The forbearance that has made her a good clinician and a good writer also makes her a good friend.

In the years since then, Jamison has produced a corpus of work that, in a very different kind of bipolarity, limns the glittering revelations of psychosis only to return to its perilous ordeals. Touched with Fire (1993) had already chronicled the artistic achievements of people with bipolar illness; Night Falls Fast (1999) tackles the impossible subject of suicide; Exuberance (2004) tells us how unipolar mania has generated many intellectual and artistic breakthroughs; and Nothing was the Same (2009) is a closely observed and deeply personal account of losing her second husband to cancer, a journey complicated by her unreliable moods. Her illness runs through these books even when it is not her explicit topic. But that recurrent theme does not narrow the books into ego studies; instead, it makes them startlingly, powerfully intimate.

Jamison consistently evinces a romantic attachment to language itself. Her sentences flow out in an often poetic rapture, and she displays a sustaining love for the poetry of others, quoting it by the apposite yard. Few doctors know poetry so well, and few poets understand so much biology, and Jamison serves as a translator between humanism and science, which are so often disparate vocabularies for the same phenomena. While poetry inflects her literary voice, it sits comfortably beside a sense of humor. Irony is among her best defenses against gloom, and the zing of her comic asides makes reading about unbearable things a great deal more bearable. The crossing point of precision, luminosity, and hilarity may be the safest domain for an inconsistent mind, a nexus of relief for someone whose stoicism cannot fully assuage her distress.

Two decades after its publication, An Unquiet Mind remains fresh. There’s been a bit more science in the field and a great deal of social change regarding mental illness, change this book helped to create: a society in which what was relentlessly shameful is more easily and frequently acknowledged. The book delineates not how to treat the condition, but how to live with the condition and its treatments, and that remains relevant even as actual treatments evolve.

Jamison does not stint on her own despair, but she has constructed meaning and built an identity from it. While she might not have opted for this illness, neither does she entirely regret it; she prefers, as she writes so movingly, a life of passionate turbulence to one of tedious calm. Learning to appreciate the things you also regret makes for a good way forward. If you have bipolar illness, this book will help you to forgive yourself for everything that has gone awry; if you do not, it will perhaps show how a steely tenacity can imbue disasters with value, a capacity that stands to enrich any and every life.

Andrew Solomon

Kay Redfield Jamison

Prologue

When it’s two o’clock in the morning, and you’re manic, even the UCLA Medical Center has a certain appeal. The hospital, ordinarily a cold clotting of uninteresting buildings, became for me, that fall morning not quite twenty years ago, a focus of my finely wired, exquisitely alert nervous system. With vibrissae twinging, antennae perked, eyes fast forwarding and fly faceted, I took in everything around me. I was on the run. Not just on the run but fast and furious on the run, darting back and forth across the hospital parking lot trying to use up a boundless, restless, manic energy. I was running fast, but slowly going mad.

The man I was with, a colleague from the medical school, had stopped running an hour earlier and was, he said impatiently, exhausted. This, to a saner mind, would not have been surprising: the usual distinction between day and night had long since disappeared for the two of us, and the endless hours of scotch, brawling, and fallings about in laughter had taken an obvious, if not final, toll. We should have been sleeping or working, publishing not perishing, reading journals, writing in charts, or drawing tedious scientific graphs that no one would read.

Suddenly a police car pulled up. Even in my less than totally lucid state of mind I could see that the officer had his hand on his gun as he got out of the car. “What in the hell are you doing running around the parking lot at this hour?” he asked. A not unreasonable question. My few remaining islets of judgment reached out to one another and linked up long enough to conclude that this particular situation was going to be hard to explain. My colleague, fortunately, was thinking far better than I was and managed to reach down into some deeply intuitive part of his own and the world’s collective unconscious and said, “We’re both on the faculty in the psychiatry department.” The policeman looked at us, smiled, went back to his squad car, and drove away. Being professors of psychiatry explained everything.

Within a month of signing my appointment papers to become an assistant professor of psychiatry at the University of California, Los Angeles, I was well on my way to madness; it was 1974, and I was twenty-eight years old. Within three months I was manic beyond recognition and just beginning a long, costly personal war against a medication that I would, in a few years’ time, be strongly encouraging others to take. My illness, and my struggles against the drug that ultimately saved my life and restored my sanity, had been years in the making.

For as long as I can remember I was frighteningly, although often wonderfully, beholden to moods. Intensely emotional as a child, mercurial as a young girl, first severely depressed as an adolescent, and then unrelentingly caught up in the cycles of manicdepressive illness by the time I began my professional life, I became, both by necessity and intellectual inclination, a student of moods. It has been the only way I know to understand, indeed to accept, the illness I have; it also has been the only way I know to try and make a difference in the lives of others who also suffer from mood disorders.

The disease that has, on several occasions, nearly killed me does kill tens of thousands of people every year: most are young, most die unnecessarily, and many are among the most imaginative and gifted that we as a society have.

The Chinese believe that before you can conquer a beast you first must make it beautiful. In some strange way, I have tried to do that with manic-depressive illness. It has been a fascinating, albeit deadly, enemy and companion; I have found it to be seductively complicated, a distillation both of what is finest in our natures, and of what is most dangerous. In order to contend with it, I first had to know it in all of its moods and infinite disguises, understand its real and imagined powers. Because my illness seemed at first simply to be an extension of myself, that is to say, of my ordinarily changeable moods, energies, and enthusiasms, I perhaps gave it at times too much quarter. And, because I thought I ought to be able to handle my increasingly violent mood swings by myself, for the first ten years I did not seek any kind of treatment. Even after my condition became a medical emergency, I still intermittently resisted the medications that both my training and clinical research expertise told me were the only sensible way to deal with the illness I had.

My manias, at least in their early and mild forms, were absolutely intoxicating states that gave rise to great personal pleasure, an incomparable flow of thoughts, and a ceaseless energy that allowed the translation of new ideas into papers and projects. Medications not only cut into these fast-flowing, highflying times, they also brought with them seemingly intolerable side effects. it took me far too long to realize that lost years and relationships cannot be recovered, that damage done to oneself and others cannot always be put right again, and that freedom from the control imposed by medication loses its meaning when the only alternatives are death and insanity.

The war that I waged against myself is not an uncommon one. The major clinical problem in treating manic-depressive illness is not that there are not effective medications, there are, but that patients so often refuse to take them. Worse yet, because of a lack of information, poor medical advice, stigma, or fear of personal and professional reprisals, they do not seek treatment at all.

Manic-depression distorts moods and thoughts, incites dreadful behaviors, destroys the basis of rational thought, and too often erodes the desire and will to live. It is an illness that is biological in its origins, yet one that feels psychological in the experience of it; an illness that is unique in conferring advantage and pleasure, yet one that brings in its wake almost unendurable suffering and, not infrequently, suicide.

I am fortunate that I have not died from my illness, fortunate in having received the best medical care available, and fortunate in having the friends, colleagues, and family that I do. Because of this, I have in turn tried, as best I could, to use my own experiences of the disease to inform my research, teaching, clinical practice, and advocacy work.

Through writing and teaching I have hoped to persuade my colleagues of the paradoxical core of this quicksilver illness that can both kill and create; and, along with many others, have tried to change public attitudes about psychiatric illnesses in general and manic depressive illness in particular. It has been difficult at times to weave together the scientific discipline of my intellectual field with the more compelling realities of my own emotional experiences. And yet it has been from this binding of raw emotion to the more distanced eye of clinical science that I feel I have obtained the freedom to live the kind of life I want, and the human experiences necessary to try and make a difference in public awareness and clinical practice.

I have had many concerns about writing a book that so explicitly describes my own attacks of mania, depression, and psychosis, as well as my problems acknowledging the need for ongoing medication. Clinicians have been, for obvious reasons of licensing and hospital privileges, reluctant to make their psychiatric problems known to others. These concerns are often well warranted.

I have no idea what the longterm effects of discussing such issues so openly will be on my personal and professional life, but, whatever the consequences, they are bound to be better than continuing to be silent. I am tired of hiding, tired of misspent and knotted energies, tired of the hypocrisy, and tired of acting as though I have something to hide.

One is what one is, and the dishonesty of hiding behind a degree, or a title, or any manner and collection of words, is still exactly that: dishonest. Necessary, perhaps, but dishonest. I continue to have concerns about my decision to be public about my illness, but one of the advantages of having had manic-depressive illness for more than thirty years is that very little seems insurmountably difficult. Much like crossing the Bay Bridge when there is a storm over the Chesapeake, one may be terrified to go toward, but there is no question of going back. I find myself somewhat inevitably taking a certain solace in Robert Lowell’s essential question, Yet why not say what happened?

Part One

THE WILD BLUE YONDER

Into the Sun

I was standing with my head back, one pigtail caught between my teeth, listening to the jet overhead. The noise was loud, unusually so, which meant that it was close. My elementary school was near Andrews Air Force Base, just outside Washington; many of us were pilots’ kids, so the sound was a matter of routine. Being routine, however, didn’t take away from the magic, and I instinctively looked up from the playground to wave. I knew, of course, that the pilot couldn’t see me, I always knew that, just as I knew that even if he could see me the odds were that it wasn’t actually my father. But it was one of those things one did, and anyway I loved any and all excuses just to stare up into the skies. My father, a career Air Force officer, was first and foremost a scientist and only secondarily a pilot. But he loved to fly, and, because he was a meteorologist, both his mind and his soul ended up being in the skies. Like my father, I looked up rather more than I looked out.

When I would say to him that the Navy and the Army were so much older than the Air Force, had so much more tradition and legend, he would say, Yes, that’s true, but the Air Force is the future. Then he would always add: And we can fly. This statement of creed would occasionally be followed by an enthusiastic rendering of the Air Force song, fragments of which remain with me to this day, nested together, somewhat improbably, with phrases from Christmas carols, early poems, and bits and pieces of the Book of Common Prayer: all having great mood and meaning from childhood, and all still retaining the power to quicken the pulses.

So I would listen and believe and, when I would hear the words “Off we go into the wild blue yonder,” I would think that “wild” and “yonder” were among the most wonderful words I had ever heard; likewise, I would feel the total exhilaration of the phrase “Climbing high, into the sun” and know instinctively that I was a part of those who loved the vastness of the sky.

The noise of the jet had become louder, and I saw the other children in my second grade class suddenly dart their heads upward. The plane was coming in very low, then it streaked past us, scarcely missing the playground. As we stood there clumped together and absolutely terrified, it flew into the trees, exploding directly in front of us. The ferocity of the crash could be felt and heard in the plane’s awful impact; it also could be seen in the frightening yet terrible lingering loveliness of the flames that followed. Within minutes, it seemed, mothers were pouring onto the playground to reassure children that it was not their fathers; fortunately for my brother and sister and myself, it was not ours either. Over the next few days it became clear, from the release of the young pilot’s final message to the control tower before he died, that he knew he could save his own life by bailing out. He also knew, however, that by doing so he risked that his unaccompanied plane would fall onto the playground and kill those of us who were there.

The dead pilot became a hero, transformed into a scorchingly vivid, completely impossible ideal for what was meant by the concept of duty. It was an impossible ideal, but all the more compelling and haunting because of its very unobtainability. The memory of the crash came back to me many times over the years, as a reminder both of how one aspires after and needs such ideals, and of how killingly difficult it is to achieve them. I never again looked at the sky and saw only vastness and beauty. From that afternoon on I saw that death was also and always there.

Although, like all military families, we moved a lot, by the fifth grade my older brother, sister, and I had attended four different elementary schools, and we had lived in Florida, Puerto Rico, California, Tokyo, and Washington, twice, our parents, especially my mother, kept life as secure, warm, and constant as possible. My brother was the eldest and the steadiest of the three of us children and my staunch ally, despite the three year difference in our ages. I idolized him growing up and often trailed along after him, trying very hard to be inconspicuous, when he and his friends would wander off to play baseball or cruise the neighborhood. He was smart, fair, and self-confident, and I always felt that there was a bit of extra protection coming my way whenever he was around. My relationship with my sister, who was only thirteen months older than me, was more complicated. She was the truly beautiful one in the family, with dark hair and wonderful eyes, who from the earliest times was almost painfully aware of everything around her. She had a charismatic way, a fierce temper, very black and passing moods, and little tolerance for the conservative military lifestyle that she felt imprisoned us all. She led her own life, defiant, and broke out with abandon whenever and wherever she could. She hated high school and, when we were living in Washington, frequently skipped classes to go to the Smithsonian or the Army Medical Museum or just to smoke and drink beer with her friends.

She resented me, feeling that I was, as she mockingly put it, “the fair-haired one”, a sister, she thought, to whom friends and schoolwork came too easily, passing far too effortlessly through life, protected from reality by an absurdly optimistic view of people and life. Sandwiched between my brother, who was a natural athlete and who never seemed to see less-than-perfect marks on his college and graduate admission examinations, and me, who basically loved school and was vigorously involved in sports and friends and class activities, she stood out as the member of the family who fought back and rebelled against what she saw as a harsh and difficult world. She hated military life, hated the constant upheaval and the need to make new friends, and felt the family politeness was hypocrisy.

Perhaps because my own violent struggles with black moods did not occur until I was older, I was given a longer time to inhabit a more benign, less threatening, and, indeed to me, a quite wonderful world of high adventure. This world, I think, was one my sister had never known. The long and important years of childhood and early adolescence were, for the most part, very happy ones for me, and they afforded me a solid base of warmth, friendship, and confidence. They were to be an extremely powerful amulet, a potent and positive countervailing force against future unhappiness. My sister had no such years, no such amulets. Not surprisingly, perhaps, when both she and I had to deal with our respective demons, my sister saw the darkness as being within and part of herself, the family, and the world. I, instead, saw it as a stranger; however lodged within my mind and soul the darkness became, it almost always seemed an outside force that was at war with my natural self.

My sister, like my father, could be vastly charming: fresh, original, and devastatingly witty, she also was blessed with an extraordinary sense of aesthetic design. She was not an easy or untroubled person, and as she grew older her troubles grew with her, but she had an enormous artistic imagination and soul. She also could break your heart and then provoke your temper beyond any reasonable level of endurance. Still, I always felt a bit like pieces of earth to my sister’s fire and flames.

For his part, my father, when involved, was often magically involved: ebullient, funny, curious about almost everything, and able to describe with delight and originality the beauties and phenomena of the natural world. A snowflake was never just a snowflake, nor a cloud just a cloud. They became events and characters, and part of a lively and oddly ordered universe. When times were good and his moods were at high tide, his infectious enthusiasm would touch everything. Music would fill the house, wonderful new pieces of jewelry would appear, a moonstone ring, a delicate bracelet of cabochon rubies, a pendant fashioned from a moody sea, green stone set in a swirl of gold, and we’d all settle into our listening mode, for we knew that soon we would be hearing a very great deal about whatever new enthusiasm had taken him over. Sometimes it would be a discourse based on a passionate conviction that the future and salvation of the world was to be found in windmills; sometimes it was that the three of us children simply had to take Russian lessons because Russian poetry was so inexpressibly beautiful in the original.

*

from

An Unquiet Mind. A Memoir of Moods and Madness

by Kay Redfield Jamison

get it at Amazon.com

The Great God of Depression. How mental illness stopped being a terrible dark secret – Pagan Kennedy * DARKNESS VISIBLE. A MEMOIR of MADNESS – William Styron.

The pain of severe depression is quite unimaginable to those who have not suffered it, and it kills in many instances because its anguish can no longer be borne.

The most honest authorities face up squarely to the fact that serious depression is not readily treatable. Failure of alleviation is one of the most distressing factors of the disorder as it reveals itself to the victim, and one that helps situate it squarely in the category of grave diseases.

One by one, the normal brain circuits begin to drown, causing some of the functions of the body and nearly all of those of instinct and intellect to slowly disconnect.

Inadvertently I had helped unlock a closet from which many souls were eager to come out. It is possible to emerge from even the deepest abyss of despair and “once again behold the stars.”

Nearly 30 years ago, the author William Styron outed himself as mentally ill. “My days were pervaded by a gray drizzle of unrelenting horror,” he wrote in a New York Times op-ed article, describing the deep depression that had landed him in the psych ward. He compared the agony of mental illness to that of a heart attack. Pain is pain, Whether it’s in the mind or the body. So why, he asked, were depressed people treated as pariahs?

A confession of mental illness might not seem like a big deal now, but it was back then. In the 1980s, “if you were depressed, it was a terrible dark secret that you hid from the world,” according to Andrew Solomon, a historian of mental illness and author of “The Noonday Demon.” “People with depression were seen as pathetic and even dangerous. You didn’t let them near your kids.”

From William Styron’s Op-Ed on Depression. “In the popular mind, suicide is usually the work of a coward or sometimes, paradoxically, a deed of great courage, but it is neither; the torment that precipitates the act makes it often one of blind necessity.”

The response to Mr. Styron’s op-ed was immediate. Letters flooded into The New York Times. The readers thanked him, blurted out their stories and begged him for more. “Inadvertently I had helped unlock a closet from which many souls were eager to come out,” Mr. Styron wrote later.

“It was like the #MeToo movement,” Alexandra Styron, the author’s daughter, told me. “Somebody comes out and says: ‘This happened. This is real. This is what it feels like.’ And it just unleashed the floodgates.”

Readers were electrified by Mr. Styron’s confession in part because he inhabited a storybook world of glamour. After his novel “Sophie’s Choice” was adapted into a blockbuster movie in 1982, Mr. Styron rocketed from mere literary success to Hollywood fame. Meryl Streep, who won an Oscar for playing Sophie, became a lifelong friend, adding to Mr. Styron’s roster of illustrious buddies, from “Jimmy” Baldwin to Arthur Miller. He appeared at gala events with his silver hair upswept in a genius-y pompadour and his face ruddy from summers on Martha’s Vineyard. And yet he had been so depressed that he had eyed the knives in his kitchen with suicide-lust.

William Styron

James L.W. West, Mr. Styron’s friend and biographer, told me that Mr. Styron had never wanted to become “the guru of depression.” But after his article, he felt he had a duty to take on that role.

His famous memoir of depression, “Darkness Visible,” came out in October 1990. It was Mr. Styron’s curiosity about his own mind, and his determination to use himself as a case study to understand a mysterious disease, that gave the book its political power. “Darkness Visible” demonstrated that patients could be the owners and describers of their mental disorders, upending centuries of medical tradition in which the mentally ill were discredited and shamed. The brain scientist Alice Flaherty, who was Mr. Styron’s close friend and doctor, has called him “the great god of depression” because his influence on her field was so profound. His book became required reading in some medical schools, where physicians were finally being trained to listen to their patients.

Mr. Styron also helped to popularize a new way of looking at the brain. In his telling, suicidal depression is a physical ailment, as unconnected to the patient’s moral character as cancer. The book includes a cursory discussion of the chemistry of the brain neurotransmitters, serotonin and so forth. For many readers, it was a first introduction to scientific ideas that are now widely accepted.

For people with severe mood disorders, “Darkness Visible” became a guidebook. “I got depressed and everyone said to me: ‘You have to read the Bill Styron book. You have to read the Bill Styron book. Have you read the Bill Styron book? Let me give you a copy of the Bill Styron book,”’ Mr. Solomon told me. “On the one hand an absolutely harrowing read, and on the other hand one very much rooted in hope.”

The book benefited from perfect timing. It appeared contemporaneously with the introduction of Prozac and other mood disorder medications with fewer side effects than older psychiatric drugs. Relentlessly advertised on TV and in magazines, they seemed to promise protection. And though Mr. Styron himself probably did not take Prozac and was rather skeptical about drugs, his book became the bible of that era.

He also inspired dozens of writers including Mr. Solomon and Dr. Flaherty to chronicle their own struggles. In the 1990s, bookstores were crowded with mental-illness memoirs, Kay Redfield Jamison’s “An Unquiet Mind,” Susanna Kaysen’s “Girl, Interrupted” and Elizabeth Wurtzel’s “Prozac Nation,” to name a few. You read; you wrote; you survived.

It was an optimistic time. In 1999, with “Darkness Visible” in its 25th printing, Mr. Styron told Diane Rehm in an NPR interview: “I’m in very good shape, if I may be so bold as to say that.” He continued, “It’s as if I had purged myself of this pack of demons.”

It wouldn’t last. In the summer of 2000, he crashed again. In the last six years of his life, he would check into mental hospitals and endure two rounds of electroshock therapy.

Mr. Styron’s story mirrors the larger trends in American mental health over the past few decades. During the exuberance of the 1990s, it seemed possible that drugs would one day wipe out depression, making suicide a rare occurrence. But that turned out to be an illusion. In fact, the American suicide rate has continued to climb since the beginning of the 21st century.

We don’t know why this is happening, though we do have a few clues. Easy access to guns is probably contributing to the epidemic: Studies show that when people are able to reach for a firearm, a momentary urge to self-destruct is more likely to turn fatal. Oddly enough, climate change may also be to blame: A new study shows that rising temperatures can make people more prone to suicide.

With suicidal depression so widespread, we find ourselves needing new ways to talk about it, name its depredations and help families cope with it. Mr. Styron’s mission was to invent this new language of survival, but he did so at high cost to his own mental health.

When he revealed his history of depression, he inadvertently set a trap for himself. He became an icon of recovery. His widow, Rose Styron, told me that readers would call the house at all hours when they felt suicidal, and Mr. Styron would counsel them. He always took those calls, even when they woke him at 3 in the morning.

When he plunged into depression again in 2000, Mr. Styron worried about disappointing his fans. “When he crashed, he felt so guilty because he thought he’d let down all the people he had encouraged in ‘Darkness Visible,’” Ms. Styron told me. And he became painfully aware that if he ever did commit suicide, that private act would ripple out all over the world. The consequences would be devastating for his readers, some of whom might even decide to imitate him.

And so, one dark day in the summer of 2000, he wrote up a statement to be released in the event of his suicide. “I hope that readers of ‘Darkness Visible’ past, present and future will not be discouraged by the manner of my dying,” his message began. It was an attempt to inoculate his fans from the downstream effects of his own selfdestruction.

Mr. Styron’s family described this sense of his that succumbing to depression a second time made him a fraud.

DARKNESS VISIBLE.

A MEMOIR of MADNESS

William Styron

For the thing which I greatly feared is come upon me, and that which I was afraid of Is come unto me. I was not in safety, neither had I rest, neither was I quiet; yet trouble came. -Job

One

IN PARIS ON A CHILLY EVENING LATE IN OCTOBER OF 1985 I first became fully aware that the struggle with the disorder in my mind, a struggle which had engaged me for several months, might have a fatal outcome. The moment of revelation came as the car in which I was riding moved down a rain slick street not far from the Champs Elysées and slid past a dully glowing neon sign that read HOTEL WASHINGTON. I had not seen that hotel in nearly thirty-five years, since the spring of 1952, when for several nights it had become my initial Parisian roosting place.

In the first few months of my Wanderjahr, I had come down to Paris by train from Copenhagen, and landed at the Hotel Washington through the whimsical determination of a New York travel agent. In those days the hotel was one of the many damp, plain hostelries made for tourists, chiefly American, of very modest means who, if they were like me, colliding nervously for the first time with the French and their droll kinks, would always remember how the exotic bidet, positioned solidly in the drab bedroom, along with the toilet far down the ill-lit hallway, virtually defined the chasm between Gallic and Anglo-Saxon cultures.

But I stayed at the Washington for only a short time. Within days I had been urged out of the place by some newly found young American friends who got me installed in an even seedier but more colorful hotel in Montparnasse, hard by Le Dome and other suitably literary hangouts. (In my mid-twenties, I had just published a first novel and was a celebrity, though one of very low rank since few of the Americans in Paris had heard of my book, let alone read it.) And over the years the Hotel Washington gradually disappeared from my consciousness.

It reappeared, however, that October night when I passed the gray stone facade in a drizzle, and the recollection of my arrival so many years before started flooding back, causing me to feel that I had come fatally full circle. I recall saying to myself that when I left Paris for New York the next morning it would be a matter of forever. I was shaken by the certainty with which I accepted the idea that I would never see France again, just as I would never recapture a lucidity that was slipping away from me with terrifying speed.

Only days before I had concluded that I was suffering from a serious depressive illness, and was floundering helplessly in my efforts to deal with it. I wasn’t cheered by the festive occasion that had brought me to France. Of the many dreadful manifestations of the disease, both physical and psychological, a sense of self-hatred, or, put less categorically, a failure of self-esteem, is one of the most universally experienced symptoms, and I had suffered more and more from a general feeling of worthlessness as the malady had progressed.

My dank joylessness was therefore all the more ironic because I had flown on a rushed four day trip to Paris in order to accept an award which should have sparklingly restored my ego. Earlier that summer I received word that I had been chosen to receive the Prix Mondial Cino del Duca, given annually to an artist or scientist whose work reflects themes or principles of a certain “humanism.” The prize was established in memory of Cino del Duca, an immigrant from Italy who amassed a fortune just before and after World War II by printing and distributing cheap magazines, principally comic books, though later branching out into publications of quality; he became proprietor of the newspaper Paris-Jour.

He also produced movies and was a prominent racehorse owner, enjoying the pleasure of having many winners in France and abroad. Aiming for nobler cultural satisfactions, he evolved into a renowned philanthropist and along the way established a book publishing firm that began to produce works of literary merit (by chance, my first novel, Lie Down in Darkness, was one of del Duca’s offerings, in a translation entitled Un Lit de Ténébres); by the time of his death in 1967 this house, Editions Mondiales, became an important entity of a multifold empire that was rich yet prestigious enough for there to be scant memory of its comic book origins when del Duca’s widow, Simone, created a foundation whose chief function was the annual bestowal of the eponymous award.

The Prix Mondial Cino del Duca has become greatly respected in France, a nation pleasantly besotted with cultural prize giving, not only for its eclecticism and the distinction shown in the choice of its recipients but for the openhandedness of the prize itself, which that year amounted to approximately $25,000. Among the winners during the past twenty years have been Konrad Lorenz, Alejo Carpentier, Jean Anouilh, Ignazio Silone, Andrei Sakharov, Jorge Luis Borges and one American, Lewis Mumford. (No women as yet, feminists take note.)

As an American, I found it especially hard not to feel honored by inclusion in their company. While the giving and receiving of prizes usually induce from all sources an unhealthy uprising of false modesty, backbiting, selftorture and envy, my own view is that certain awards, though not necessary, can be very nice to receive. The Prix del Duca was to me so straightforwardly nice that any extensive self-examination seemed silly, and so I accepted gratefully, writing in reply that I would honor the reasonable requirement that I be present for the ceremony. At that time I looked forward to a leisurely trip, not a hasty turnaround. Had I been able to foresee my state of mind as the date of the award approached, I would not have accepted at all.

Depression is a disorder of mood, so mysteriously painful and elusive in the way it becomes known to the self, to the mediating intellect, as to verge close to being beyond description.

It thus remains nearly incomprehensible to those who have not experienced it in its extreme mode, although the gloom, “the blues” which people go through occasionally and associate with the general hassle of everyday existence are of such prevalence that they do give many individuals a hint of the illness in its catastrophic form. But at the time of which I write I had descended far past those familiar, manageable doldrums. In Paris, I am able to see now, I was at a critical stage in the development of the disease, situated at an ominous way station between its unfocused stirrings earlier that summer and the near violent denouement of December, which sent me into the hospital. I will later attempt to describe the evolution of this malady, from its earliest origins to my eventual hospitalization and recovery, but the Paris trip has retained a notable meaning for me.

On the day of the award ceremony, which was to take place at noon and be followed by a formal luncheon, I woke up at midmorning in my room at the Hétel Pont Royal commenting to myself that I felt reasonably sound, and I passed the good word along to my wife, Rose. Aided by the minor tranquilizer Halcion, I had managed to defeat my insomnia and get a few hours’ sleep. Thus I was in fair spirits.

But such wan cheer was an habitual pretense which I knew meant very little, for I was certain to feel ghastly before nightfall. I had come to a point where I was carefully monitoring each phase of my deteriorating condition. My acceptance of the illness followed several months of denial during which, at first, I had ascribed the malaise and restlessness and sudden fits of anxiety to withdrawal from alcohol; I had abruptly abandoned whiskey and all other intoxicants that June.

During the course of my worsening emotional climate I had read a certain amount on the subject of depression, both in books tailored for the layman and in weightier professional works including the psychiatrists’ bible, DSM (The Diagnostic and Statistical Manual of the American Psychiatric Association). Throughout much of my life I have been compelled, perhaps unwisely, to become an autodidact in medicine, and have accumulated a better than average amateur’s knowledge about medical matters (to which many of my friends, surely unwisely, have often deferred), and so it came as an astonishment to me that I was close to a total ignoramus about depression, which can be as serious a medical affair as diabetes or cancer. Most likely, as an incipient depressive, I had always subconsciously rejected or ignored the proper knowledge; it cut too close to the psychic bone, and I shoved it aside as an unwelcome addition to my store of information.

At any rate, during the few hours when the depressive state itself eased off long enough to permit the luxury of concentration, I had recently filled this vacuum with fairly extensive reading and I had absorbed many fascinating and troubling facts, which, however, I could not put to practical use.

The most honest authorities face up squarely to the fact that serious depression is not readily treatable. Unlike, let us say, diabetes, where immediate measures taken to rearrange the body’s adaptation to glucose can dramatically reverse a dangerous process and bring it under control, depression in its major stages possesses no quickly available remedy: failure of alleviation is one of the most distressing factors of the disorder as it reveals itself to the victim, and one that helps situate it squarely in the category of grave diseases.

Except in those maladies strictly designated as malignant or degenerative, we expect some kind of treatment and eventual amelioration, by pills or physical therapy or diet or surgery, with a logical progression from the initial relief of symptoms to final cure. Frighteningly, the layman sufferer from major depression, taking a peek into some of the many books currently on the market, will find much in the way of theory and symptomatology and very little that legitimately suggests the possibility of quick rescue. Those that do claim an easy way out are glib and most likely fraudulent. There are decent popular works which intelligently point the way toward treatment and cure, demonstrating how certain therapies, psychotherapy or pharmacology, or a combination of these, can indeed restore people to health in all but the most persistent and devastating cases; but the wisest books among them underscore the hard truth that serious depressions do not disappear overnight.

All of this emphasizes an essential though difficult reality which I think needs stating at the outset of my own chronicle: the disease of depression remains a great mystery. It has yielded its secrets to science far more reluctantly than many of the other major ills besetting us. The intense and sometimes comically strident factionalism that exists in present day psychiatry, the schism between the believers in psychotherapy and the adherents of pharmacology, resembles the medical quarrels of the eighteenth century (to bleed or not to bleed) and almost defines in itself the inexplicable nature of depression and the difficulty of its treatment. As a clinician in the field told me honestly and, I think, with a striking deftness of analogy: “If you compare our knowledge with Columbus’s discovery of America, America is yet unknown; we are still down on that little island in the Bahamas.”

In my reading I had learned, for example, that in at least one interesting respect my own case was atypical. Most people who begin to suffer from the illness are laid low in the morning, with such malefic effect that they are unable to get out of bed. They feel better only as the day wears on. But my situation was just the reverse. While I was able to rise and function almost normally during the earlier part of the day, I began to sense the onset of the symptoms at midafternoon or a little later, gloom crowding in on me, a sense of dread and alienation and, above all, stifling anxiety. I suspect that it is basically a matter of indifference whether one suffers the most in the morning or the evening: if these states of excruciating near paralysis are similar, as they probably are, the question of timing would seem to be academic. But it was no doubt the turnabout of the usual daily onset of symptoms that allowed me that morning in Paris to proceed without mishap, feeling more or less self-possessed, to the gloriously ornate palace on the Right Bank that houses the Fondation Cino del Duca. There, in a rococo salon, I was presented with the award before a small crowd of French cultural figures, and made my speech of acceptance with what I felt was passable aplomb, stating that while I was donating the bulk of my prize money to various organizations fostering French-American goodwill, including the American Hospital in Neuilly, there was a limit to altruism (this spoken jokingly) and so I hoped it would not be taken amiss if I held back a small portion for myself.

What I did not say, and which was no joke, was that the amount I was withholding was to pay for two tickets the next day on the Concorde, so that I might return speedily with Rose to the United States, where just a few days before I had made an appointment to see a psychiatrist. For reasons that I’m sure had to do with a reluctance to accept the reality that my mind was dissolving, I had avoided seeking psychiatric aid during the past weeks, as my distress intensified. But I knew I couldn’t delay the confrontation indefinitely, and when I did finally make contact by telephone with a highly recommended therapist, he encouraged me to make the Paris trip, telling me that he would see me as soon as I returned. I very much needed to get back, and fast.

Despite the evidence that I was in serious difficulty, I wanted to maintain the rosy view. A lot of the literature available concerning depression is, as I say, breezily optimistic, spreading assurances that nearly all depressive states will be stabilized or reversed if only the suitable antidepressant can be found; the reader is of course easily swayed by promises of quick remedy. In Paris, even as I delivered my remarks, I had a need for the day to be over, felt a consuming urgency to fly to America and the office of the doctor, who would whisk my malaise away with his miraculous medications. I recollect that moment clearly now, and am hardly able to believe that I possessed such ingenuous hope, or that I could have been so unaware of the trouble and peril that lay ahead.

Simone del Duca, a large dark-haired woman of queenly manner, was understandably incredulous at first, and then enraged, when after the presentation ceremony I told her that I could not join her at lunch upstairs in the great mansion, along with a dozen or so members of the Académie Frangaise, who had chosen me for the prize. My refusal was both emphatic and simpleminded; I told her point-blank that I had arranged instead to have lunch at a restaurant with my French publisher, Frangoise Gallimard. Of course this decision on my part was outrageous; it had been announced months before to me and everyone else concerned that a luncheon, moreover, a luncheon in my honor, was part of the day’s pageantry. But my behavior was really the result of the illness, which had progressed far enough to produce some of its most famous and sinister hallmarks: confusion, failure of mental focus and lapse of memory. At a later stage my entire mind would be dominated by anarchic disconnections; as I have said, there was now something that resembled bifurcation of mood: lucidity of sorts in the early hours of the day, gathering murk in the afternoon and evening. It must have been during the previous evening’s murky distractedness that I made the luncheon date with Frangoise Gallimard, forgetting my del Duca obligations. That decision continued to completely master my thinking, creating in me such obstinate determination that now I was able to blandly insult the worthy Simone del Duca. “Alors!” she exclaimed to me, and her face flushed angrily as she whirled in a stately volte-face, “au revoir!”

Suddenly I was flabbergasted, stunned with horror at what I had done. I fantasized a table at which sat the hostess and the Académie Frangaise, the guest of honor at La Coupole. I implored Madame’s assistant, a bespectacled woman with a clipboard and an ashen, mortified expression, to try to reinstate me: it was all a terrible mistake, a mixup, a malentendu. And then I blurted some words that a lifetime of general equilibrium, and a smug belief in the impregnability of my psychic health, had prevented me from believing I could ever utter; I was chilled as I heard myself speak them to this perfect stranger.

“I’m sick,” I said, “un probleme psychiatrique.”

Madame del Duca was magnanimous in accepting my apology and the lunch went off without further strain, aIthough I couldn’t completely rid myself of the suspicion, as we chatted somewhat stiffly, that my benefactress was still disturbed by my conduct and thought me a weird number. The lunch was a long one, and when it was over I felt myself entering the afternoon shadows with their encroaching anxiety and dread. A television crew from one of the national channels was waiting (I had forgotten about them, too), ready to take me to the newly opened Picasso Museum, where I was supposed to be filmed looking at the exhibits and exchanging comments with Rose.

This turned out to be, as I knew it would, not a captivating promenade but a demanding struggle, a major ordeal. By the time we arrived at the museum, having dealt with heavy traffic, it was past four o’clock and my brain had begun to endure its familiar siege: panic and dislocation, and a sense that my thought processes were being engulfed by a toxic and unnameable tide that obliterated any enjoyable response to the living world. This is to say more specifically that instead of pleasure, certainly instead of the pleasure I should be having in this sumptuous showcase of bright genius, I was feeling in my mind a sensation close to, but indescribably different from, actual pain.

This leads me to touch again on the elusive nature of such distress. That the word “indescribable” should present itself is not fortuitous, since it has to be emphasized that if the pain were readily describable most of the countless sufferers from this ancient affliction would have been able to confidently depict for their friends and loved ones (even their physicians) some of the actual dimensions of their torment, and perhaps elicit a comprehension that has been generally lacking; such incomprehension has usually been due not to a failure of sympathy but to the basic inability of healthy people to imagine a form of torment so alien to everyday experience.

For myself, the pain is most closely connected to drowning or suffocation, but even these images are off the mark. William James, who battled depression for many years, gave up the search for an adequate portrayal, implying its near-impossibility when he wrote in The Varieties of Religious Experience:

“It is a positive and active anguish, a sort of psychical neuralgia wholly unknown to normal life.”

The pain persisted during my museum tour and reached a crescendo in the next few hours when, back at the hotel, I fell onto the bed and lay gazing at the ceiling, nearly immobilized and in a trance of supreme discomfort. Rational thought was usually absent from my mind at such times, hence trance.

I can think of no more apposite word for this state of being, a condition of helpless stupor in which cognition was replaced by that “positive and active anguish.”

And one of the most unendurable aspects of such an interlude was the inability to sleep. It had been my custom of a near lifetime, like that of vast numbers of people, to settle myself into a soothing nap in the late afternoon, but the disruption of normal sleep patterns is a notoriously devastating feature of depression; to the injurious sleeplessness with which I had been afflicted each night was added the insult of this afternoon insomnia, diminutive by comparison but all the more horrendous because it struck during the hours of the most intense misery. It had become clear that I would never be granted even a few minutes’ relief from my full-time exhaustion. I clearly recall thinking, as I lay there while Rose sat nearby reading, that my afternoons and evenings were becoming almost measurably worse, and that this episode was the worst to date. But I somehow managed to reassemble myself for dinner with, who else? -Francoise Gallimard, co-victim along with Simone del Duca of the frightful lunchtime contretemps.

The night was blustery and raw, with a chill wet wind blowing down the avenues, and when Rose and I met Francoise and her son and a friend at La Lorraine, a glittering brasserie not far from L’Etoile, rain was descending from the heavens in torrents. Someone in the group, sensing my state of mind, apologized for the evil night, but I recall thinking that even if this were one of those warmly scented and passionate evenings for which Paris is celebrated I would respond like the zombie I had become. The weather of depression is unmodulated, its light a brownout.

And zombielike, halfway through the dinner, I lost the del Duca prize check for $25,000. Having tucked the check in the inside breast pocket of my jacket, I let my hand stray idly to that place and realized that it was gone. Did I “intend” to lose the money? Recently I had been deeply bothered that I was not deserving of the prize. I believe in the reality of the accidents we subconsciously perpetrate on ourselves, and so how easy it was for this loss to be not loss but a form of repudiation, offshoot of that seIf-loathing (depression’s premier badge) by which I was persuaded that I could not be worthy of the prize, that I was in fact not worthy of any of the recognition that had come my way in the past few years. Whatever the reason for its disappearance, the check was gone, and its loss dovetailed well with the other failures of the dinner: my failure to have an appetite for the grand plateau de fruits de mer placed before me, failure of even forced laughter and, at last, virtually total failure of speech.

At this point the ferocious inwardness of the pain produced an immense distraction that prevented my articulating words beyond a hoarse murmur; I sensed myself turning walleyed, monosyllabic, and also I sensed my French friends becoming uneasily aware of my predicament. It was a scene from a bad Operetta by now: all of us near the floor, searching for the vanished money. Just as I signaled that it was time to go, Francoise’s son discovered the check, which had somehow slipped out of my pocket and fluttered under an adjoining table, and we went forth into the rainy night. Then, while I was riding in the car, I thought of Albert Camus and Romain Gary.

Two

WHEN I WAS A YOUNG WRITER THERE HAD BEEN A stage where Camus, almost more than any other contemporary literary figure, radically set the tone for my own view of life and history. I read his novel The Stranger somewhat later than I should have, I was in my early thirties, but after finishing it I received the stab of recognition that proceeds from reading the work of a writer who has wedded moral passion to a style of great beauty and whose unblinking vision is capable of frightening the soul to its marrow.

The cosmic loneliness of Meursault, the hero of that novel, so haunted me that when I set out to write The Confessions of Nat Turner I was impelled to use Camus’s device of having the story flow from the point of view of a narrator isolated in his jail cell during the hours before his execution. For me there was a spiritual connection between Meursault’s frigid solitude and the plight of Nat Turner, his rebel predecessor in history by a hundred years, likewise condemned and abandoned by man and God.

Camus’s essay “Reflections on the Guillotine” is a virtually unique document, freighted with terrible and fiery logic; it is difficult to conceive of the most vengeful supporter of the death penalty retaining the same attitude after exposure to scathing truths expressed with such ardor and precision. I know my thinking was forever altered by that work, not only turning me around completely, convincing me of the essential barbarism of capital punishment, but establishing substantial claims on my conscience in regard to matters of responsibility at large. Camus was a great cleanser of my intellect, ridding me of countless sluggish ideas, and through some of the most unsettling pessimism I had ever encountered causing me to be aroused anew by life’s enigmatic promise.

The disappointment I always felt at never meeting Camus was compounded by that failure having been such a near miss. I had planned to see him in 1960, when I was traveling to France and had been told in a letter by the writer Romain Gary that he was going to arrange a dinner in Paris where I would meet Camus. The enormously gifted Gary, whom I knew slightly at the time and who later became a cherished friend, had informed me that Camus, whom he saw frequently, had read my Un Lit de Te’nebres and had admired it; I was of course greatly flattered and felt that a get-together would be a splendid happening. But before I arrived in France there came the appalling news: Camus had been in an automobile crash, and was dead at the cruelly young age of forty-six. I have almost never felt so intensely the loss of someone I didn’t know. I pondered his death endlessly. Although Camus had not been driving he supposedly knew the driver, who was the son of his publisher, to be a speed demon; so there was an element of recklessness in the accident that bore overtones of the near-suicidal, at least of a death flirtation, and it was inevitable that conjectures concerning the event should revert back to the theme of suicide in the writer’s work.

One of the century’s most famous intellectual pronouncements comes at the beginning of The Myth of Sisyphus: “There is but one truly serious philosophical problem, and that is suicide. Judging whether life is or is not worth living amounts to answering the fundamental question of philosophy.” Reading this for the first time I was puzzled and continued to be throughout much of the essay, since despite the work’s persuasive logic and eloquence there was a lot that eluded me, and I always came back to grapple vainly with the initial hypothesis, unable to deal with the premise that anyone should come close to wishing to kill himself in the first place.

A later short novel, The Fall, I admired with reservations; the guilt and seIf-condemnation of the lawyer-narrator, gloomily spinning out his monologue in an Amsterdam bar, seemed a touch clamorous and excessive, but at the time of my reading I was unable to perceive that the lawyer was behaving very much like a man in the throes of clinical depression. Such was my innocence of the very existence of this disease. Camus, Romain told me, occasionally hinted at his own deep despondency and had spoken of suicide. Sometimes he spoke in jest, but the jest had the quality of sour wine, upsetting Romain. Yet apparently he made no attempts and so perhaps it was not coincidental that, despite its abiding tone of melancholy, a sense of the triumph of life over death is at the core of The Myth of Sisyphus with its austere message: in the absence of hope we must still struggle to survive, and so we doby the skin of our teeth.

It was only after the passing of some years that it seemed credible to me that Camus’s statement about suicide, and his general preoccupation with the subject, might have sprung at least as strongly from some persistent disturbance of mood as from his concerns with ethics and epistemology. Gary again discussed at length his assumptions about Camus’s depression during August of 1978, when I had lent him my guest cottage in Connecticut, and I came down from my summer home on Martha’s Vineyard to pay him a weekend visit. As we talked I felt that some of Romain’s suppositions about the seriousness of Camus’s recurring despair gained weight from the fact that he, too, had begun to suffer from depression, and he freely admitted as much. It was not incapacitating, he insisted, and he had it under control, but he felt it from time to time, this leaden and poisonous mood the color of verdigris, so incongruous in the midst of the lush New England summer. A Russian Jew born in Lithuania, Romain had always seemed possessed of an Eastern European melancholy, so it was hard to tell the difference. Nonetheless, he was hurting. He said that he was able to perceive a flicker of the desperate state of mind which had been described to him by Camus.

Gary’s situation was hardly lightened by the presence of Jean Seberg, his lowa-born actress wife, from whom he had been divorced and, I thought, long estranged. I learned that she was there because their son, Diego, was at a nearby tennis camp. Their presumed estrangement made me surprised to see her living with Romain, surprised too, no, shocked and saddened, by her appearance: all her once fragile and luminous blond beauty had disappeared into a puffy mask. She moved like a Sleepwalker, said little, and had the blank gaze of someone tranquilized (or drugged, or both) nearly to the point of catalepsy. I understood how devoted they still were, and was touched by his solicitude, both tender and paternal. Romain told me that Jean was being treated for the disorder that afflicted him, and mentioned something about antidepressant medications, but none of this registered very strongly, and also meant little.

This memory of my relative indifference is important because such indifference demonstrates powerfully the outsider’s inability to grasp the essence of the illness. Camus’s depression and now Romain Gary’s, and certainly Jean’s, were abstract ailments to me, in spite of my sympathy, and I hadn’t an inkling of its true contours or the nature of the pain so many victims experience as the mind continues in its insidious meltdown.

In Paris that October night I knew that I, too, was in the process of meltdown. And on the way to the hotel in the car I had a clear revelation. A disruption of the circadian cycle, the metabolic and glandular rhythms that are central to our workaday life, seems to be involved in many, if not most, cases of depression; this is why brutal insomnia so often occurs and is most likely why each day’s pattern of distress exhibits fairly predictable alternating periods of intensity and relief. The evening’s relief for me, an incomplete but noticeable letup, like the change from a torrential downpour to a steady shower, came in the hours after dinner time and before midnight, when the pain lifted a little and my mind would become lucid enough to focus on matters beyond the immediate upheaval convulsing my system. Naturally I looked forward to this period, for sometimes I felt close to being reasonably sane, and that night in the car I was aware of a semblance of clarity returning, along with the ability to think rational thoughts. Having been able to reminisce about Camus and Romain Gary, however, I found that my continuing thoughts were not very consoling.

The memory of Jean Seberg gripped me with sadness. A little over a year after our encounter in Connecticut she took an overdose of pills and was found dead in a car parked in a cul-de-sac off a Paris avenue, where her body had lain for many days. The following year I sat with Romain at the Brasserie Lipp during a long lunch while he told me that, despite their difficulties, his loss of Jean had so deepened his depression that from time to time he had been rendered nearly helpless. But even then I was unable to comprehend the nature of his anguish. I remembered that his hands trembled and, though he could hardly be called superannuated, he was in his mid-sixties, his voice had the wheezy sound of very old age that I now realized was, or could be, the voice of depression; in the vortex of my severest pain I had begun to develop that ancient voice myself. I never saw Romain again. Claude Gallimard, Francoise’s father, had recollected to me how, in 1980, only a few hours after another lunch where the talk between the two old friends had been composed and casual, even lighthearted, certainly anything but somber, Romain Gary, twice winner of the Prix Goncourt (one of these awards pseudonymous, the result of his having gleefully tricked the critics), hero of the Republic, valorous recipient of the Croix de Guerre, diplomat, bon vivant, womanizer par excellence, went home to his apartment on the rue du Bac and put a bullet through his brain.

It was at some point during the course of these musings that the sign HOTEL WASHINGTON swam across my vision, bringing back memories of my long ago arrival in the city, along with the fierce and sudden realization that I would never see Paris again. This certitude astonished me and filled me with a new fright, for while thoughts of death had long been common during my siege, blowing through my mind like icy gusts of wind, they were the formless shapes of doom that I suppose are dreamed of by people in the grip of any severe affliction. The difference now was in the sure understanding that tomorrow, when the pain descended once more, or the tomorrow after that, certainly on some not too distant tomorrow, I would be forced to judge that life was not worth living and thereby answer, for myself at least, the fundamental question of philosophy.

Three

TO MANY OF US WHO KNEW ABBIE HOFFMAN EVEN slightly, as I did, his death in the spring of 1989 was a sorrowful happening. Just past the age of fifty, he had been too young and apparently too vital for such an ending; a feeling of chagrin and dreadfulness attends the news of nearly anyone’s suicide, and Abbie’s death seemed to me especially cruel.

I had first met him during the wild days and nights of the 1968 Democratic Convention in Chicago, where I had gone to write a piece for The New York Review of Books, and I later was one of those who testified on behalf of him and his fellow defendants at the trial, also in Chicago, in 1970. Amid the pious follies and morbid perversions of American life, his antic style was exhilarating, and it was hard not to admire the hellraising and the brio, the anarchic individualism.

I wish I had seen more of him in recent years; his sudden death left me with a particular emptiness, as suicides usually do to everyone. But the event was given a further dimension of poignancy by what one must begin to regard as a predictable reaction from many: the denial, the refusal to accept the fact of the suicide itself, as if the voluntary act, as opposed to an accident, or death from natural causes, were tinged with a delinquency that somehow lessened the man and his character.

Abbie’s brother appeared on television, grief, ravaged and distraught; one could not help feeling compassion as he sought to deflect the idea of suicide, insisting that Abbie, after all, had always been careless with pills and would never have left his family bereft. However, the coroner confirmed that Hoffman had taken the equivalent of 150 phenobarbitals.

It’s quite natural that the people closest to suicide victims so frequently and feverishly hasten to disclaim the truth; the sense of implication, of personal guilt, the idea that one might have prevented the act if one had taken certain precautions, had somehow behaved differently, is perhaps inevitable. Even so, the sufferer, whether he has actually killed himself or attempted to do so, or merely expressed threats, is often, through denial on the part of others, unjustly made to appear a wrongdoer.

A similar case is that of Randall Jarrell, one of the fine poets and critics of his generation, who on a night in 1965, near Chapel Hill, North Carolina, was struck by a car and killed. Jarrell’s presence on that particular stretch of road, at an odd hour of the evening, was puzzling, and since some of the indications were that he had deliberately let the car strike him, the early conclusion was that his death was suicide. Newsweek, among other publications, said as much, but Jarrell’s widow protested in a letter to that magazine; there was a hue and cry from many of his friends and supporters, and a coroner’s jury eventually ruled the death to be accidental. Jarrell had been suffering from extreme depression and had been hospitalized; only a few months before his misadventure on the highway and while in the hospital, he had slashed his wrists.

Anyone who is acquainted with some of the jagged contours of Jarrell’s life, including his violent fluctuations of mood, his fits of black despondency, and who, in addition, has acquired a basic knowledge of the danger signals of depression, would seriously question the verdict of the coroner’s jury. But the stigma of selfinflicted death is for some people a hateful blot that demands erasure at all costs. (More than two decades after his death, in the Summer 1986 issue of The American Scholar, a one time student of Jarrell’s, reviewing a collection of the poet’s letters, made the review less a literary or biographical appraisal than an occasion for continuing to try to exorcise the vile phantom of suicide.)

Randall Jarrell almost certainly killed himself. He did so not because he was a coward, nor out of any moral feebleness, but because he was afflicted with a depression that was so devastating that he could no longer endure the pain of it.

This general unawareness of what depression is really like was apparent most recently in the matter of Primo Levi, the remarkable Italian writer and survivor of Auschwitz who, at the age of sixty-seven, hurled himself down a stairwell in Turin in 1987. Since my own involvement with the illness, I had been more than ordinarily interested in Levi’s death, and so, late in 1988, when I read an account in The New York Times about a symposium on the writer and his work held at New York University, was fascinated but, finally, appalled. For, according to the article, many of the participants, worldly writers and scholars, seemed mystified by Levi’s suicide, mystified and disappointed. It was as if this man whom they had all so greatly admired, and who had endured so much at the hands of the Nazis, a man of exemplary resilience and courage, had by his suicide demonstrated a frailty, a crumbling of character they were loath to accept. In the face of a terrible absolute self-destruction, their reaction was helplessness and (the reader could not avoid it) a touch of shame.

My annoyance over all this was so intense that I was prompted to write a short piece for the op-ed page of the Times. The argument I put forth was fairly straightforward:

The pain of severe depression is quite unimaginable to those who have not suffered it, and it kills in many instances because its anguish can no longer be borne.

The prevention of many suicides will continue to be hindered until there is a general awareness of the nature of this pain. Through the healing process of time, and through medical intervention or hospitalization in many cases, most people survive depression, which may be its only blessing; but to the tragic legion who are compelled to destroy themselves there should be no more reproof attached than to the victims of terminal cancer.

I had set down my thoughts in this Times piece rather hurriedly and spontaneously, but the response was equally spontaneous, and enormous. It had taken, I speculated, no particular originality or boldness on my part to speak out frankly about suicide and the impulse toward it, but I had apparently underestimated the number of people for whom the subject had been taboo, a matter of secrecy and shame. The overwhelming reaction made me feel that inadvertently I had helped unlock a closet from which many souls were eager to come out and proclaim that they, too, had experienced the feelings I had described. It is the only time in my life I have felt it worthwhile to have invaded my own privacy, and to make that privacy public. And I thought that, given such momentum, and with my experience in Paris as a detailed example of what occurs during depression, it would be useful to try to chronicle some of my own experiences with the illness and in the process perhaps establish a frame of reference out of which one or more valuable conclusions might be drawn.

Such conclusions, it has to be emphasized, must still be based on the events that happened to one man. In setting these reflections down I don’t intend my ordeal to stand as a representation of what happens, or might happen, to others. Depression is much too complex in its cause, its symptoms and its treatment for unqualified conclusions to be drawn from the experience of a single individual. Although as an illness depression manifests certain unvarying characteristics, it also allows for many idiosyncrasies; I’ve been amazed at some of the freakish phenomena, not reported by other patients, that it has wrought amid the twistings of my mind’s labyrinth.

Depression afflicts millions directly, and millions more who are relatives or friends of victims. It has been estimated that as many as one in ten Americans will suffer from the illness. As assertively democratic as a Norman Rockwell poster, it strikes indiscriminately at all ages, races, creeds and classes, though women are at considerably higher risk than men. The occupational list (dressmakers, barge captains, sushi chefs, cabinet members) of its patients is too long and tedious to give here; it is enough to say that very few people escape being a potential victim of the disease, at least in its milder form. Despite depression’s eclectic reach, it has been demonstrated with fair convincingness that artistic types (especially poets) are particularly vulnerable to the disorder, which, in its graver, clinical manifestation takes upward of twenty percent of its victims by way of suicide.

Just a few of these fallen artists, all modern, make up a sad but scintillant roll call: Hart Crane, Vincent van Gogh, Virginia Woolf, Arshile Gorky, Cesare Pavese, Romain Gary, Vachel Lindsay, Sylvia Plath, Henry de Montherlant, Mark Rothko, John Berryman, Jack London, Ernest Hemingway, William Inge, Diane Arbus, Tadeusz Borowski, Paul Celan, Anne Sexton, Sergei Esenin, Vladimir Mayakovsky, the list goes on. (The Russian poet Mayakovsky was harshly critical of his great contemporary Esenin’s suicide a few years before, which should stand as a caveat for all who are judgmental about self destruction.)

When one thinks of these doomed and splendidly creative men and women, one is drawn to contemplate their childhoods, where, to the best of anyone’s knowledge, the seeds of the illness take strong root; could any of them have had a hint, then, of the psyche’s perishability, its exquisite fragility? And why were they destroyed, while others, similarly stricken, struggled through?

Four

WHEN I WAS FIRST AWARE THAT I HAD BEEN LAID low by the disease, I felt a need, among other things, to register a strong protest against the word “depression.” Depression, most people know, used to be termed “melancholia,” a word which appears in English as early as the year 1303 and crops up more than once in Chaucer, who in his usage seemed to be aware of its pathological nuances. “Melancholia” would still appear to be a far more apt and evocative word for the blacker forms of the disorder, but it was usurped by a noun with a bland tonality and lacking any magisterial presence, used indifferently to describe an economic decline or a rut in the ground, a true wimp of a word for such a major illness. It may be that the scientist generally held responsible for its currency in modern times, a Johns Hopkins Medical School faculty member justly venerated, the Swiss born psychiatrist Adolf Meyer, had a tin ear for the finer rhythms of English and therefore was unaware of the semantic damage he had inflicted by offering “depression” as a descriptive noun for such a dreadful and raging disease. Nonetheless, for over seventy-five years the word has slithered innocuously through the language like a slug, leaving little trace of its intrinsic malevolence and preventing, by its very insipidity, a general awareness of the horrible intensity of the disease when out of control.

As one who has suffered from the malady in extremis yet returned to tell the tale, I would lobby for a truly arresting designation. “Brainstorm,” for instance, has unfortunately been preempted to describe, somewhat jocularly, intellectual inspiration. But something along these lines is needed. Told that someone’s mood disorder has evolved into a storm, a veritable howling tempest in the brain, which is indeed what a clinical depression resembles like nothing else, even the uninformed layman might display sympathy rather than the standard reaction that “depression” evokes, something akin to “So what?” or “You’ll pull out of it” or “We all have bad days.” The phrase “nervous breakdown” seems to be on its way out, certainly deservedly so, owing to its insinuation of a vague spinelessness, but we still seem destined to be saddled with “depression” until a better, sturdier name is created.

The depression that engulfed me was not of the manic type, the one accompanied by euphoric highs, which would have most probably presented itself earlier in my life. I was sixty when the illness struck for the first time, in the “unipolar” form, which leads straight down. I shall never learn what “caused” my depression, as no one will ever learn about their own. To be able to do so will likely forever prove to be an impossibility, so complex are the intermingled factors of abnormal chemistry, behavior and genetics. Plainly, multiple components are involved, perhaps three or four, most probably more, in fathomless permutations.

That is why the greatest fallacy about suicide lies in the belief that there is a single immediate answer, or perhaps combined answers, as to why the deed was done.

The inevitable question “Why did he, or she do it?” usually leads to odd speculations, for the most part fallacies themselves. Reasons were quickly advanced for Abbie Hoffman’s death: his reaction to an auto accident he had suffered, the failure of his most recent book, his mother’s serious illness. With Randall Jarrell it was a declining career cruelly epitomized by a vicious book review and his consequent anguish. Primo Levi, it was rumored, had been burdened by caring for his paralytic mother, which was more onerous to his spirit than even his experience at Auschwitz.

Any one of these factors may have lodged like a thorn in the sides of the three men, and been a torment. Such aggravations may be crucial and cannot be ignored. But most people quietly endure the equivalent of injuries, declining careers, nasty book reviews, family illnesses. A vast majority of the survivors of Auschwitz have borne up fairly well. Bloody and bowed by the outrages of life, most human beings still stagger on down the road, unscathed by real depression.

To discover why some people plunge into the downward spiral of depression, one must search beyond the manifest crisis, and then still fail to come up with anything beyond wise conjecture.

The storm which swept me into a hospital in December began as a cloud no bigger than a wine goblet the previous June. And the cloud, the manifest crisis, involved alcohol, a substance I had been abusing for forty years. Like a great many American writers, whose sometimes lethal addiction to alcohol has become so legendary as to provide in itself a stream of studies and books, I used alcohol as the magical conduit to fantasy and euphoria, and to the enhancement of the imagination. There is no need to either rue or apologize for my use of this soothing, often sublime agent, which had contributed greatly to my writing; although I never set down a line while under its influence, I did use it, often in conjunction with music, as a means to let my mind conceive visions that the unaltered, sober brain has no access to. Alcohol was an invaluable senior partner of my intellect, besides being a friend whose ministrations I sought daily, sought also, I now see, as a means to calm the anxiety and incipient dread that I had hidden away for so long somewhere in the dungeons of my spirit.

The trouble was, at the beginning of this particular summer, that I was betrayed. It struck me quite suddenly, almost overnight: I could no longer drink. It was as if my body had risen up in protest, along with my mind, and had conspired to reject this daily mood bath which it had so long welcomed and, who knows? perhaps even come to need. Many drinkers have experienced this intolerance as they have grown older. I suspect that the crisis was at least partly metabolic, the liver rebelling, as if to say, “No more, no more”, but at any rate I discovered that alcohol in minuscule amounts, even a mouthful of wine, caused me nausea, a desperate and unpleasant wooziness, a sinking sensation and ultimately a distinct revulsion. The comforting friend had abandoned me not gradually and reluctantly, as a true friend might do, but like a shot, and I was left high and certainly dry, and unhelmed.

Neither by will nor by choice had I became an abstainer; the situation was puzzling to me, but it was also traumatic, and I date the onset of my depressive mood from the beginning of this deprivation. Logically, one would be overjoyed that the body had so summarily dismissed a substance that was undermining its health; it was as if my system had generated a form of Antabuse, which should have allowed me to happily go my way, satisfied that a trick of nature had shut me off from a harmful dependence. But, instead, I began to experience a vaguely troubling malaise, a sense of something having gone cockeyed in the domestic universe I’d dwelt in so long, so comfortably. While depression is by no means unknown when people stop drinking, it is usually on a scale that is not menacing. But it should be kept in mind how idiosyncratic the faces of depression can be.

It was not really alarming at first, since the change was subtle, but I did notice that my surroundings took on a different tone at certain times: the shadows of nightfall seemed more somber, my mornings were less buoyant, walks in the woods became less zestful, and there was a moment during my working hours in the late afternoon when a kind of panic and anxiety overtook me, just for a few minutes, accompanied by a visceral queasiness, such a seizure was at least slightly alarming, after all. As I set down these recollections, I realize that it should have been plain to me that I was already in the grip of the beginning of a mood disorder, but I was ignorant of such a condition at that time.

When I reflected on this curious alteration of my consciousness, and I was baffled enough from time to time to do so, I assumed that it all had to do somehow with my enforced withdrawal from alcohol. And, of course, to a certain extent this was true. But it is my conviction now that alcohol played a perverse trick on me when we said farewell to each other: although, as everyone should know, it is a major depressant, it had never truly depressed me during my drinking career, acting instead as a shield against anxiety.

Suddenly vanished, the great ally which for so long had kept my demons at bay was no longer there to prevent those demons from beginning to swarm through the subconscious, and I was emotionally naked, vulnerable as I had never been before.

Doubtless depression had hovered near me for years, waiting to swoop down. Now I was in the first stage, premonitory, like a flicker of sheet lightning barely perceived, of depression’s black tempest.

I was on Martha’s Vineyard, where I’ve Spent a good part of each year since the 1960s, during that exceptionally beautiful summer. But I had begun to respond indifferently to the island’s pleasures. I felt a kind of numbness, an enervation, but more particularly an odd fragility, as if my body had actually become frail, hypersensitive and somehow disjointed and clumsy, lacking normal coordination. And soon I was in the throes of a pervasive hypochondria. Nothing felt quite right with my corporeal self; there were twitches and pains, sometimes intermittent, often seemingly constant, that seemed to presage all sorts of dire infirmities. (Given these signs, one can understand how, as far back as the seventeenth century, in the notes of contemporary physicians, and in the perceptions of John Dryden and others, a connection is made between melancholia and hypochondria; the words are often interchangeable, and were so used until the nineteenth century by writers as various as Sir Walter Scott and the Brontés, who also linked melancholy to a preoccupation with bodily ills.) It is easy to see how this condition is part of the psyche’s apparatus of defense: unwilling to accept its own gathering deterioration, the mind announces to its indwelling consciousness that it is the body with its perhaps correctable defects, not the precious and irreplaceable mind, that is going haywire.

In my case, the overall effect was immensely disturbing, augmenting the anxiety that was by now never quite absent from my waking hours and fueling still another strange behavior pattern, a fidgety restlessness that kept me on the move, somewhat to the perplexity of my family and friends. Once, in late summer, on an airplane trip to New York, I made the reckless mistake of downing a scotch and soda, my first alcohol in months, which promptly sent me into a tailspin, causing me such a horrified sense of disease and interior doom that the very next day I rushed to a Manhattan internist, who inaugurated a long series of tests. Normally I would have been satisfied, indeed elated, when, after three weeks of high-tech and extremely expensive evaluation, the doctor pronounced me totally fit; and I was happy, for a day or two, until there once again began the rhythmic daily erosion of my mood, anxiety, agitation, unfocused dread.

By now I had moved back to my house in Connecticut. It was October, and one of the unforgettable features of this stage of my disorder was the way in which my old farmhouse, my beloved home for thirty years, took on for me at that point when my spirits regularly sank to their nadir an almost palpable quality of ominousness. The fading evening light, akin to that famous “slant of light” of Emily Dickinson’s, which spoke to her of death, of chill extinction, had none of its familiar autumnal loveliness, but ensnared me in a suffocating gloom. I wondered how this friendly place, teeming with such memories of (again in her words) “Lads and Girls,” of “laughter and ability and sighing, and Frocks and Curls,” could almost perceptibly seem so hostile and forbidding. Physically, I was not alone. As always Rose was present and listened with unflagging patience to my complaints. But I felt an immense and aching solitude. I could no longer concentrate during those afternoon hours, which for years had been my working time, and the act of writing itself, becoming more and more difficult and exhausting, stalled, then finally ceased.

There were also dreadful, pouncing seizures of anxiety. One bright day on a walk through the woods with my dog I heard a flock of Canada geese honking high above trees ablaze with foliage; ordinarily a sight and sound that would have exhilarated me, the flight of birds caused me to stop, riveted with fear, and I stood stranded there, helpless, shivering, aware for the first time that I had been stricken by no mere pangs of withdrawal but by a serious illness whose name and actuality I was able finally to acknowledge. Going home, I couldn’t rid my mind of the line of Baudelaire’s, dredged up from the distant past, that for several days had been skittering around at the edge of my consciousness: “I have felt the wind of the wing of madness.”

Our perhaps understandable modern need to dull the sawtooth edges of so many of the afflictions we are heir to has led us to banish the harsh old-fashioned words: madhouse, asylum, insanity, melancholia, lunatic, madness.

But never let it be doubted that depression, in its extreme form, is madness. The madness results from an aberrant biochemical process. It has been established with reasonable certainty (after strong resistance from many psychiatrists, and not all that long ago) that such madness is chemically induced amid the neurotransmitters of the brain, probably as the result of systemic stress, which for unknown reasons causes a depletion of the chemicals norepinephrine and serotonin, and the increase of a hormone, cortisol.

With all of this upheaval in the brain tissues, the alternate drenching and deprivation, it is no wonder that the mind begins to feel aggrieved, stricken, and the muddied thought processes register the distress of an organ in convulsion. Sometimes, though not very often, such a disturbed mind will turn to violent thoughts regarding others. But with their minds turned agonizingly inward, people with depression are usually dangerous only to themselves. The madness of depression is, generally speaking, the antithesis of violence. It is a storm indeed, but a storm of murk. Soon evident are the slowed-down responses, near paralysis, psychic energy throttled back close to zero. Ultimately, the body is affected and feels sapped, drained.

That fall, as the disorder gradually took full possession of my system, I began to conceive that my mind itself was like one of those outmoded small town telephone exchanges, being gradually inundated by flood waters: one by one, the normal circuits began to drown, causing some of the functions of the body and nearly all of those of instinct and intellect to slowly disconnect.

There is a well known checklist of some of these functions and their failures. Mine conked out fairly close to schedule, many of them following the pattern of depressive seizures. I particularly remember the lamentable near disappearance of my voice. It underwent a strange transformation, becoming at times quite faint, wheezy and spasmodic, a friend observed later that it was the voice of a ninety year old. The libido also made an early exit, as it does in most major illnesses, it is the superfluous need of a body in beleaguered emergency. Many people lose all appetite; mine was relatively normal, but I found myself eating only for susistence: food, like everything else within the scope of sensation, was utterly without savor. Most distressing of all the instinctual disruptions was that of sleep, along with a complete absence of dreams.

Exhaustion combined with sleeplessness is a rare torture. The two or three hours of sleep I was able to get at night were always at the behest of the Halcyon, a matter which deserves particular notice. For some time now many experts in psychopharmacology have warned that the benzodiazepine family of tranquilizers, of which Halcion is one (Valium and Ativan are others), is capable of depressing mood and even precipitating a major depression. Over two years before my siege, an insouciant doctor had prescribed Ativan as a bedtime aid, telling me airily that I could take it as casually as aspirin. The Physicians’ Desk Reference, the pharmacological bible, reveals that the medicine I had been ingesting was (a) three times the normally prescribed strength, (b) not advisable as a medication for more than a month or so, and (c) to be used with special caution by people of my age. At the time of which I am speaking I was no longer taking Ativan but had become addicted to Halcion and was consuming large doses. It seems reasonable to think that this was still another contributory factor to the trouble that had come upon me. Certainly, it should be a caution to others.

At any rate, my few hours of sleep were usually terminated at three or four in the morning, when I stared up into yawning darkness, wondering and writhing at the devastation taking place in my mind, and awaiting the dawn, which usually permitted me a feverish, dreamless nap. I’m fairly certain that it was during one of these insomniac trances that there came over me the knowledge, a weird and shocking revelation, like that of some long beshrouded metaphysical truth, that this condition would cost me my life if it continued on such a course. This must have been just before my trip to Paris.

Death, as I have said, was now a daily presence, blowing over me in cold gusts. I had not conceived precisely how my end would come. In short, I was still keeping the idea of suicide at bay. But plainly the possibility was around the corner, and I would soon meet it face to face.

What I had begun to discover is that, mysteriously and in ways that are totally remote from normal experience.

The gray drizzle of horror induced by depression takes on the quality of physical pain. But it is not an immediately identifiable pain, like that of a broken limb. It may be more accurate to say that despair, owing to some evil trick played upon the sick brain by the inhabiting psyche, comes to resemble the diabolical discomfort of being imprisoned in a fiercely overheated room. And because no breeze stirs this caldron, because there is no escape from this smothering confinement, it is entirely natural that the victim begins to think ceaselessly of oblivion.

*

Five

. . .

*

from

DARKNESS VISIBLE. A MEMOIR of MADNESS

by William Styron

get it at Amazon.com

Depressive Realism. Interdisciplinary perspectives – Colin Feltham.

Depressive Realism argues that people with mild-to-moderate depression have a more accurate perception of reality than nondepressives.

This book challenges the tacit hegemony of contemporary positive thinking, as well as the standard assumption in cognitive behavioural therapy that depressed individuals must have cognitive distortions.

The kind of world we live in, and that we are, cyclically determines how we feel and think. Some of us perceive and construe the world in dismal terms and believe our construal to be truer than competing accounts. Depending on what the glass is half-full of, the Depressive Realist may regard it as worthless, tasteless, poisonous or ultimately futile to drink.

I do not mean to say that people who experience clinical depression should not have therapy if they wish to, nor even that it does not sometimes help. Rather, I believe the assumption should not be made that depressive or negative views about life and experience necessarily correlate with psychological illness.

Depressive Realism seriously questions the standard assumption in cognitive behaviour therapy that depressed individuals must have cognitive distortions, and indeed reverses this to ask whether DRs might have a more objective grasp of reality than others, and a stubborn refusal to embrace illusion.

I argue that human life contains many glaringly tragic and depressing components and the denial or minimisation of these adds yet another level of depression.

Depressive realism is a worldview of human existence that is essentially negative, and which challenges assumptions about the value of life and the institutions claiming to answer life’s problems. Drawing from central observations from various disciplines, this book argues that a radical honesty about human suffering might initiate wholly new ways of thinking, in everyday life and in clinical practice for mental health, as well as in academia.

Divided into sections that reflect depressive realism as a worldview spanning all academic disciplines, chapters provide examples from psychology, psychotherapy, philosophy and more to suggest ways in which depressive realism can critique each discipline and academia overall. This book challenges the tacit hegemony of contemporary positive thinking, as well as the standard assumption in cognitive behavioural therapy that depressed individuals must have cognitive distortions. It also appeals to the utility of depressive realism for its insights, its pursuit of truth, as well as its emphasis on the importance of learning from negativity and failure. Arguments against depressive realism are also explored.

This book makes an important contribution to our understanding of depressive realism within an interdisciplinary context. It will be of key interest to academics, researchers and postgraduates in the fields of psychology, mental health, psychotherapy, history and philosophy. It will also be of great interest to psychologists, psychotherapists and counsellors.

Colin Feltham is Emeritus Professor of Critical Counselling Studies at Sheffield Hallam University. He is also External Associate Professor of Humanistic Psychology at the University of Southern Denmark.

Introduction

One could declare this to be simply a book about pessimism but that term would be inaccurate and insufficient. A non-verbal shortcut into the subject could be had by listening to Tears for Fears’ Mad World or Dinah Washington’s This Bitter Earth, or perhaps just by reading today’s newspaper. Depressive realism is the term used throughout this book but it will often be abbreviated to DR for ease of reading, referring to the negative worldview and also to anyone subscribing to this worldview (a DR, or DRs). DRs themselves may regard the ‘depressive’ part of the label as gratuitous, thinking their worldview to be simply realism just as Buddhism holds dukkha to be a fact of life.

Initially, it may seem that this book has a traditional mental health or psychological focus, but it draws from a range of interdisciplinary sources, is pertinent to diverse contexts and hopefully of interest to readers in the fields of philosophical anthropology, philosophy of mental health and existentialism and psychotherapy. I imagine it may be of negative, argumentative interest to some theologians, anthropologists, psychologists, social scientists and related lay readers.

Although more implicitly than explicitly, the message running throughout the book is that the kind of world we live in, and that we are, cyclically determines how we feel and think. We will disagree about what kind of world it is, but I hope we might agree that the totality of our history and surroundings has much more impact on us than simply what goes round in our heads.

Depressive realism can be defined, described and contextualised in several ways. its first use appears to have been by Alloy and Abramson (1979) in a paper describing a psychology experiment comparing the judgements of mildly depressed and non-depressed people. It is necessary to make some clarification at the outset about ‘clinical depression’. I do not believe that depression is a desirable state, or that those who are severely depressed are more accurate in their evaluations of life than others (Carson et al., 2010). This is not a book advocating suicide as a solution to life’s difficulties, nor am I advocating voluntary human extinction, nor is the text intended to promote hatred of humanity. The DR discussed here should not be mistaken for a consensual, life-hating suicide cult even if it includes respect for the challenging views of Benatar (2006) and Perry (2014). Nor can one assume that all ‘depressives’ necessarily have permanently and identically pessimistic worldviews, nor indeed that the lines drawn by the psychological professionals between all such mood states are accurate. But one can ask that the majority worldview that ‘Iife is alright’ be set against the DR view that life contains arrestingly negative features (Ligotti, 2010).

The strictly psychological use of DR has now expanded into the world of literary criticism, for example, in Jeffery’s (2011) text on Michel Houellebecq. It is this second, less technical sense of DR on which I focus mainly in this book, that is, on the way in which some of us perceive and construe the world in dismal terms and believe our construal to be truer than competing accounts. Inevitably, within this topic we find ourselves involved in rather tedious realism wars or epistemological battles between yea-sayers, nay-sayers and those who fantasise that objective evidence exists that can end the wars.

Insofar as any term includes ‘realism’, we can say it has a philosophical identity. In the case of DR, the philosophical pessimism most closely associated with Schopenhauer may be its natural home. Existentialism is often considered a negative philosophy, and sometimes wholly nihilistic, but in fact it includes or allows for several varieties of worldview. DR receives the same kind of criticism as existentialism often has, which is that it is less an explicit philosophy than a mood, or a rather vague expression of the personalities, projections and opinions of certain writers or artists.

Depressive realism as it is translated from psychology to philosophy can be said to refer to the belief that phenomena are accurately perceived as having negative weighting. Put differently, we can say that ‘the truth about life’ always turns out to be more negative than positive, and hence any sustained truth-seeking must eventually find itself mired in unpleasant discoveries.

We then come to synonyms or closely related terms and ideas. These include, in alphabetical order, absurdism, anthropathology, antihumanism, cynicism, depressionism, disenchantment, emptiness, existential anxiety and depression, futilitarianism, meaninglessness, melancholia, misanthropy, miserabilism, nihilism, pessimism, radical scepticism, rejectionism, tedium vitae, tragedy, tragicomedy or Weltschmerz. We could add saturninity, melancology and other terms if we wanted to risk babellian excess, or flag up James Joyce’s ‘unhappitants of the earth’ as a suitable descriptor for DRs. We could stray into Buddhist territory and call up the concepts of samsara and dukkha. I do not claim that such terms are synonymous or that those who would sign up to DR espouse them all but they are closely associated, unless you are a semantically obsessive philosopher.

Dienstag (2006) denies any necessary commonality between different intellectual expressions of pessimism, and Weller (2011) demonstrates a connoisseur-ship of nuances of nihilism. Kushlev et al. (2015) point out that sadness and unhappiness are not identical. But Daniel (2013) stresses the assemblage of melancholy, and Bowring (2008) provides a very useful concise history, geography and semantics of melancholy.

Here is one simple illustration of how the shades of DR blend into one, not in any linear progression but pseudo-cyclically. The DR often experiences the weariness of one who has seen it all before, is bored and has had enough; the melancholy of the one who feels acutely the elusiveness and illusion of happiness, the impermanence of life and always smells death in the air; the pessimism of one whose prophetic intuition knows that all proposed quasi-novel solutions must eventually fade to zero; the nihilism of one whose folly-spotting and illusion-sensing radar never rests; the depression of one whose black dog was always there, returns from time to time and may grow a little blacker in old age; the sorrowful incredulity at the gullible credulity of hope-addicts and faith-dealers; the deep sadness of one who travels extensively and meets many people whose national and personal suffering is written all over their faces; and the bleakly aloof fundamentalism of one who believes his epistemology to be superior to other, always shallower accounts. In some cases an extreme form of DR may tip into contemptuous or active nihilism, for example, DeCasseres’s (2013) ‘baleful vision’.

But DR need not be, seldom is, a state of maximum or unchanging bleakness or sheer unhappiness, and many DRs like Cioran, Beckett and Zapffe could be very funny, as is Woody Allen. But grey-skies thinking is the DR’s natural default position and ambivalence his highest potential.

A broad, working definition of depressive realism runs as follows: depressive realism is a worldview of human existence as essentially negative. To qualify this, we have to say that some DRs regard the ‘world’ (everything from the cosmos to everyday living) as wholly negative, as a burdensome absurdity, while some limit its negativity to human experience, or to certain aspects or eras of humanity or to sensate life. ‘Existence is no good at all’ probably covers the first outlook (see Ligotti, 2010), and ‘existence contains much more bad than good’ the second (Benatar, 2006). We might also speak of dogmatic DR and a looser, attitudinal DR that seeks dialogue.

Critics of DR, of whom there are many as we shall see, often joke lamely about the perceived glass half empty mentality underlying this view, and tirelessly point out the cliché that a glass half empty is half-full. DR may not deny that life includes or seems to include some positive values, sometimes, but it is founded on the belief, the assertion, that it is overall more negative than positive. And, depending on what the glass is haIf-full of, the DR may regard it as worthless, tasteless, poisonous or ultimately futile to drink.

The succinct ingredients of DR are perhaps as follows. The human species is overdeveloped into two strands, the clever and inventive, and the destructive and distressing, all stemming from evolutionarily accidental surplus consciousness. We have developed to the point of outgrowing the once necessary God myth, confronting the accidental origins of everything and realising that our individual lives end completely at death. We have to live and grow old with these sad and stubborn facts. We must sometimes look at the vast night sky and see our diminutive place reflected in it, and we realise that our species’ existence itself is freakishly limited and all our earthly purposes are ultimately for nought.

We can never organise optimal living conditions for ourselves, and we realise that our complex societies contain abundant absurdities. World population increases, information overload increases and new burdens outweigh any benefits of material progress however clever and inventive we are. We claim to value truth but banish these facts from our consciousness by all manner of mendacious, tortuous mental and behavioural devices. The majority somehow either denies all of the above or manages not to think about it. But it unconsciously nags at even the most religious and optimistic, and the compulsion to deny it drives fundamentalist religious revival, capitalist growth, war and mental illness.

Depressive realism may generate a range of attitudes from decisive suicidality or leaden apathy through to cheerful cynicism, eloquent disenchantment and compassionate or violent nihilism. We can argue that everyone has a worldview whether implicit or explicit, unconscious or conscious, inarticulate or eloquent. Wilhelm von Humboldt is credited with the origins of the concept, using the term Weltansicht (world meaning), with Weltanschauung arriving a little later with Kant and Hegel.

DR may contain idiosyncratic affects, perceptions and an overall worldview, the scale of negativity of which fluctuates. It may be embodied at an early age or emerge later with ageing and upon reflection, or after suffering a so-called ‘nadir experience’, and may even be overturned, although this event is probably rare. Often, we cannot help but see the world in the way we happen to see it, whether pessimistically or optimistically, even if our moods sometimes fluctuate upwards or downwards. Typically, no matter how broadminded or open to argument we consider ourselves to be, we all feel that we are right. The DR certainly fits this position, often regarding himself as a relentlessly sceptical truth-seeker where others buy into complacent thought and standard social illusions.

The person who has no particular take on existence, who genuinely takes each day or moment as it comes, is arguably rare.

We should ask what it is that is depressed in DR and what it is to which the realism points. Melancholy was once the more common term, depression simply meaning something being pushed downwards, as in dejected spirits. This downwardness places depression in line etymologically with the downwardness of pessimism, not to mention countless metaphors such as Bunyan’s trough of despond.

From the 17th century depression gained its clinical identity but the roots lie in much earlier humoral theory. Whichever metaphor is employed, however, we might ask why ‘upwards’ is implied to be the norm, and in what sense ‘downwards’ should be applied to ‘unhappy consciousness’. Heaven has always been located upwards and hell downwards. More accurate metaphors for depression might involve inward or horizontal states. But this would still leave the question of why outwardness and verticality should be regarded as more normal, or the view of the depressed, melancholic, downward, inward or horizontal human being as less acceptable or normal than its opposite, unless on purely statistical grounds.

I think it is fair and proper to make my own position as transparently clear as possible. In spite of critiques of writing from ‘the view from nowhere’, most academic writing persists in a quasi-objective style resting on the suspiciously erased person of the author. Like most DRs, my personality and outlook has always included a significantly depressive or negative component. I was once diagnosed in my early 30s in a private psychotherapy clinic as having chronic mild depression. I have often been the butt of teasing and called an Eeyore or cynic. I am an atheist.

I have had a fair amount of therapy during my life but in looking back I have to say that:

a. none of that therapy has fundamentally changed the way I experience life, and

b. my mature belief is that I was always this way, that is, someone with a ‘depressive outlook’.

Only quite recently have I come to regard this as similar to the claim made by most gay people that they were born gay, or have been gay for as long as they remember, that they do not think of themselves in pathological terms and they do not believe homosexuality to be a legitimate object for therapeutic change.

I do not mean to say that people who experience clinical depression should not have therapy if they wish to, nor even that it does not sometimes help. Rather, I believe the assumption should not be made that depressive or negative views about life and experience necessarily correlate with psychological illness.

Since I have worked in the counselling and psychotherapy field for about 35 years, I have some explaining to do, which appears mainly in Chapter 6.

Appearing in the series Explorations in Mental Health as this book does, I should like to give a brief sense of location here. In truth this is an interdisciplinary subject that by its nature has no exclusive home. On the other hand, given my academic background, there are some clear links with psychology, psychotherapy and counselling. On the question of mental health, the contribution of DR is to re-examine assumptions about ‘good’ mental health and in particular to challenge the standard pathological view of depression as sick, and with therapists as having a clinical mandate to pronounce on everything with depressive or gloomy connotations.

The line between so-called existential anxiety and so-called death and health anxiety can be a fine one, and we should question the agonised revisions and diagnostic hyperinflation by the contributors to the DSM over such matters (APA, 2013; Frances, 2014).

DR seriously questions the standard assumption in cognitive behaviour therapy that depressed individuals must have cognitive distortions, and indeed reverses this to ask whether DRs might have a more objective grasp of reality than others, and a stubborn refusal to embrace illusion.

In conducting this challenge we are taken well beyond psychology into ontology, history, the philosophy of mental health and other disciplines. The mission of this book is hardly to revolutionise the field of mental health, but it is in part to reassess the link between perceived depression, pessimism and negative worldviews.

But a book of this kind emerges not only from a personal position and beliefs. I may experience my share of low mood, insomnia, conflict and death anxiety, but my views are also informed abundantly by wide reading, observations of everyday life and friends. Mirroring the ‘blind, pitiless indifference and cruelty of nature’ (Dawkins, 2001), I see around me a man in his 80s passing his days in the fog of Alzheimer’s, another in his 70s with Parkinson’s disease, a woman suffering from many sad medical after-effects of leg amputation, another woman suffering from menopausal mood swings, couples revealing the cracks in their allegedly smooth relationships, several young men struggling gloomily to find any fit between their personalities and the workplace, colleagues putting a brave face on amid insane institutional pressures and the list of merely first world suffering could go on and on.

The sources of this common brutalism are biological and social. The examples of suffering easily outnumber any clear examples of the standard optimistic depiction of happy humans, yet this latter narrative continues to assert itself, backed up by cheerful statistics and miserabilism countering examples.

I argue that human life contains many glaringly tragic and depressing components and the denial or minimisation of these adds yet another level of depression.

The lead characters in DR will emerge during the book. It may be useful here, however, to mention those who feature prominently in the DR gallery. These include Gautama Buddha, Arthur Schopenhauer, Giacomo Leopardi, Philipp Mainlander, Thomas Hardy, Edgar Saltus, Sigmund Freud, Samuel Beckett, E.M. Cioran, Peter Wessel Zapffe, Thomas Ligotti, John Gray, David Benatar and Michel Houellebecq.

One of the admitted difficulties in such billing is that those still alive might well disown membership of this or any group. Another problem is who can really be excluded: for example, why not include Kierkegaard, Nietzsche, Dostoevsky, Kafka, Camus? As well as the so-called greats, we should pause to remember more minor writers, for example, the Scottish poet James Thomson (1834-82) whose The City of Dreadful Night captures perfectly many DR themes (see Chapter 4). Sloterdijk (1987) included in his similar ‘cabinet of cynics’ an idiosyncratic trawl from Diogenes to Heidegger; Feld’s (2011) ‘children of Saturn’ features Dante and Ficino.

In truth DRs may be scattered both interdisciplinarily and transhistorically (Breeze, 2014). To some extent questions of DR membership are addressed in the text, but it is true to say such discriminations are not my main focus.

This book is structured loosely by disciplines in order to demonstrate the many sources and themes involved. My treatment of these disciplines will not satisfy experts in those disciplines and must appear at times náive, imprecise or inaccurate, but these fields impinge on us, claim to define how we live and suffer and what remedies might exist. In another kind of civilisation we might have no such epistemological divisions. I look at how these disciplines inform DR but also use DR as critical leverage to examine their shortcomings.

Hence, Chapter 1 excavates some of the relevant evolutionary and common historical themes.

Chapter 2 looks at some religious themes and the theologies explicating these, as well as the contemporary fascination with spirituality and its downsides.

In Chapter 3 I examine a number of philosophical themes connecting with DR.

Some examples in literature and film are analysed in Chapter 4.

Psychology comes into focus in Chapter 5, to be complemented and contrasted with psychotherapy and the psychological therapies in Chapter 6.

In Chapter 7 socio-political themes are scrutinised insofar as they illustrate DR.

I then move on to science, technology and the future in Chapter 8, again in order to depict the dialectic between these and DR.

The ‘lifespan and everyday life’ is the focus of Chapter 9, which takes a partial turn away from academic disciplines to the more experiential.

Arguments against DR, as comprehensive as I can make them in a concise form, comprise Chapter 10, while the final chapter envisages the possible utility of DR.

One of the many things DRs find depressing about the societies we live in is that those of us shaped ironically by twisted educational systems to think and write about such matters, and lucky to find a haIf-accommodating employment niche, are likely to be in or associated with academia. This institution has survived for many centuries and in spite of its elitist niche remains somewhat influential, although far less influential than its personnel imagine.

In its current form it is being ravaged by the so-called new public management but at the same time in its social science, arts and humanities departments is defiantly dominated by left-wing academics whose writing style is often highly symbolic, obfuscatory, arguably often meaningless (Sokal, 2009) and designed for coded communication with a mere minutiae of the general population, that is, academic peers.

On the other hand, academia can also suffer from a kind of censorship-by-demand-for-evidence, meaning that common observation, subjectivity and anecdote are erased or downgraded and a statistics inebriated tyranny reigns supreme. Once when presenting some of the themes in this book to an academic ‘research group’, I was told I had cherry-picked too many bad examples, as if my colleagues were all paragons of balanced argument and nothing short of watertight pseudo-objectivity could be tolerated: in my view this itself is an example of silencing the DR nihilism that threatens an uncritically ‘life is good’ assumption.

A dilemma facing anyone who hopes to capture the essence of depressive realism and the parrhesia within it concerns the style in which to write and the assumptions and allusions to make. Universities seem barely fit for purpose any longer, or their purpose is unclear and some have predicted their demise (Readings, 1997; Evans, 2005). This should not surprise us, on the contrary, we should learn to expect such decline as an inescapable part of the entropy of human institutions but it is a current aspect of our depressing social landscape.

I have only partly followed the academic convention of obsessively citing evidence and precise sources of evidence. In some cases, where no references are given, my figures and examples derive from unattributed multiple internet sources; I do not necessarily make any claims to authority or accuracy, and the reader should check on sources if he or she has such a need. In many instances I use terms such ‘many people believe’, which might irritate conventional social scientists. I also use anecdote, opinion and naturalistic observations fairly freely. Academic discourse is, I think, very similar to the ‘rhetoric’ exposed by Michelstaedter (2004), in contrast with the persuasion of personally earned insights and authentic observation, as Kierkegaard too would have recommended.

A confession. What appears above is what is expected of a writer, a logical outline, a promise of reading pleasures to come and of finding and offering meaning even in the teeth of meaninglessness (a trick accomplished by the sophistry of Critchley [1997], among other academic prestidigitators). As I moved from the publisher’s acceptance of my proposal to the task of actual composition I began to wonder if I could in fact do it. ‘Let’s do this thing’ is a common American expression of committed and energetic project initiation. As befits a text on depressive realism, the author is bedevilled by doubt: more of a Beckettian ‘is this thing even worth beginning?’ The topic is so massive that one is suffocated on all sides by the weight of precedents and related information, the beckoning nuances, the normative opposition to it and the hubris of attempting it. I anguished over the possibility of a subtitle, something like ‘perspectives on pointlessness’, that might convey a mixture of nihilism and humour. Such are our needs for and struggles with sublimation, and our neophilia, that it is tempting not to bother. However, here it is.

Chapter 1

Big history, anthropathology and depressive realism

Can we say there is something intrinsically fantastic (unlikely), admirable (beautifully complex) and simultaneously tragic (entropically doomed from the outset) about the universe? And about ourselves, the only selfconscious part of the universe as far as we know, struggling to make sense of our own existence, busily constructing and hoping for explanations even as we sail individually and collectively into oblivion? Was the being or something that came out of nothing ever a good thing (a random assertion of will in Schopenhauerian terms), a good thing for a while that then deteriorated, a good thing that has its ups and downs but will endure or a good thing that must sooner or later end? Or perhaps neither good nor bad?

Depressive realism looks not only to the distant future but into the deepest past, interpreting it as ultimately negatively toned.

It is quite possible and indeed common practice for depressive realists and others to explicate their accounts without recourse to history. It appears that much contemporary academic discourse, certainly in the social sciences, is tacitly structured abiologically and ahistorically, as if in spite of scientific accounts we have not yet accepted any more than creationists that we are blindly evolved and evolving beings. In other words, in spite of much hand-wringing, many maintain a resignedly agnogenic position as regards the origins of the human malaise: we do not and may never know the causes.

But we have not appeared from nowhere, we are not selfcreating or God-created, we were not born as a species a few hundred or a few thousand years ago, we are not in any deep sense merely Plato’s heirs. Neither Marxist dialectical materialism nor Engels’ dialectics of nature capture the sheer temporal depth of evolution and its ultimate cosmogony (Shubin, 2014). Existence, beyond the animal drive to survive, is atheleological and unpromising. Religious and romantic theleologies largely avoid examination of our material roots and probable limits. From a certain DR perspective it is not only the future that has a dismal hue; an analysis of the deep past also yields much sorry material.

My preference is to begin with certain historical and materialist questions. The reasoning behind this is that (a) we have accounts of and claims to explain the existence of life as once benign but having become at some stage corrupt; (b) we might find new, compelling explanations for the negative pathways taken by humanity; (c) recorded observations of human tragedy that can be loosely called depressive realism are found in some of the earliest literature; (d) this procedure helps us to compare large scale and long-term DR propositions with relevant microphenomena and transient patterns. This anchorage in deep history does not necessarily imply a materialist reductionism to follow but it tends, I believe, to show a ceaselessly adaptive, evolutionarily iterative process and entropic trajectory via complexity.

The emerging disciplines of deep and big history challenge the arbitrary starting points, divisions and events of traditional history by going back to the earliest known of cosmic and non-human events, charting any discernible patterns and drawing tentative conclusions. Spier (2011) offers an excellent condensed account of this kind, but we probably need to add as a reinforcer the argument from Kraus (2012) that something from nothing is not only possible but inevitable and explicable by scientific laws. Indeed, it is necessary to begin here as a way of further eroding theistic claims that want to start with God and thereby insist on God’s (illusory) continuing sustenance and guiding purpose.

It is not the creation ex nihilo of the mythological, pre-scientific God, the omnipotent being who brought forth the universe from chaos that any longer helps us to understand our world, but modern science.

We do not know definitively how we evolved, but we have convincing enough causal threads at our disposal. Here I intend to sift through those of most interest in exploring the question of why our world has become such a depressing place.

We are animals but apparently higher animals, so far evolved beyond even our nearest relatives that some regard human beings as of another order of nature altogether. Given the millennia of religious belief that shaped our picture of ourselves, the Darwinian revolution even today is not accepted by all. Even some scientists who purport to accept the standard evolutionary account do not seem to accept our residual animal nature emotionally (Tallis, 2011).

But it is important to begin by asking about the life of wild animaIs. They must defend themselves against predators by hiding or fighting, and they must eat by grazing, scavenging or predation; they must reproduce and where necessary protect their young. Many animals spend a great deal of their time asleep, and some play. Social animals cultivate their groups by hunting together, communicating or grooming. Some animals protect their territory, build nests or rudimentary homes and a few make primitive tools; some migrate, and some maintain hierarchical structures. Most animals live relatively short lives, live with constant risk and are vigilant.

However it happened, human beings differ from animals in having developed a consciousness linked with tool-making, language and massive, highly structured societies that have taken us within millennia into today’s complex, earth spanning and nature dominating civilisation. Wild animals certainly suffer, contrary to idyllic fantasies of a harmonious nature but their suffering is mostly acute, resulting from injury, hunger and predation, and their lives are not extended beyond their natural ability to survive.

Our ingenuity and suffering are two sides of the same coin.

Weapon making and cooperation allowed us to rise above constant vulnerability to predators, but our lives are now often too safe, bland and boring, since we have forfeited the purpose of day-to-day survival. We have also benefited from becoming cleverer at the cost of loss of sensory acuity. Accordingly, and with painful paradox, we are driven to seek ‘meaning’ and we are gratuitously violent (Glover, 2001; White, 2012). Animals have no such problems.

*

from

Depressive Realism. Interdisciplinary perspectives

by Colin Feltham

get it at Amazon.com

Breaking Down Is Waking Up. Can psychological suffering be a spiritual gateway? – Dr Russell Razzaque.

There are as many types of mental illness as there are people who suffer them.

The World Health Organization estimates that approximately 450 million people worldwide have a mental health problem.

None of us is immune from the existential worry that nags away in the back of our mind. We are all vulnerable to emotional and psychological turmoil in our lives and there is something fundamental about the human condition that makes it so.

There is something at the core of the experience of mental illness that draws sufferers towards the spiritual. Their suffering is an echo of the suffering we all contain within us.

EVERYONE NEEDS A BANISTER; a fixed point of reference from which we understand and engage with life. We need something to hold on to, so that when we’re hit by life’s inevitable disappointments, pain or traumas, we won’t fall too far into confusion, despair or hopelessness. With a weak banister we risk getting knocked off course, losing our bearings and falling prey to stress, psychological turmoil and mental illness. A strong banister will stand the test of time in an ever changing world, giving us more confidence to face the knocks and hardships of life more readily.

Understanding who we are and how we fit into the world is a quest we start at birth and continue through the whole of our lives. Sometimes these questions come to the fore, but usually they bubble away somewhere beneath the surface: ‘Who am I?’ ‘Am I normal?’ ‘Why am I here?’ ‘Is there any real point to life?’ Deep down inside we know that nothing lasts, the trees, landscapes and life around us will all one day perish, just as surely as we ourselves will, and everyone we know too. But we have evolved ways to hold this reality and the questions it hurls up at bay.

We construct banisters to help us navigate our way round this maze of pain and insecurity: a set of beliefs and lifestyles that help us form a concrete context to make sense of things and, as the saying goes, ‘keep calm and carry on’. But, for most of us, the core beliefs and lifestyles that hold us together still leave us vulnerable to instability. The sense of identity we evolve is so precarious that we’re often buffeted by life onto shaky ground. And, as a consequence, we become prone to various forms of psychological distress; indeed, for vast swathes of society this proceeds all the way to mental illness, whether that be labelled as anxiety, depression, bipolar disorder or the most severe form of mental illness, psychosis.

There are as many types of mental illness as there are people who suffer them. One of the reasons I decided to specialize in psychiatry, shortly after qualifying from medical school, was that, unlike any other branch of medicine, no two people I saw ever came to me with the same issues. Although different presentations might loosely fit into different categories, there appeared to me to be as many ways of becoming mentally unwell as there were ways of being human. I have since specialized in the more severe and acute end of psychiatry. I currently work in a secure, intensive care facility but to this day, in 16 years of practice, I have never seen two cases that were exactly the same.

And the numbers just seem to be going up. In the UK today, one in four adults experiences at least one diagnosable mental health problem in any one year. In the USA, the figure is the same and this equates to just over 20 million people experiencing depression and 2.4 million diagnosed with schizophrenia, a severe form of mental illness where the individual experiences major disturbances in thoughts and perceptions. The World Health Organization estimates that approximately 450 million people worldwide have a mental health problem.

Beyond these figures, however, are all the people who struggle with various levels of stress throughout life and, all the while, carry a fear at the back of their minds, that they too may one day slide into mental illness. In my experience, this is a fear that pervades virtually every stratum of society. Rarely am I introduced as a psychiatrist to new people in a social gathering without at least some of them quietly feeling, or even explicitly reporting, that they worry that one day they are going to need my help. Such comments are often made in jest, but the genuine anxiety that underlies them is rarely far beneath the surface. There is a niggling worry at the back of many people’s minds that something might be wrong with them; that something isn’t quite right. What they don’t realize, however, in their own private suffering, is just how much company they have in this fear. Indeed, I include myself and my colleagues among them, too. None of us is immune from the existential worry that nags away in the back of our mind.

But, if we look closely, there is also another process that can be discerned underneath all of this. Deep down inside every bubbling cauldron of insecurity, we can also find the seeds of a kind of liberation. Something is just waiting to burst forth. This something is hard to define or describe in language, but it is often in our darkest hours that we can feel it the most. And the further we fall the closer to it we get. This is why, I believe, mental illness can be so powerful, not just because of the deep distress that it contains, but also because of the authentic potential that it represents.

Mental illness, however, is just one aspect of a continuum we are all on. All of us have different ways of reacting emotionally to the experiences we encounter in life and the ones that involve a high level of distress either for oneself or for others are the ones we choose to label as mental illness. And it is this end of the spectrum that l will focus on most in this book, as it is these most stark forms of distress that present us with the greatest opportunity to observe the seeds within, and thus, ultimately, learn what is in all of us too.

There may be a variety of factors that contribute to the various forms of mental illness, of course, from childhood traumas to one’s genetic make up, but as the cut-off point always centres around distress which is grounded in subjective experience the definition itself will always remain somewhat arbitrary. That’s not to say that such definitions have no utility. By helping us communicate with each other about these complex shapes of suffering, they will also help us communicate our ideas with one another about how to help reduce the suffering encountered.

That is why I use these terms in this book, but it should be noted that I attach this large caveat from the outset. Ultimately, the only person who can really describe a person’s suffering is the sufferer himself; outside that individual, the rest of us are always necessarily off the mark. What must invariably be remembered, however, is that there is no ‘them’ and ‘us’. We are all vulnerable to emotional and psychological turmoil in our lives and there is something fundamental about the human condition that makes it so.

That is why I believe, as a psychiatrist, that the best research I ever engage in is when I explore my own vulnerabilities. That is when I start to connect with threads of the suffering that my patients are undergoing too. And what I find particularly fascinating about this process is that the deeper I descend into my own world of emotional insecurity, the more I grow to appreciate an indescribable dimension to reality that so many of my patients talk about in spiritual terms, engage with, and indeed rely upon so much of the time.

In a survey of just under 7,500 people, published in early 2013, researchers from University College London found a strong correlation between people suffering mental illness and those with a spiritual perspective on life. Though the results confused many, to me they made perfect sense.

There is something at the core of the experience of mental illness that draws sufferers towards the spiritual. Their suffering is an echo of the suffering we all contain within us.

That is why I can say from the outset, and without reticence, that my insights are based largely on a subjective pathway to our shared inner world. And it is through this perspective that I have evolved what I believe is a new banister: a new way of seeing the world and being within it. It is, however, not just that my introspection has taught me about my patients, but that my patients have also taught me about myseIf. Indeed I can safely say that I have gleaned just as much from the individuals I have cared for as I have from the professionals and teachers I have learnt from.

I consider myself hugely lucky to work in a profession in which looking into myself and learning about my own inner world has been, and continues to be, a vital requirement of my work (though, it has to be said that, sadly, many within my profession do not recognize this). It has propelled me into a journey of limitless exploration of both myself and the people I care for and this has led me to ever deeper understandings of the nature of mental illness, the mind and reality itself. I have drawn upon a diverse array of wisdom along the way, and my journey has ultimately led me to construct a synthesis of modern psychiatry and ancient philosophy; of new scientific findings and old spiritual practices.

But this banister comes with a health warning, as indeed all should. Just as a set of perspectives and insights can be a useful support in times of instability, so too can overreIiance on them become counterproductive. That is why a banister needs to be held lightly. Gripping too tightly to anything in life is a recipe for exhaustion and, consequently, even greater instability.

What we need is a banister that, when held lightly, can allow us to move forward, rather than hold us back. I believe that such an understanding of reality and our place within it actually exists; it is also imperative to our survival as a species. I believe that life’s potential is far greater than most of us are ever aware of, and that our limitations are a lot more illusory than we know. In a sense I feel we are all suffering from a form of mental illness a resistance to the realization of our true nature, and to that end I humbly offer this book as a guiding rail out of the turmoil.

My Journey. An Exploration of Inner and Outer Worlds

Chapter 1

Wisdom in Bedlam

‘One must still have chaos in oneself to be able to give birth to a dancing star.’ Friedrich Nietzsche

MENTAL ILLNESS IS SOMETHING that most of us shy away from. Someone who exhibits behaviour or feelings that are considered out of the ordinary will, sooner or later, experience a fairly broad radius of avoidance around them. Even in psychiatric hospitals this is evident, where the less ill patients will veer away from those who are more unwell. The staff themselves are often prone to such avoidance, too. But contrary to this natural reflex that exists within all of us, moving closer to, and spending time with, someone suffering mental illness can often be quite an enlightening experience. It took me many years to realize this myself, but through the cloud of symptoms, a fascinating display of insight and depth can often be found in even the most acutely unwell. And this turned out to be true whatever the type of mental illness. The problem might be mood related for example, depression or bipolar or what we term neurotic like anxiety, panic or post-traumatic stress disorder or all the way up to the paranoia or hearing voices that we see at the most severe stage of mental illness termed psychosis. Indeed, the more severe the symptoms, the deeper the wisdom that appeared to be contained (though often hidden) within it.

A frequent observation of mine, for example, is just how perceptive the people I treat can be, regardless of the very evident turbulence that is going on inside. It is not uncommon for those who are newly admitted to share with me their impressions of the nursing and other staff on the ward with an uncanny degree of accuracy within only a few days of arrival. They’ll sometimes rapidly intuit the diverse array of temperaments, perspectives and personality traits among staff members and so have a feel for who is best to approach, avoid, or even wind up, depending on their mental state and needs at the time. It is likely that this acute sensitivity is one of the initial causes of their mental illness in the first place, but the flip side is that they have also managed to glean a lot about life from their experiences to date. This wisdom is often hidden by the symptoms of their illness, but it lurks there under the surface, often ready to flow out after a little gentle probing. I am frequently struck by the profundity of what I hear from my patients during our sessions and I often find myself feeding this same wisdom back to them even when, at the same time, they are undoubtedly experiencing and manifesting a degree of almost indescribable psychological pain.

Most of us spend our lives going to work, earning a salary, feeding our families and perhaps indulging in sport or entertainment at the weekends. Rarely are we able to step back from it all and wonder what the purpose of all this is, or whether or not we have our perspectives right. During the football World Cup one year, a patient told me that he felt such events served a deeper purpose for society, ‘It stops us thinking about the plight of the poor around the world.’ Events such as this kept us anaesthetized, he believed, so we could avoid confronting the depths of inequality and injustice around the globe, and that would ultimately enable the system that propped up the very corporations who were sponsoring these events to keep going. I had to admit that I had never thought of it that way before.

Compassion is a frequent theme I observe in those suffering mental illness, even though they are usually receiving treatment in a hospital setting because, on some level, they are failing to demonstrate compassion towards either themselves or others. I have often been moved by hearing of an older patient with a more chronic history of mental ill-health, perhaps due to repeated long-term drug use, or failure to engage with therapy, taking the time to approach a younger man, maybe admitted to hospital for the first time, and in effect tell him, ‘Don’t do what I did, son. Please learn from my mistakes.’ There are few moments, I believe, that are more powerfully therapeutic than that.

It is only in the last few years that we have discovered, after trialling a variety of treatments, that one of the most powerful interventions for what are known as the ‘negative symptoms’ of schizophrenia, is exercise. These negative features relate to a lack of energy, drive, motivation and, often, basic functional activity. Whatever the diagnostic label you choose to put on it, this can often be the most disabling part of such illnesses, and there are hardly any known treatments for it. Although an evidence base has recently evolved around the practice of regular exercise. I never quite understood why this could be until a patient one day put forward a hypothesis to me. It takes you out of your mind, he explained to me. ‘You see doc, you can’t really describe a press-up. You just do it.’ The whirlwinds within could be overcome for a few moments at least, while attention is paid, instead, to the body. Suddenly I realized why going to the gym was the highlight of his week.

A rarely described but key feature of mental illness, therefore, is just how paradoxical it can be, with the same person who is plagued by negative, obsessional or irrational thoughts, also able to demonstrate an acute and perceptive understanding of the people and world around him. It is as if one mental faculty deteriorates, only for another one to branch out somewhere else; or rather, consciousness constricts in one area only to expand in another. There is actually some quite startling experimental evidence to back this up. An interesting study was conducted by neuroscientists at Hannover Medical School in Germany and University College London, Institute of Cognitive Neuroscience. It involved a hollowmask experiment. Essentially, when we are shown a two-dimensional photograph of a white face mask, it will look exactly the same whether it is pointing outwards with the convex face towards the camera or inwards with the concave inside of the face towards the camera. This is known as the hollow-mask illusion.

Such photographs were shown to a sample of control volunteers.

Sometimes the face pointed outwards, and sometimes inwards. Almost every time the hollow, inward-pointing concave face was shown to them, they misinterpreted it and reported that they were seeing the outward-pointing face of the mask instead. This miscategorization of the illusion actually occurred 99% of the time. The same experiment was then performed on a sample of individuals with a diagnosis of schizophrenia. They did not fall for the illusion: 93% of the time, this group was actually correctly able to identify when the photo placed before them was, in fact, an inward-pointing concave mask.

Clearly what we see here is an expansion in perceptual ability compared to normal controls. Data like this has begun to pierce the notion that mental illness is purely a negative or pathological experience. In fact, in this study, it was the normal controls who were less in touch with reality than those with a psychotic illness!

The most interesting aspect of this is that, whether they be suffering neurosis, depression, bipolar or even psychotic disorders, many people actually have some awareness of the fact that they are also somehow connecting, through this process, to a more profound reality that they were like the rest of us hitherto ignorant of. The experience might be disconcerting, even acutely frightening, but there is a sense that there is also something restorative about it too; they are rediscovering some roots they, perhaps along with the rest of us, had long forgotten about. One patient put it to me this way, ‘I feel like I am waking up. But it’s very scary because I feel like I have been regressing at the same time. It’s almost as if I needed to go through this in order to wake up.’

This sense of a wider meaning and purpose behind a breakdown is not an uncommon theme among the people I see but it is, nevertheless, so counterintuitive that it continues to halt me in my tracks whenever I encounter it. In psychiatry, for genuinely caring reasons, we are striving to reduce the distress that the people we see are experiencing. That, after all, is the reason we became health-care professionals in the first place: to heal the sick. So our reflex, whenever we see people in any kind of pain, is to remove it. But when one senses that the sufferer himself/herself sees value in the experience then we need to stop and think. So long as they are not a risk to themselves or others, perhaps our usual reflex to extinguish such an experience might lead to the suppression of something that could otherwise have been valuable or even potentially transformative.

I have had many experiences of treating people who, even after a terrible episode of psychotic breakdown, came out the other end saying that this was good for them and that the experience, despite being horrendous, was something they needed to go through. This has sometimes been attributed to an expansion of awareness that they felt they needed, and that they believed the illness brought to them. A patient once talked with me about a profound, almost overwhelming, sense of gentleness and warmth he felt when listening to music one evening, just hours before his relapse into psychosis, and as we were talking in the session, he suddenly looked up at me and said, with a mixture of awe and joy on his face, and tears in his eyes, ‘Sometimes I feel that there is something out there so beautiful and so much bigger than me, but I just can’t handle it.’

Though we will be exploring the whole gamut of psychological distress and mental illness in this book, it is the psychotic experience that usually invokes the greatest stereotype and stigma, and so merits extra attention in this opening chapter. Psychosis is when someone is said to have lost touch with reality, and this may involve hearing voices, seeing things or holding some delusional ideas. The idea that someone suffering psychosis can also be the conduit of genuinely deep wisdom and insight, therefore, surprises most people, even mental-health professionals who might not be familiar with this client group. First-person accounts of this are not easy to find in the academic literature, but one particularly good case study was published by David Lukoff in the Journal of Transpersonal Psychology. He wrote it in conjunction with a gentleman who had himself suffered a psychotic breakdown and went by the pseudonym of Howard Everest. Howard was able, in a very articulate way, to describe his own breakdown which he referred to as a form of personal odyssey both during and after it actually happened.

. . .

*

Dr Russell Razzaque is a London based psychiatrist with sixteen years experience in adult mental health. He has worked for a number of national and international organizations during his career including the University of Cambridge, the UK Home Office and the Ministry of Justice, and he currently works in acute mental health services in the NHS in east London. He is also a published author in human psychology with several books on the subject, and he writes columns for a number of publications including Psychology Today, The Independent, The Guardian and USA Today.

*

from

Breaking Down Is Waking Up. Can psychological suffering be a spiritual gateway?

by Dr Russell Razzaque

get it at Amazon.com

Meditation increases prosociality? Meditation under the microscope – Ute Kreplin.

It’s hailed as the panacea for everything from cancer to war.

Inflated study results for the power of meditation fuel magical beliefs about its benefits. Mindfulness websites market it as a ‘happy pill, with no side effects’; it is said it can bring world peace in a generation, if only children would breathe deep and live in the moment.

But what if meditation doesn’t work for you? Or worse, what if it makes you feel depressed, anxious or psychotic?

Does research into its efficacy meet scientific standards? Can we be sure that there are no unexpected outcomes that neither benefit the individual nor society? Is it possible that meditation can fuel dysfunctional environments and indeed itself create a path to mental illness?

One day there will be a more complete picture of this potent and poorly understood practice. For now, our understanding is mostly warped.

Among the promised psychological and physical benefits of meditation are the elimination or reduction of stress, anxiety and depression, as well as bipolar disorder, eating disorders, diabetes, substance abuse, chronic pain, blood pressure, cancer, autism and schizophrenia. It is a panacea for the individual.

There are also apparent interpersonal and collective effects. Mindfulness and other Buddhist-derived meditation techniques, such as compassion and loving-kindness meditation, can perhaps increase prosocial emotions and behaviours, yielding greater social connection and altruism, tampering aggression and prejudice.

‘If every eight year old in the world is taught meditation,’ the Dalai Lama purportedly said, ‘the world will be without violence within one generation.’ The quote is widely shared online.

Such a useful activity naturally finds a variety of applications. Meditation techniques have been deployed in the military with the aim of increasing the wellbeing and work effectiveness of soldiers. Snipers are known to meditate in order to disengage emotionally from the act of killing, to steady the hand that takes a life (the element of peacefulness associated with meditation having been rather set aside). Corporations counteract stress and burnout with meditation which, on the surface, is an amiable aim, but it can also help create compliant workers. And in schools, meditation interventions aim to calm children’s minds, offering students the ability to better deal with the pressure of attaining high grades. Here, too, the goal is to reduce misbehaviour and aggression in a bid to increase prosociality and compliance.

Psychological research often upholds this optimism about the efficacy of meditation. Indeed, studies on the prosocial effects of meditation almost always support the power of meditation, the power not only of transforming the individual but of changing society. So it appears well grounded that meditation might improve socially advantageous behaviour. This brings with it the prospect of applications in a variety of contexts, where it might find its use in social conflicts, such as mitigation of war and terrorism. The problem, however, is with the research that bolsters such claims.

Last year, the experimental psychologists Miguel Farias, Inti A Brazil and I conducted a systematic review and meta-analysis that examined the scientiiic literature behind the claim that meditation increases prosociality. We looked at randomised controlled studies, where meditators were compared with nonmeditating individuals, and reviewed more than 20 studies that evaluated the effect of various types of meditation on prosocial feelings and behaviours such as how compassionate, empathetic or connected individuals felt.

The studies we reviewed used a variety of methodologies and interventions. For example, one used an eight-week meditation intervention called ‘mindfulness-based stress-reduction’. Individuals learned how to conduct mindful breathing and to practise ‘being in the moment’, letting go of their thoughts and feelings. Meanwhile the control group, with which the meditators were compared, engaged in a weekly group discussion about the benefits of compassion. Another study compared guided relaxation (participants listening to an audio recording about deep breathing and unwinding) with a control group that simply did nothing in a waiting room. Most studies required participants to fill in questionnaires about their experience of the meditation intervention, and their levels of compassion towards themselves and others. Some studies also included behavioural measures of compassion, in one case assessed by how willing a person was to give up a chair in a (staged) full waiting room.

Initially, the results were promising. Our meta-analysis indicated that meditation did indeed have a positive, though moderate, impact on prosociality. But digging deeper, the picture became more complicated. While meditation made people feel somewhat more compassionate or empathetic, it did not reduce aggression or prejudice, nor did it improve how socially connected one felt. So the prosocial benefits are not straightforward, but they are apparently measurable. The issue is the way in which those benefits were measured.

To fully dissect the studies, we conducted a secondary comparison to see how methodological considerations would change our initial findings. This analysis looked at the use of control groups and whether the teacher of the intervention was also an author of the study, which might be an indication of bias. The results were astounding.

Let’s start with the control groups. The purpose of the control group is to isolate the effects of the intervention (in our case, meditation) and to eliminate unintentional bias. The importance of adequate control conditions was first brought to light by the discovery of the placebo effect in drug trials, which is when a treatment is effective even though no active agent (or drug) is used. To avoid this effect, each group in a drug trial receives identical treatments, except one group receives a placebo (or sugar pill) and the other gets the real drug. Neither the experimenter nor the participants know who is in which trial (this is called a double-blind design), which helps to eliminate unintentional bias. This way they can tell if it’s the active agent that is effective and not something else.

But the use of adequate controls is tricky in studies that look at behavioural change, because it is harder to create a control group (or placebo) when the treatment is not just a pill but an action. The control has to be similar to the intervention but lack some important components that differentiate it from the experimental counterpart. This is known as an active control. A passive control group simply does nothing, compared with the group that has the intervention.

Meditation did indeed improve compassion when the intervention was compared with a passive control group, that is, a group that completed only the questionnaires and surveys but did not engage in any real activity. So participants who undertook eight weeks of loving-kindness meditation were found to have improved compassion following the intervention compared with a passive waiting-room control group.

Our analysis suggests that meditation per se does not, alas, make the world a more compassionate place.

But have we isolated the effects of meditation or are we simply demonstrating that doing something is better than doing nothing? It might be that compassion improved simply because individuals spent eight weeks thinking about being more compassionate, and felt good about having engaged in a new activity. An active control group (eg, participants taking part in a discussion about compassion) is a more effective tool to isolate the effects of the meditation intervention because both groups have now engaged in a new activity that involves cultivating compassion. And here the results of our analysis suggest that meditation per se does not, alas, make the world a more compassionate place.

A well designed control condition allows studies with a double-blind design. Developing an effective placebo for a meditation intervention is often said to be impossible, but it has in fact been done and with considerable success. In the heydays of transcendental meditation research in the 1970s, Jonathan C Smith developed a 71-page manual describing the rationale and beneiits of a meditation technique. He gave the manual to a research assistant, who was unaware that the technique was completely made-up therefore, a placebo and who then proceeded to give a lecture to participants in the control group about the merits of the technique. (When it came to the actual placebo technique, participants were instructed to sit quietly for 20 minutes twice per day in a dark room, and to think of anything they wanted.) The point is, the placebo can work in studying meditation, it’s just not often used.

Double-blind designs can help to eliminate the accidental bias of the participants through the researcher. These biases have a longstanding history in psychology, and are called experimenter biases (when the experimenter inadvertently influences the participant’s behaviour) and demand characteristics (when participants behave in a way that they think will please the experimenter). The importance of avoiding experimenter bias and demand characteristics was discussed as early as the 1960s. Recent work indicates that experimenter biases remain, particularly in the study of meditation.

In light of the discussion around experimenter bias and demand characteristics, it is surprising to find that, in 48 per cent of the studies we looked at, the meditation intervention was taught by one of the studv’s authors, often its lead author.

More importantly, little attempt was made to control for any potential bias that an enthusiastic teacher and researcher might have had on the participants. Such a bias is often not intentional but stems from subconsciously giving preferential treatment or being particularly enthusiastic to participants in the experimental group. The prevalence of authors as teachers was so great that we decided to look at it statistically in our meta-analysis. We compared studies that had used an author with studies that had used an external teacher or other form of instruction (eg, an audio recording).

We found that compassion increased only in those studies where the author was also the teacher of the intervention.

Experimenter bias often goes hand-in-hand with demand characteristics, where participants behave or respond in a way that they think is in line with the expectations of the researcher. For example, participants might respond regardless of their true feelings more enthusiastically on a questionnaire about compassion because the researcher herself was enthusiastic about compassion. The media buzz around meditation which portrays it as a cure for a range of mental health problems, the key to improved wellbeing and to changing one’s brain for the better is also very likely to feed back to participants, who will expect to see benefits from a meditation intervention.

Yet, almost none of the studies we examined controlled for expectation effects, and this methodological concern is generally absent in the meditation literature.

The prevalence of experimenter bias is only one side of the coin. Another troubling but rarely discussed bias concerns data-analysis and reporting. Interpreting statistical results and choosing what to highlight is challenging. Data do not speak for themselves: they are interpreted by academics whose minds are not blank states. Academics often tread a thin line between the duty of impartial data-analysis and their own beliefs, desires and expectations. In 2003, Ted Kaptchuk of Harvard Medical School summarised a number of interpretative biases that have become widespread in science reporting: confirmation bias, rescue bias (finding selective fault with an experiment to justify an expectation), and ‘time will tell’ bias (holding on to an expectation discounted by data because additional data might in fact support it), among others. All were overwhelmingly present in the meditation literature we reviewed.

The most common bias we encountered was a ‘confirmation bias’, in which evidence that supports one’s preconceptions is favoured over evidence that challenges these convictions. Confirmation bias was particularly prevalent in the form of an overreporting of marginally significant results. When using statistical testing, a p-value of 0.05 and below typically indicates that the results are statistically significant in psychological research. But it has become common practice to report results as ‘trends’ or as ‘marginally significant’ if they are close to, but don’t quite reach the desired 0.05 cut-off. The problem is that there is little consensus in psychology as to what might constitute ‘marginal significance’, which in our review ranged from p-values of 0.06 to 0.14 hardly even marginal. (It is debatable whether p-values are not the most accurate way to conduct science anyway, but we should stick to the rules if we are using this type of testing.)

The positive view of meditation and the fight to protect its reputation make it harder to publish negative results.

Being liberal with statistical methods that were designed to have clear cut-offs increases the chance of finding an effect when there is none. A further problem with the use of ‘marginal significance’ is reporting it free from bias. For instance, in one study the authors reported a marginally significant difference (p = 0.069) in favour of the meditation intervention relative to the control group. However, on the following page, when the authors reported a different set of results that did not favour the meditation group, they claimed the exact same p-level as non-significant. When the results confirmed their hypothesis, it was ‘significant’ but only in that case.

In fact, the majority of studies in our review discussed the marginally significant as equal to statistically significant.

Confirmation bias is difficult to overcome. Journals rely on reviewers to spot them, but because some of these biases have become standard practice (through the reporting of marginally significant effects, say) they often slip through. Reviewers and authors also face academic pressures that make these biases more likely since journals favour the reporting of positive results.

But in the study of meditation there is another complication: many of the researchers, and therefore the reviewers of journal articles, are personally invested in meditation not only as practitioners and enthusiasts but also as providers of meditation programmes from which their institutions or themselves financially profit. The overly positive view of meditation and the fierce fight to protect its untarnished reputation make it harder to publish negative results.

My aim is not to discredit science, but scientists do have a duty to produce an evidence base that aims to be bias-free and aware of its limitations. This is important because the inflated results for the power of meditation fuel magical beliefs about its benefits. Mindfulness websites market it as a ‘happy pill, with no side effects’; it is said it can bring world peace in a generation, if only children would breathe deep and live in the moment. But can we be sure that there are no unexpected outcomes that neither benefit the individual nor society? Is it possible that meditation can fuel dysfunctional environments and indeed itself create a path to mental illness?

The utilisation of meditation techniques by large corporations such as Google or Nike has created growing tensions within the wider community of individuals who practise and endorse its benefits. Those of a more traditional bent argue that meditation without the ethical teachings can lead into the wrong kind of meditation (such as the sniper who steadies the killing shot, or the compliant worker who submits to an unhealthy work environment). But what if meditation doesn’t work for you? Or worse, what if it makes you feel depressed, anxious or psychotic? The evidence for such symptoms is predictably scarce in recent literature, but reports from the 1960s and ’70s warn of the dark side of transcendental meditation. There is a danger that those few cases that receive psychiatric attention are discounted by psychologists as having had a predisposition to mental illness.

In The Buddha Pill (2015), Miguel Farias and Catherine Wikholm take a critical look at the symptoms of depression, anxiety, restlessness, mania and psychosis that are triggered directly by meditation. They argue that the prevalence of adverse effects has not been assessed by the scientific community, and it is easy to think that the few anecdotal cases that might surface are due to an individual’s predisposition to mental-health problems. But a simple search on Google shows that reports of depression, anxiety and mania are not uncommon in meditation forums and blogs. For example, one Buddhist blog features a number of reports on adverse mental-health effects that are framed as ‘dark nights’. One blogger writes:

I’ve had one pretty intense dark night, it lasted for nine months, included misery, despair, panic attacks, inability to concentrate (to the point that it was difficult to do simple tasks), inability to socialise (because of bad feelings, but also because I had a hard time following and understanding what others were saying, due to lack of concentration), loneliness, auditory hallucinations, mild paranoia, treating my friends and family badly, long episodes of nostalgia and regret, obsessive thoughts (usually about death), etc, etc, etc.

In Buddhist circles, these so-called ‘dark nights’ are part of meditation. In an ideal situation, ‘dark nights’ are worked through with an experienced teacher under the framework of Buddhist teachings, but what about those who don’t have such a teacher or who meditate in a secular context?

Those who meditate alone can be left isolated in the claws of mental ill-health.

The absence of reported adverse effects in the current literature might be accidental, but it is more likely that those suffering from them believe that such effects are a part of meditation, or they don’t connect them to the practice in the first place. Considering its positive image and the absence of negative reports on meditation, it is easy to think that the problem lies within. In the best-case scenario, one might simply stop meditating, but many webpages and articles often frame these negative or ambivalent feelings as a part of meditation that will go away with practice. Yet continuing to practise can result in a full-blown psychotic episode (at worst), or have more subtle adverse effects. For example, in 1976 the clinical psychologist Arnold A Lazarus reported that a ‘young man found that the benefits he had been promised from transcendental meditation simply did not emerge, and instead of questioning the veracity of the exaggerated claims, he developed a strong sense of failure, futility, and ineptitude’.

In a best-case scenario, individuals will have a psychiatrist or experienced meditation teacher to guide them, but those who practise alone can be left isolated in the claws of mental ill-health. Lazarus warned that meditation is not for everyone, and we need to consider individual differences and be aware of adverse effects in its application in a secular context. ‘One man’s meat is another man’s poison,’ he once said about transcendental meditation. Researchers and therapists need to know both the benefits and the risks of meditation for different kinds of people, it is not unvarnished good news.

In The Buddha Pill, Farias and Wikholm write:

We haven’t stopped believing in meditation’s ability to fuel change but we are concerned that the science of meditation is promoting a skewed view: meditation wasn’t developed so we could lead less stressful lives or improve our wellbeing. Its primary purpose was more radical to rupture your idea of who you are; to shake to the core your sense of self so that you realise there is ‘nothing there’. But that’s not how we see meditation courses promoted in the West. Here, meditation has been revamped as a natural pill that will quieten your mind and make you happier.

There must be a more balanced view of meditation, one that understands the limitations of meditation and its adverse effects. One day there will be a more complete picture of this potent and poorly understood practice. For now, our understanding is mostly warped.

Ute Kreplin is lecturer in psychology at Massey University in New Zealand. Her research has been published in Nature and Neuropsychologia, among others.

“We will change the world, starting from the very beginning.” Building Babies Brains. Criança Feliz, Brazil’s audacious plan to fight poverty – Jenny Anderson * Advancing Early Childhood Development: from Science to Scale – The Lancet * A groundbreaking study offers undeniable proof that the fight against inequality starts with moms – Jenny Anderson.

“How can we most dramatically improve the quality of life for our citizens, their health, their education? The answer to that question lies in starting at the beginning, at pregnancy, and in the first few years of a child’s life.” Osmar Terra

Decades of groundbreaking research shows that the love and sense of safety experienced by a baby directly impacts how the child’s brain is wired. Adversity, especially persistent, stress-triggering adversity like neglect and abuse, hampers that development, and can result in poorer health, educational attainment, and early death.

“Children who experience profound neglect early in life, if you don’t reverse that by the age of two, the chance they will end up with poor development outcomes is high. The strongest buffer to protect against that? A parent, or caring adult.” Charles Nelson

The best investment a policymaker can make is in the earliest years of childhood, because that’s when intervention has the highest payoffs. Strong biological, psychosocial, and economic arguments exist for intervening as early as possible, starting from and even before conception, to promote, protect, and support children’s development.

Studies have found that children whose mothers received coaching made significant developmental gains, and not just in the short term. Twenty-two years later, the kids from one group who had received those home visits as young children not only had higher scores on tests of reading, math, and general knowledge, they had stayed in school longer. They were less likely to exhibit violent behavior, less likely to experience depression, and had better social skills. They also earned 25% more on average than a control group of kids whose mothers had not received the coaching.

Osmar Terra is a tall man with a deep voice and an easy laugh, one that disguises the scale of his ambition to transform Brazilian society. A federal representative for nearly two decades, he is the driving force behind the world’s biggest experiment to prove that teaching poor parents how to love and nurture their infants will dramatically influence what kind of adults they become, and give Brazil its best shot at changing its current trajectory of violence, inequality, and poverty.

Terra, aged 68, first became obsessed with the question of how humans develop nearly 30 years ago. As a cardiologist in the 1990s, he would read endless research papers about the neuroscience of early childhood. When he entered politics, becoming mayor of Santa Rosa in Rio Grande do Sul in 1992, he continued to grapple with the question, even studying for a master’s degree in neuroscience. The science, he believed, should lead to smart policy. As a doctor and a manager, a mayor and a state health secretary, he was always trying to figure out how to to tackle poverty head-on. “In every single activity I always ask myself, ‘What is the public policy that can be more transformative?’” he says. “How can we most dramatically improve the quality of life for our citizens, their health, their education?”

The answer to that question, he came to realize, lay in starting at the beginning, at pregnancy, and in the first few years of a Child’s life.

Decades of groundbreaking research shows that the love and sense of safety experienced by a baby directly impacts how the child’s brain is wired. Adversity, especially persistent, stress-triggering adversity like neglect and abuse, hampers that development, and can result in poorer health, educational attainment, and early death. While science underpins his mission, Terra’s palpable passion for the topic and his skill at politicking eventually led him to create Criança Feliz, a highly ambitious parent coaching program he helped launch in 2017 to try and reach four million pregnant women and children by 2020.

Under Criança Feliz, an army of trained social workers, a sort of national baby corps, are dispatched to the poorest corners of Brazil. Traveling by boat, sometimes battling crocodiles and floods, by foot, by car, by truck and by bus, these social workers go to people’s homes to show them how to play, sing, and show affection to their infants and young children. They explain to parents why this matters:

Emotional safety underpins cognitive growth. Intelligence is not fixed, but formed through experience.

Parent coaching, and specifically, home visiting, is not new. The most famous study, which took place in Jamaica in the 1970s, showed that well trained home visitors supporting poor mothers with weekly visits for two years led to big improvements in children’s cognition, behavior, and future earnings. One group of infants in that program who received coaching in their earliest years earned 25% more than a control group more than 20 years later.

But Brazil’s ambition is audacious. No city or country has ever attempted to reach so many people in such a short amount of time. (The largest program doing this now is probably in Peru, reaching about 100,000 families; Criança Feliz is already reaching 300,000.) “They are raising the bar for what is possible nationally,” says Jan Sanderson, the former deputy minister of children from Manitoba, Canada, who is an expert in home visiting and recently traveled to observe the program.

Just how Brazil, a massive country with endemic poverty and grating inequality, came to embrace parent coaching as the next frontier in combating poverty is a story of Terra’s political will, the strategic savvy of a few foundations, the pivotal role of a Harvard program, and the compassion of a growing group of unlikely allies, from communists to far-right wing politicians. Talking to lawmakers in Brazil can feel like wandering around a neuroscience convention: One senator from the south can’t stop talking about working memory, while a mayor from the northern town of Boa Vista in Roirama state is fixated on synapse connection.

At least 68 senators and congresspeople, judges, and mayors have converted to the cause, becoming evangelical in their focus on early childhood development.

“I believe that this is the solution, not only for Brazil, but for any country in the world in terms of security, public security, education, and health care,” says Iosé Medeiros, a senator from the state of Mato Grosso who heads the parliamentary committee on early childhood development. “It’s a cheap solution.”

Terra’s claims are more dramatic. “We will change the world, starting from the very beginning.”

Those words are hardly surprising coming from the man whom Ely Harasawa, Criança Feliz’s director, calls the program’s “godfather.” But the devil, of course, is in the details, and in Terra and his allies’ ability to steer a course through some rather treacherous political terrain.

Criança Feliz in action

On a hot day in May, Adriana Miranda, a 22-year-old accounting student, visits Gabriela Carolina Herrera Campero, also 22, who is 36 weeks pregnant with her third child. Campero arrived in Brazil less than a year ago from Venezuela, fleeing with her husband and two children from that country’s financial collapse and ensuing chaos. She lives in Boa Vista, a city in the north of Brazil where 10% of the population are estimated to be refugees.

The two women greet each other warmly and start chatting, in spite of the fact that Miranda is speaking in Portuguese and Campero in Spanish. They sit together on plastic chairs on a concrete patio as Miranda goes through a checklist of questions about the pregnancy. Has Campero been to her prenatal visits? (Yes.) How is she feeling? (Hot.) Is she drinking enough water? (Yes.) And walking? (When it’s not too hot.) Is she depressed or anxious? (No, but worried, yes.) Does she feel supported by her husband? (Yes.) How is she sleeping and what kinds of foods is she eating? (She’s not sleeping well because she always has to pee, and she is eating a lot of fruit.)

Miranda moves on to talking with Campero about attachment, how to create a strong bond with a baby in utero, and also once the baby is born. Does she know that at five months, the baby can hear her and that her voice will provide comfort to the baby when it is born?

“It’s important the baby feel the love we are transmitting. When he is in distress, he will know your voice and it will calm him,” says Miranda.

It’s a topic they have discussed before. Campero is eager to show what she has learned about the baby. (A part of the program requires that visitors check for knowledge.) “It has five senses, and if I talk, he will know my voice,” she says. “The baby will develop more.” They discuss the importance of cuddling a baby and being patient.

Having a baby in the best of circumstances can be challenging. As an impoverished refugee, in a new country, it can be utterly overwhelming.

I ask Campero, in Spanish, whether the program has been helpful. After all, she already has two kids. Doesn’t she know what to expect? She starts to cry. “They have helped me emotionally,” she says. “She has taught me so many things I didn’t know.” For example, she didn’t know to read to a baby, or that her baby could hear her in utero. Her son used to hit her belly; he now sings songs to the baby because she explained to him what she learned from Miranda. “I feel supported,” she tells me.

Many people, rich and poor alike, have no idea what infants are capable of. Psychologists and neuroscientists believe they are creative geniuses, able to process information in far more sophisticated ways than we ever knew. But for that genius to show itself, the baby needs to feel safe and loved and to have attention.

Medeiros explains how he viewed parenting before he went to the Harvard program.

”I raised my kids as if I were taking care of a plant,” he recalls. “You give them food, you take care of them.” He says he did the best he could, but “I did not have all this information. If I had encouraged them, stimulated them more, I would have been able to contribute much more to their development.”

He is hardly the exception. A 2012 nationally representative survey in Brazil asked mothers, 5200 of whom were college educated, what things were most important for the development of their children up to three years of age. Only 19% mentioned playing and walking, 18% said receiving attention from adults, and 12% picked receiving affection. “So playing, talking to the child, attachment, it’s not important for more than 80% of the people who are interviewed,” says Harasawa, the director of Criança Feliz.

Criança Feliz is part of Brazil’s welfare program for its poorest citizens, called Bolsa Familia. Started 15 years ago, the welfare program is rooted in a cash transfer system that makes payments contingent on kids getting vaccines and staying in school, and pregnant mothers getting prenatal care. Vaccination rates in Brazil exceed 95% and primary school enrollment is near universal. Originally derided, and still criticized by some in Brazil as a handout program for the poor, Bolsa Familia is nevertheless being replicated worldwide.

But a powerful coterie of Brazil’s political leaders believe it’s not enough. Cash transfers alleviate the conditions of poverty, but do not change its trajectory.

That’s where Criança Feliz comes in. The program is adapted from UNICEF and the World Health Organization’s Care for Child Development parent coaching program. Trained social workers visit pregnant women every month and new parents once a week for the hrst three years of a child’s life. Sessions last about an hour. The goal is to not to play with the baby or train the parent, but to help parents have a more loving relationship with their children. The program costs $20 per child per month. The ministry of social development allocated $100 million in 2017 and $200 million in 2018.

Cesar Victoria, an epidemiology professor at the Federal University of Pelotas in Brazil, will conduct a three year randomized control trial comparing kids in the program to kids who are not, on measures of cognition, attachment, and motor development. Caregivers will be evaluated to see what they have learned about stimulation and play.

Criança Feliz neither pities poverty nor romanticizes it. It recognizes that low income people often lack information about how to raise their children and offers that information up, allowing parents to do what they will with it. “It’s one thing to say ‘read to your baby twice a day,”’ says Sanderson. “It’s another thing to say, ‘when your baby hears your voice, there are little sparks firing in his brain that are helping him get ready to learn.’”

Of course, it’s a delicate balance between respecting the right of a family to raise their children the way they see fit and offering information and evidence that could help the child and the family. “You’re in their home, you can’t interfere,” says Teresa Surrita, mayor of Boa Vista. “But you are there to change their mindset.”

Liticia Lopes da Silva 23, a home visitor from Arujé, outside Sao Paulo, says that the initial Visits with families can be hard. “They don’t understand the importance of stimulation and they are resistant to the idea of playing with children,” she says. “They are raised a different way, their parents did not have this interaction with them.” The issue is not just that some mothers don’t play with their babies; some barely look at them. Others treat the visitors as nannies, leaving them to play with the child, thus thwarting the very purpose of the visit, the interaction between parent and child.

But after a few weeks of watching a social worker sit on the floor, playing with the child, and talking with her about the baby’s development, the mothers sometimes join in. “It’s amazing to see the families evolve,” says one home visitor in Arujé. “Three to four months after, you see the difference in how the mother plays with the child. In a different way, the whole family gets involved. Fathers often get involved and many families start to ask the visitors to come more often, although the visitors cannot oblige.

When a home visitor named Sissi Elisabeth Gimenes visits a family in Aruié, she brings a color wheel painted onto a piece of recycled cardboard, along with painted clothespins. She asks Agatha, age three, to put a brown clip on the brown color.

Agatha doesn’t know her colors and gets very shy. Sissi encourages Agatha while chatting with her mother, Alda Ferreira, about how play beneflts brain development. She quietly models how to use encouragement and praise, praising Agatha for finding white, ”the color of clouds”, as the girl slowly gets more confident and gets off her mother’s lap to play.

The activity is intentional. The clips hone Agatha’s fine motor skills as well as her cognitive ones; the interaction with her mother helps create the synaptic connections that allow her brain to grow and pave the way to more effective learning later on. Alda tells us her daughter knows many things that her older daughter did not at the same age.

Agatha

The process changes the social workers as well. One social worker, who has a three year old herself, says that as parents, we think we know everything. “But I knew nothing.” In Aruja, where the home visitors are all psychology students at the local university, working with the program as part-time interns, many admitted to being shocked at seeing the reality of what they’d been taught in the classroom. Poverty looks different off the page. “We are changing because we are out of the bubble,” said one. “Theory is very shallow.”

As we leave Campero’s house, I ask Miranda what she thought of the visit. She too starts to cry. “Gabriella recognizes the program is making a difference in her life,” she says, embarrassed and surprised at her own emotions. Campero had told Miranda a few weeks earlier that she was worried because the baby was not moving. Miranda suggested that Campero try singing to the child in her womb; the baby started to move.

The man who made it happen

In 2003, as secretary of health in Rio Grande do Sul, Terra created Programa Primeira Infancia Melhor (the Better Early Childhood Development Program, or PIM), a home visiting program based on Educa tu Hijo, a very successful case study from Cuba. Results have been mixed, but Terra saw the impact it had on families and communities. He set his sights on expanding the program nationally.

One of the most persuasive arguments for the program, he knew, was the science. But he had to build votes for that science. In 2011, he started lobbying everyone he could to try and get financial backing from congress to fund a week-long course that he helped create at Harvard University’s Center for the Developing Child. He thought if lawmakers, who would be attracted to the prestige of a course at Harvard, could learn from the neuroscientists and physicians there, they might also become advocates for the policy.

“Anybody in the corridor he sees, it’s a hug, it’s a tap on the chest, and then it’s early childhood development,” says Mary Young, director of the Center for Child Development at the China Development Research Foundation and an advisor to Criança Feliz. “He’s got the will and the skill.”

One convert, Michel Temer, who was vice president from 2011 and became president in 2016 when his boss was impeached, tapped Terra to be minister of social development. Soon after, Criança Feliz was born. But trying to get Terra to talk about legislation can be a challenge. What he wants to talk about are neurons, synapses, and working memory. Did I know that one million new neural connections are formed every second in the first few years of life?

And that those neural connections are key to forming memories?

“The number of connections depends on the stimuli of the environment,” he says. And the environment of poverty is relentlessly unkind to the stimuli available to children.

Attachment, he explains, is key, not just psychologically, but neurobiologically. “If a child feels emotionally safe and secure and attached they explore the world in a better way. The safer they feel, the safer their base, the faster they learn,” he says.

The first 1,000 days

Over the past 20 years, scientists have focused on the importance of the first 1,000 days of life. Brains build themselves, starting with basic connections and moving to more complex ones. Like a house, the better the foundation of basic connections, the more complex are the ones that can be built on top. In an infant’s earliest days, it’s not flashcards that create their brains, but relationships, via an interactive process that scientists call “serve and return.” When an infant or young child babbles, looks at an adult, or cries, and the adult responds with an affectionate gaze, words, or hugs, neural connections are created in the child’s brain that allow them to later develop critical tools like self-control and communication.

If kids do not experience stimulation and nurturing care, or if they face repeated neglect or abuse, the neural networks do not organize well. And that, says Charles Nelson, a pediatrics professor at Harvard Medical School, can affect the immune system, the cardiovascular system, the metabolic system, and even alter the physical structure of the brain. “Children who experience profound neglect early in life, if you don’t reverse that by the age of two, the chance they will end up with poor development outcomes is high,” he says.

The strongest buffer to protect against that? A parent, or caring adult.

The case for early childhood as policy was elevated by Nobel Prize winning economist James Heckman. As founder of the Center for the Economics of Human Development at the University of Chicago, he demonstrated the economic case for why the best investment a policymaker can make is in the earliest years of childhood, because that’s when intervention has the highest payoffs.

“The highest rate of return in early childhood development comes from investing as early as possible, from birth through age five, in disadvantaged families,” Heckman said in 2012. His work showed that every dollar invested in a child over those years delivers a 13% return on investment every year. “Starting at age three or four is too little too late, as it fails to recognize that skills beget skills in a complementary and dynamic way,” he said.

More than 506 Brazilian legislators, judges, mayors, state politicians and and prosecutors have attended the Harvard course that Terra helped set up. There, Jack Shonkoff, a pediatrician and professor, explains what infants need to thrive, what toxic stress does to a child and how to build resilience. The attendees are put in groups, maybe a state senator from one state with council members from municipalities in the same state, to spend the week on a project; in the next two-and-a-half months, they finish it with the help of a technical facilitator.

”It’s a little facilitation and a little manipulation,” says Eduardo Queiroz, outgoing head of the Fundaeéo Maria Cecilia Souto Vidigal, a foundation which has played an integral role in supporting and shepherding Criança Feliz. “We create a community.”

It costs $8,800 to attend the program. Some pay their own way. Congress pays for lawmakers to go, and the Fundagéo Maria Cecilia Souto Vidigal funds between 10 and 12 scholarships a year. The fellowship does not require the participants to do anything with their knowledge. But many have. Surrita, who is in her fifth term as mayor of Boa Vista, focused her early governing efforts on working with teens, tackling drugs and gangs as a way to help them. After her week at Harvard, she changed her approach, deciding to make Boa Vista the “early childhood development capital of Brazil.” Investing in young children, she argues, will mean not so many problems with teens:

”After taking this course Harvard on the ECD I realized how important it would be for us to work with the kids from pregnancy up to 6 years old that to develop them mentally and cognitively and that way I realized that it would be possible for us to improve the performance of the teenagers lives by working on them when they’re kids.”

Obstacles and opportunities

Criança Feliz faces two significant threats: the prospect of being shut down, and the challenges created by its own ambition.

Although the Legal Framework for Early Childhood Development, passed in 2016, underpins Criança Feliz, it currently exists as a decree of the president. Of the last three presidents, one is in jail, one was impeached and the current one, Temer, faces criminal charges. With approval ratings of around 3%, Temer has decided not to run again, and the program’s supporters are worried that whoever wins the election will dismantle what the previous government has done (a common practice in Brazil). “We are concerned every day because the program is ongoing and we don’t know if the [next] president will support it,” says Ilnara Trajano, the state coordinator from Roirama state.

Mederios and Terra say the solution to avoiding political death is to create a law that will automatically fund Criança Feliz at the state level, rather than relying on presidential support. Terra, who exudes confidence and optimism, is sure such a law can be passed before the October date set for presidential elections. Others, including Harasawa, are not so sanguine. “We are in a race against time,” she says. She is working around the clock to build support one municipality at a time. She worries that not everyone thinks the government should play a role in parenting. “We are not trying to replace the family,” she says. “We are trying to support it.”

Beyond its political future, the program itself faces a host of issues. In many places, there aren’t enough skilled workers to act as home visitors. There’s also the fraught logistics of getting around. In Careiro da Varzea, in Amazonas state, home visitors often travel five hours, by foot, to reach pregnant women and young children; they are tired when they arrive. In Arujé, seven home visitors share one car to visit 200 families, or 30 visits each, per week. Internet services can be terrible, and wild, dogs often chase the social workers.

The visitors are trained in a curriculum that tells them which materials to use, what to teach and when, and the research that underpins the guidance they give to mothers. But they need more training, and the curriculum does not always prepare them for the poverty and distress they see. Some mothers want to give up their babies; they did not want them in the first place.

Many suffer from depression. The social workers are trained to support nurturing care, but they are not mental health experts. Inevitably, turnover is high.

The evidence for the value of home visiting at scale is at once highly compelling and frustratingly imprecise. Consider the case of Colombia: From 2009 to 2011, researchers there studied 1,419 children between the ages of 12 to 24 months to see whether coaching their mothers on interactions with their babies could help the children’s development. After 18 months, the researchers found a host of benefits. The children whose mothers had received coaching got smarter. Their language skills improved, and their home environments were judged to be more stimulating. But when researchers went back two years later, they found the children, now about five years old, had not maintained those benetits. “Two years after the intervention ended, we found no effects on children’s cognition, language, school readiness, executive functioning, or behavioral development,” the study reported. (Criança Feliz run for a longer period of time, however.)

Governments face notoriously hard choices about where to invest their money. “Early childhood development is a really valuable investment,” says Dave Evans, an economist at the World Bank. “But so is primary education and the quality of primary education, and if you spend a dollar in one place, it’s a dollar you aren’t spending in another place.”

Samuel, Keith, and Giliane

One of the Virtues of a home visiting program, compared to say, building childcare centers, is that social workers can see what is happening inside a home: signs of domestic violence, other children in need, a mother’s depression, a father’s unemployment. They can help with kids like Samuel, who was born with cerebral palsy.

At two-and-a-half years old, Samuel loves his ball, and shrieks with delight when he is presented with a truck. He can’t stop smiling at his mother, Giliane de Almedida Trindade Dorea. She and social worker Keith Mayara Ribeiro da Silva, gather around him to talk and play.

“Where is the dog? Yes! That’s the dog. Very good Samuel!” says da Silva.

The two encourage Samuel to try and stand up. He struggles. “Get up, use your legs,” says Dorea. “You are lazy. Be strong!”

Samuel ignores the women’s requests. He wants to play. They shift gears. “Where is the ball?” da Silva asks. He grabs it and plays. “He’s very smart!” she says. She and Dorea are trying to get Samuel to use one hand, which cannot open, to play with the ball and then the truck. They work together for 15 minutes to find a way to get him to use his weak hand, but he just wants to play with his dominant hand.

Dorea adores her son and plays with him patiently. But it has been hard, she says. When da Silva started to visit, Samuel could not sit up, he was quite shy and often cried. Da Silva has helped the family access the services and care that Samuel needs: a physiotherapist, an occupational therapist, an acupuncturist, and a doctor to check his hearing. These are services the government will provide, but finding them and organizing the appointments is time consuming and can be overwhelming.

Dorea says Samuel has changed since Keith has been coming. “His interaction with people, he’s totally different. He was so shy.” In fact, she says the whole family has benefited. Her older daughter also knows how to play with Samuel and loves to help. She appreciates the support. Raising a child with a disability is hard work. “The visitor is a like a friend who comes every week not just for fun but also to share my concerns,” she says. Her biggest complaint about the program? “It’s too short.”

Will it survive?

There is a maxim in investing that you have to survive short-run volatility to get to the long run, you can’t make money if you don’t have any. Criança Feliz faces the same problem. Child development takes time. It is not a jobs program or a construction project, which voters can see.

The benefits can take years to show up, and politicians have never been known for their long-term thinking.

Alberto Beltrame, the current minister of social development, is a believer. Start early and you shape character, transforming the child into a better young adult and, eventually, creating an improved workforce, he says. You reduce violence and crime. He agrees that Bolsa Familia alone is not enough. It does not promote autonomy, or break the cycle of poverty. What is needed is a two-pronged approach: In the short term, promote training, microcredit, and entrepreneurialism to create jobs. For the medium and long term, Criança Feliz.

“We have a huge array of benefits that we are going to gain with this one program, and the cost is very, very low compared to others,” he says.

In every home we visited, mothers said they loved the support, be it information, toys, or more often, company to share their challenges and triumphs. Priscila Soares da Silva has three children, including six month old Allyce, and another on the way. With Allyce, she says, she has changed her approach to parenting, setting time aside to play every day now. “You raise children your way,” she explains cooing over Allyce. “When you see there are other visions, you see the way you did it was not so right.” She is also refreshingly honest about something all parents know: We do it better when someone is watching. “There are things we know, but we are lazy. When she comes, we are better.”

When I quietly ask her teenage daughter, who is lingering in the corner, what she thinks of the visits, she answers immediately: “She’s so much more patient,” she says of her mother. Her own takeaway: Parenting is hard, and she does not want to do it anytime soon. Priscila smiles at this, agreeing she started too soon, and noting the benefits of the program have extended beyond Allyce and the baby she will soon have. “The program got the family closer.”

Evans, from the World Bank, is watching the program closely. “I see Criança Feliz as a big, bold, gamble about which I am optimistic,” he says. “But I think the measurement and the evaluation is crucial to see if it is a model that other countries want to echo.”

If it survives the near term political turbulence, Beltrame says it can go way beyond the poor to beneiit everyone. “We are trying to make the Brazilian people realize, independent from their level of income, that stimulating children from pregnancy through the first 1,000 days of life is important,” he says. Better young people equal healthier and better adults, who are more emotionally connected and can be better citizens.

With Crianea Feliz, Beltrame says, we have the “possibility of having a new destiny and future for each one of these children.”

The Lancet

Advancing Early Childhood Development: from Science to Scale

An Executive Summary for The Lancet’s Series

Overview of the Series

The 2016 Lancet Early Childhood Development Series highlights early childhood development at a time when it has been universally endorsed in the 2030 Sustainable Development Goals.” This Series considers new scientific evidence for interventions, building on the findings and recommendations of previous Lancet Series on child development (2007, 2011), and proposes pathways for implementation of early childhood development at scale.

The Series emphasises “nurturing care”, especially of children below three years of age, and multi-sectoral interventions starting with health, which can have wide reach to families and young children through health and nutrition.

Key messages from the Series

The burden and cost of inactian is high.

A staggering 43 percent of children under five years of age, an estimated 250 million, living in low and middle income countries are at risk of suboptimal development due to poverty and stunting. The burden is currently underestimated because risks to health and wellbeing go beyond these two factors. A poor start in life can lead to poor health, nutrition, and inadequate learning, resulting in low adult earnings as well as social tensions. Negative consequences impact not only present but also future generations. Because of this poor start, affected individuals are estimated to suffer a loss of about a quarter of average adult income per year while countries may forfeit up to twice their current GDP expenditures on health and education.

– Young children need nurturing care from the start.

Development begins at conception. Scientific evidence indicates that early childhood is not only a period of special sensitivity to risk factors, but also a critical time when the benefits of early interventions are amplified and the negative effects of risk can be reduced. The most formative experiences of young children come from nurturing care received from parents, other family members, caregivers, and community based services. Nurturing care is characterised by a stable environment that promotes children’s health and nutrition, protects children from threats, and gives them opportunies for early learning, through affectionate interactions and relationships. Benefits of such care are life long, and include improved health, wellbeing, and ability to learn and earn. Families need support to provide nurturing care for young children, including material and financial resources, national policies such as paid parental leave and provision of population based services in a range of sectors, includlng health, nutrition, education, and child and social protection.

We must deliver multi-sector interventions, with health as a starting point for reaching the youngst children.

Interventions, including support for families to provide nurturing care and solving difficulties when they occur, target multiple risks to development, and can be integrated into existing maternal and child health services. Services should be two pronged, considering the needs of the child as well as the primary caregiver, and include both (are for child development as well as maternal and family health and wellbeing. This affordable approach is an important entry point for multi-sectoral collaborations that support families and reach very young children. Essential among these are nutrition, to support growth and health, child protection, for violence prevention and family support. social protection, for family financial stability and capacity to access services; and education, for quality early learning opportunities.

– We must strengthen government leadership, to scale up what works.

It is possible to scale up projects to nationwide programmes that are effective and sustainable, as indicated by four country case studies in diverse world regions. However, government leadership and political prioritisation are prerequisites. Governments may choose different pathways for achievmg early childhood development goals and targets, from introducing tansformative government wide initiatives to progressively enhancing existing services. Services and interventions to support early childhood development are essential to ensuring that everyone reaches their potential over their life course and into the next generation, the vision that is core to the Sustainable Development Goals.

Risks to early childhood development remain high

Updated definitions of stunting and extreme poverty and improved source data were used to re-estimate the number of children under 5 years in low and middle income countries who are at risk of not reaching their developmental potential. Between 2004 and 2010, this number declined from 279 million (51 percent of children in 2004) to 249 million (43 percent of chiidren in 2010), with the highest prevalence in sub Saharan Africa (70 percent in 2004 and 66 percent in 2010).” An illustrative analysis from 15 countries with available Multiple indicator Cluster Surveys in 2010 or 2011 demonstrates the implications of additional risks to chiidren’s development beyond poverty and stunting, induding low maternal schooling (completed primary school) and child physical abuse by either parent or by caregivers (severe punishment of children aged 2 to 5 years, such as hitting a child as hard as possible, or with a belt or stick). Estimates of children at risk increase dramatically when low maternal schooling and this kind of physmal abuse are added, from 62.7 percent (exposed to risks of stunting or extreme poverty), to 754 percent, with large disparities among sub national social and economic groups.

Global commitments to early childhood development are growing

Since 2000, the rapid increase in publications on the topic of early childhood development surpassed the general trend for health sciences publications. However, only a few of the publications reported on interventions.

The numbers of countries with national multi sectoral early childhood development policies increased from seven in 2000 to 68 in 2014, of which 45 percent were low and middle income countries. There has also been substantial investment in early childhood development during that time period. For example, since 2000 the Inter American Development Bank has approved more than 150 projects for over US$17 billion. From 2000 to 2013, the World Bank Invested $3.3 billion in 273 projects, primarily through health, nutrition, and population programmes. Still, investment falls short of the need and the impact of available interventions.

Early childhood development from a life course perspective

Childhood development is a maturational process resulting in an ordered progression of perceptual, motor, cognitive, language, socio emotional, and selfregulation skills. Thus, the acquisition of skills through the life cycle builds on the foundational capacities established in early childhood.

Multiple factors influence the acquisition of competences and skills, including health, nutrition. security and safety, responsive caregiving, and early learning (Figure 1), Each are necessary for nurtunng care. Nurturing care reduces the detrimental effects of disadvantage on brain snucture and function which, in turn, improves children’s health, growth, and development.

Interventions, including nurturing care, benefit early childhood development

Interventions identified by reviews between 2011 and 2015, and country policies shown to have significant benefits for childhood development, are summarised and organised into packages in Figure 2. Many of the health and nutrition interventions have additional beneflts for improved child survival and growth, as well as reduced morbidnes and disabilities.

Family support and strengthening package

Three elements of family strengthening increase the likelihood that families are able to provide nurturing care for their children: access to quality services (eg, antenatal care, immunisation, nutrition), skills building (29, nurturing care and reduction of harsh discipline); and support (eg, social protection, safety networks, and family support policies)

Caring for the caregiver package

This two generation package emphasises care and protection of parents’ physical and mental health and wellbeing, while enhancing caregivers’ capacnty to provide nurturing care to their child.

Early learning and protection package

This set of interventions integrates the support of young children with parental support and the facilitation of teachers’ and caregivers’ ability to create a nurturing environment in day care and early childhood centres. The emphasis is on quality and family support through parental empowerment, guidance on nutrition and care, and child protection.

Parent support pvogrammes

Parent support programmes that promote nurturing care, particularly those employing several behaviour change techniques, can substantially augment the positive effects on early childhood development outcomes of basic health and nutrition, education, and protection interventions. In contrast, maltreatment during childhood is associated with reduced volume in brain regions involved in learning and memory. Children who receive inadequate care, especially in the first 24 months of life, and often from mothers who themselves were neglected or abused, are more sensitive to the effects of stress and display more behavioural problems than do children who receive nurtunng care.

Multi sectoral interventions improve childhood development

The effectiveness of interventions could be improved by taking into consideration the major insights gained over the past decade about how human development is affected across generations by complex and multi faceted experiences. Sectoral interventions combined with elements of nurturing care and protection, can boost the effect on child outcomes. This approach encourages interventions directed at the family as a unit rather than the child alone.

Learning from early childhood development programmes at scale

An analysis of country programmes illustrates the importance of political prioritisation, legislation, and policy, and the use of existing systems and financing to scale up. These programs focus on addressing poverty, inequality, and social exclusion, starting early. Scaledup early childhood development programmes most often have a vision of comprehensive and integrated services for children and families; have been founded by statute or other formally communicated government strategy; have been funded by government; and have been led by a government department or agency working collaboratively with other departments and civil society organisations.

Framework for action

To promote health and wellbeing across the life course at scale requires interventions provided through several sectors, and a supportive environment of policies, cross sectoral coordination, and financing (Figure 3).

At the heart of this intervention framework is the nurturing care of young children, provided by parents, families, and other caregivers Particularly successful are parent support programmes to promote nurturing care, among which the most widely implemented in low and middle income country settings are the WHOIUNICEF Care for Chiid Development and Reach Up and Learn, a parenting programme tested in trials in Jamaica over the past 20 years and now expanding to other regions.

Affordability of early childhood development interventions

To assess the affordability of including interventions to promote early childhood development in existing health and nutrition services, this paper estimates the additional costs of incorporating two interventions aimed at supporting nurturing care of children into the services identified in the Global Investment Framework for Women’s and Children’s Health.“ The First intervention is based on Care for Child Development and the second on support for maternal depression, because it bolsters nurturing care. The estimated average additional investment needed is half a dollar per capita in the year 2030, ranging from US$01 in low income countries to US$07 in upper middle income countries This represents an additional 10 percent over published estimates for a comprehensive set of women’s and children’s health and nutrition services.

The cost of inaction

At an individual level, the loss of average adult income per year for the 43 percent of children at risk of not reaching their developmental potential is likely to be 26 percent, exerting a strong downward economic pull and trapping families in poverty. At a societal level, the cost of inaction for not improving stunting to a prevalence of 15 percent or less and not addressing developmental delays through preschools and home visits is several times more than what some countries currently expend on health or education respectively. The cost of inaction for not improving childhood development through preschool and home visits rises sharply in settings with fewer preschool services, as well as in settings with a higher prevalence of children at risk of poor development.

Pathway to scale

Action 1: Expand political will and funding through advocacy for the Sustainable Development Goals (SDGs)

Under the broader SDG umbrella, investing in early childhood development has become not only an aim in itself, but a requisite for achieving many other SDGs (eg, SDGs 1, 5, 10, 16, and 17). For example, SDG Target 4.2 under the learning goal, calling for universal access to quality eady childhood development, care, and pre-primary education, provides unprecedented opportunity to scale up early childhood development services,

Action 2: Create a policy environment that supports nurturing care of young children

Laws and policies can improve childhood development by increasing access to and quality of health and other services, as well as money and time for parents to provide nurturing care for their young children. Five transformative policies for which there is robust global data on levels, duration, coutry coverage, and progress achieved in the past two decades include: 1) paid parental leave for new mothers and fathers; 2) breastfeeding breaks at work, 3) paid leave for parents to care for sick children; 4) income support through a minimum wage; and 5) tuition free pre-primary education. Governments, with the technical and funding assistance of development partners, must also ramp up efforts to analyse their situation, identify gaps and priority areas for intervention, and develop sustainable and costed action plans to promote early childhood development at scale.

Action 3: Build capacity to promote early child development through multi sectoral coordination

Many efforts to promote early childhood development are dependent on non governmental services, which are frequently limited in scope and inequitable in coverage. Interventions are highly dependent on skilled human resources and, unless built on existing service systems such as health, education, social and child protection, face severe supply side constraints. This is illustrated by lessons learned from the scale up between 2000 and 2009 of more than 120 cash transfer programmes in low and middle income countries

We identified multiple examples in health and nutrition services into which interventions to promote nurturing care and improve childhood developmental outcomes have been feasibly and effectively incorporated. Opportunities also exist in other sectors. which is important for the continuity of support from early childhood into schooling. For example, in the education sector, childhood development can be supported through a variety of early learning opportunities, including the prvisiin of child day care services, preschool, and parent education. Interventions can also be provided through child and social protection services, including cash transfer programmes. Thus, the integration of early childhood development interventions into existing service delivery platforms, starting with health, is an effective and efficient way to reach large numbers of families and children.

Action 4: Ensure accountability for early child development services, increase research, and foster global and regional leadership and action

Ensuring the inclusion of a core set of early childhood development indicators, which go beyond access and process and hold stakeholders accountable for childhood development in the global metrics for the SDGs, is of paramount importance. Research that links detailed longitudinal data on policies and programmes with outcomes, allowing causal modelling, is essential.

Conclusion

Strong biological, psychosocial, and economic arguments exist for intervening as early as possible, starting from and even before conception, to promote, protect, and support children’s development. An emphasis on the first years of life is articulated within a life course perspective. High quality care in families, child day care services, and preschools during the earliest years needs to be followed by high quallty schooling and services into adolescence in order to capitalise on interdependence between investments made in the successive stages of the life cycle.

Multi sectoral interventions, with health services as an entry point, are particularly well-placed to reach children early with services that support families to deliver nurturing care and promote, protect, and support early childhood development, Interventions to promote nurturing care can feasibly build on existing health and nutrition services at only a limited additional cost. Coordination with education is needed to promote learning, and with social and child protection, to reach the most vulnerable population:

Evidence consolidated in this series points to effective interventuons and delivery approaches at a scale that was not envisaged before, During the next fifteen years. world leaders have a unique opportunity to invest in the early years for long-term individual and societal gains and achievement of the SDGs. All sectors must play their part in supporting families to prowde nurturing care for children.

However, the time has come for the health sector to expand its vision of health beyond prevention and treatment of disease to include the promotion of nurturing care for young children as a critical factor In the realisation of the human potential of all people.

A groundbreaking study offers undeniable proof that the fight against inequality starts with moms

Jenny Anderson

Children born into poverty start at a big disadvantage. To thrive, they need food, shelter, and health care. But a growing body of evidence shows there are other ways to help close the vast gap in development between poor kids and their wealthier peers: singing, talking, and playing with them.

If this sounds obvious or inconsequential, it’s not. Dealing with the stress of poverty makes it hard for many parents to establish critical bonds with their babies, bonds that lay the foundations for learning, emotional regulation, and relationships. Poor parents are “focused on survival and illness and food and health care,” says Sally Grantham-McGregor, an emeritus professor of international child health at University College London and University of the West Indies. “There’s no time to play with children, it seems frivolous.”

But playing with babies turns out to be anything but frivolous. Grantham-McGregor and her colleagues have spent more than 40 years pioneering research which showed just how much supporting mothers in the earliest days of a child’s life can directly benefit that child. In the 1970s, Grantham-McGregor and Christine Powell, from the University of the West Indies, began a research project aimed at helping young children from poor backgrounds and their moms in Kingston, Jamaica. They designed programs that sent doctors and nurses to visit mothers every week in their homes for two years, bringing toys and books that would help parents become better teachers to their babies and to increase stimulation and play.

The resulting studies found that children whose mothers received coaching made significant developmental gains, and not just in the short term. Twenty-two years later, the kids from one group who had received those home visits as young children not only had higher scores on tests of reading, math, and general knowledge, they had stayed in school longer. They were less likely to exhibit violent behavior, less likely to experience depression, and had better social skills. They also earned 25% more on average than a control group of kids whose mothers had not received the coaching.

The highly influential Jamaica studies have influenced the way many countries think about investing in early childhood development. Brazil, Guatemala, Zimbabwe, Bolivia, Peru, Colombia, Bangladesh, and India are all trying parent coaching programs, many based on the Jamaica model. It’s easy to see why some countries are embracing such an approach. After all, it’s in every country’s best interest to ensure that its most disadvantaged citizens get the support they need to live productive, fullilling lives.

“If we want to attack poverty, the place to start is very early in life,” says Paul Gertler, an economist who studied the long-term effects of the Jamaica program. Research shows that poverty affects a young child’s development on multiple levels, from their cognitive and educational performance to their physical health and social and emotional development. Compared to the cost of unemployment benefits or other social safety net programs, “getting it right to start with is cheaper.”

To tackle the lasting effects that inequality can have on a child’s life, we have to start early. The work of Grantham-McGregor and her team in Jamaica offers some of the best evidence we have about what governments can do to support families in an effort to close the intractable gap between rich and poor children everywhere.

The Jamaica experiments

Much as caregivers in poor countries typically want their children to succeed, it’s not necessarily obvious that a key way to do this is to talk and sing to babies, respond to them when they cry, and find other ways to engage them with the world. Consider a 2012 nationally representative survey in Brazil, which asked mothers, 52% of whom were college educated, what things were most important for the development of their children up to three years of age: only 19% mentioned playing and walking, 18% said receiving attention from adults, and 12% picked receiving affection.

The Jamaica studies showed how much these things matter. Through randomized controlled trials supporting poor, often uneducated mothers, the programs dramatically improved children’s development. (The effect sizes have been described as “astounding.”) It expanded the scope of helping poor children from health and nutrition to stimulation and responsiveness.

While the earliest studies used health professionals as home visitors and relatively expensive toys and materials, Grantham-McGregor and Powell quickly changed the program’s model to save money, using community health workers instead of doctors and nurses and homemade toys. Over the course of seven studies, they also experimented with different levels of frequency for the home visits and worked with babies experiencing different kinds of deprivation, including severely malnourished infants and children who had been born at a low birth weight.

They found that the effects of early intervention were both long-lasting and complex. One study tracked 129 stunted children, that is, babies smaller than well nourished children of the same age and gender, who show persistent developmental delays as they grow up. Researchers followed a group of children and mothers that received weekly home visits for two years, as well as other groups of children, including a control group. The study then tracked the children’s development for up to 22 years.

The beneflts of the intervention seemed to vary as the children grew up. After two years, the infants in the visiting group showed significant developmental gains. They actually caught up to kids who were not stunted, an enormous victory.

Over time, however, some of the effects seem to fade or fluctuate. At 7 to 8 years of age, the mean IQ from the intervention group was no higher than that of the control group. By age 11 to 12, the children who had been in the home visiting group had signincantly higher IQs than the control group, but showed no significant improvements in behavior or school achievement.

Then, when researchers tested the intervention group again at age 22, they found a battery of benefits, from higher income to better social skills and less violent tendencies.

Many researchers might have given up when the effects of the early intervention programs seemed to fade. But the benefits resurfaced with a bang, proving that programs that coach mothers can bring about lasting, significant, long-term results. In 2016, Grantham-McGregor and Smith published research in the Journal of Applied Research on Children exploring 12 published trials in five different countries, all of which were based on the original findings of the Jamaica program.

“Jamaica was so important because it shows us the potential of what can be done, the importance of stimulation, and that impacts can be long lasting,” says Amanda Devercelli, global lead for early childhood development at the World Bank. The challenge lay in taking Jamaica’s small program with big effects and making it accessible to the millions of poor families who need it.

The brain science behind nurturing care

In the years since the Jamaica studies, the science underscoring the critical opportunities and risks of early childhood has exploded. Neuroscience revealed the incredible plasticity of the early brain, showing that the foundations for learning opportunities and risks of early childhood has exploded.

Neuroscience shows that the foundations for learning as well as children’s social, emotional, and moral development start as early as pregnancy, and spike in a baby’s earliest years. Like a house, children’s brains need strong foundations. Their brains cannot fully develop without responsive caregiving; people who help them form deep and trusting attachments; and stimulation. Stress during a child’s early years, whether from poverty, malnutrition, neglect, or abuse, can negatively affect their nervous system in ways that can create lifelong problems with learning, behavior, and physical and mental health.

A foundational tenet of nurturing care is the importance of serve and return, which refers to adults’ responses to a child’s attempts at communication, from crying and babbling to gazing and smiling. According to the National Scientific Council on the Developing Child and the Center for the Developing Child at Harvard, “The interactive influences of genes and experience literally shape the architecture of the developing brain, and the active ingredient is the ‘serve and return’ nature of children’s engagement in relationships with their parents and other caregivers in their family or community.”

The neurobiology of early childhood presents a challenge to policymakers. Until fairly recently, policy makers focused their dollars and attention for children on education, usually starting around age five.

But five years old is too late. Research shows that developmental deficits between richer and poorer children can show up in kids as young as seven months. By the time children are in school, the gaps between advantaged children and disadvantaged ones are already enormous. School tends to exacerbate those rifts.

“It’s fairy well established that how well a child has developed cognitively, language development, socially, emotionally, when they enter school will determine to a large extent how well they do in school, and that will have repercussions in adulthood including the intergenerational cycle of poverty,” says Grantham-McGregor. This means the bigger a developmental deficit is early on, the harder it is for poor kids to catch up.

Grantham-McGregor is excited about the developments in neuroscience. But she’s emphatic that it’s already well established that mothers from disadvantaged homes benefit from this kind of help. “The brain research is exciting and it’s helpful because people pay attention,” she said. “It’s good for advocacy, but we were doing these programs before this data came out. And we’re still doing them.”

Expanding the lessons of Jamaica

Economists have joined the neuroscientists, arguing with data, that investing in early childhood is the most cost-effective way to affect long-term outcomes like education and employment.

James Heckman runs the Center for the Economics of Human Development at the University of Chicago, and won the Nobel prize in 2000 for his work in microeconometrics. He has since focused on applying his work to early childhood, including analyzing of the Jamaica research. He estimates that the best investment any policymaker can make is in the earliest years of childhood, because these interventions have the highest payoffs.

“The highest rate of return in early childhood development comes from investing as early as possible, from birth through age five, in disadvantaged families,” Heckman said in 2012. “Starting at age three or four is too little too late, as it fails to recognize that skills beget skills in a complementary and dynamic way.”

The key, it seems, is ensuring that families have the support and tools they need to bond with young children and provide them with engaging environments. “We know from developmental science that families are the biggest builders of skills and abilities in their children in the earliest years,” Heckman tells Quartz. “Jamaica shows that simple but effective parental education can produce better child outcomes.”

Jamaica inspired programs now exist all over the world, as do hundreds of other parenting programs. The biggest issue they face? How to get the strongest outcomes in the most affordable way. In a sense, Jamaica set the bar uncomfortably high for this, due to its small size and the fact that the home visitors were highly trained, and the coaching quite intensive.

“Our challenge now is to take what we learned from Jamaica and design programs that are affordable and feasible in many diverse low-income settings,” says Devercelli from the World Bank.

One study in Colombia looked at whether a more affordable, and scalable, version of the Jamaica program could produce the same effects. It used a large sample, studying 1,420 children aged 12-24 months and their primary caregivers in 96 municipalities, and tied the implementation of the home visits to an existing social protection program, conditional cash transfers. The results showed positive and significant effects on cognition and language, though smaller than the effects in Jamaica, as would be expected.

Meanwhile, in 2012, the Peruvian government implemented Cuna Mas, a home-visiting program based on many of the materials and foundations used in Jamaica and perhaps the best example of Jamaica operating at scale. The program has reached over 90,000 Peruvian families. Early research shows positive and significant effects on children’s cognition and language, as well as parenting practices, although the effects are smaller than in either Jamaica or Colombia.

“As you scale, the impacts are smaller,” says Marta Rubio Codina, a senior economist at the Inter-American Development Bank. Reducing costs to make the programs more affordable for governments means that quality can suffer. The goal, she says, is to figure out how to minimize those compromises. “My bet is that we have to invest in the workforce: training the home visitors and training their mentors.”

To help other countries develop and measure their own programs, an international collaboration of academics headed by the Jamaican group at the University of the West Indies developed Reach Up and Learn, a web-package of materials and curriculum and training manuals which are being used in places from Colombia, India, Peru, and Brazil. One Challenge: making sure the curriculum reflects the country’s culture, including local games, rhymes, songs, and stories.

“Adapting to culture is a lot of work,” says Grantham-McGregor. Pretend games taught to parents may need to be adapted, going to the field to work, or spinning wool, depending on common occupations. Local artists also need to redraw pictures to reflect a given culture’s typical housing, landscape, and style of dress, among other things.

Countries are experimenting with other variations on the program. Bangladesh has built a strong body of evidence that Jamaica-type programs are effective. They are experimenting with small groups of mothers visiting health workers in clinics, rather than having workers come to their homes.

As the long-term benefits of such programs materialize, early childhood advocates are urging governments to find more ways to support mothers and families. In 2016, the Lancet published a series of articles on early childhood highlighting the unique opportunity the early years offer to policymakers. Writing for the Lancet, Pia Britto, an adviser to Unicef, wrote that we now know the critical importance of “nurturing care,” which she defines as a set of interrelated concepts around caregiving, ranging from hygiene to stimulation (talking, singing, playing), responsiveness (early bonding, secure attachment, trust, and sensitive communication), and safety (routines and protection from harm).

“The single most powerful context for nurturing care is the immediate home and care settings of young children often provided by mothers, but also by fathers and other family members, as well as by childcare services,” Britto writes. Thanks to the Jamaica experiments, the world has increasingly accepted this fundamental truth: The best way to help poor kids is to start early, and give mothers and families the support they need.

Music and Empathy are psychological neighbours. Empathetic people process music differently – Stephen Johnson * Music, Empathy, and Cultural Understanding – Eric Clarke, Tia DeNora, Jonna Vuoskoski * Current Disciplinary and Interdisciplinary Debates on Empathy – Eva-Maria Engelen, Birgitt Röttger-Rössler * Neurophysiological Effects of Trait Empathy in Music Listening – Zachary Wallmark, Choi Deblieck, Marco Iacaboni. * Interpersonal Reactivity Index (IRI).

“The ‘other’ need not be a person: it can be music.” Clifton (1983)

There are two pathways when it comes to understanding each other: thinking or mind reading and feeling or empathy.

Empirical investigations have shown that people who have a tendency to be more empathic experience more intense emotions in response to music.

Listening to sounds, even outside of a musical context, significantly activates empathy circuits in the brains of high empathy people. In particular, sounds trigger parts of the brain linked to emotional contagion, a phenomenon that occurs when one takes on the emotions of another.

Musical engagement can function as a mediated form of social encounter, even when listening by ourselves. Recent research has shown that trait empathy is linked to musical preferences and listening style. If we consider music through a social psychological lens, it is plausible that individuals with a greater dispositional capacity to empathize with others might also respond to music’s social stimulus differently on a neurophysiological level by preferentially engaging brain networks previously found to be involved in trait empathy.

Music can be conceived as a Virtual Social Agent… listening to music can be seen as a socializing activity in the sense that it may train the listener’s self in social attuning and empathic relationships. In short, musical experience and empathy are psychological neighbors.

Esenherg et al (1991) define empathy as, “an emotional response that stems from another’s emotional state or condition and is congruent with the other’s emotional state or condition.”

Who or what do we empathize with when listening to music?

For some people music is able to represent a virtual person with whom to empathize, and whom they can experience as empathizing with their felt emotions. Studies that have investigated people’s reasons for listening to sad music when they already feel sad have found that some listeners can experience the music itself as providing empathy and understanding for the feelings that they are going through, functioning as a surrogate for an empathic friend.

Mirror neurons may be as much a consequence of a culture of inter-subjective engagement as they are a foundation for it.

It is quite conceivable that people who are inclined to imagine themselves from others’ perspectives also tend to take up the physical actions implied by others’ musical sounds, whether a smooth and gentle voice, a growled saxophone, or any other musical sound reflecting human actions.

It’s no surprise our level or empathy impacts how we process social interactions with other people. But how might empathy affect the way we process music?

That’s the question addressed in a first of-its-kind study published in Frontiers in Behavioral Neuroscience. The results showed that high empathy people not only got more pleasure from listening to music, but also experienced more activity in brain regions associated with social interactions and rewards.

The implication is that empathy can make you interact with music as if it were a person, or a “virtual persona,” as described in a 2007 study:

“Music can be conceived as a virtual social agent… listening to music can be seen as a socializing activity in the sense that it may train the listener’s self in social attuning and empathic relationships.”

The researchers conducted two experiments to examine how empathy impacts the way we perceive music. In the first, 15 UCLA students listened to various sounds made by musical instruments, like a saxophone, while undergoing an fMRI scan.

Activation sites correlating with trait empathy (IRI subscales) in selected contrasts.

Some of the instrument sounds were distorted and noisy. The idea was that the brain might interpret these sounds as similar to the “signs of distress, pain, or aggression” that humans and animals emit in stressful scenarios, and these “cues may elicit heightened responses” among high-empathy people. Participants also completed the Interpersonal Reactivity Index, a selfreported survey commonly used by scientists to measure one’s level of empathy.

The results confirmed what the team had hypothesized: listening to the sounds, even outside of a musical context, significantly activated empathy circuits in the brains of high-empathy people. In particular, the sounds triggered parts of the brain linked to emotional contagion, a phenomenon that occurs when one takes on the emotions of another.

But how does empathy affect the way we listen to a complete piece of music?

To find out, the researchers asked students to listen to music that they either liked or disliked, and which was either familiar or unfamiliar to them. They found that listening to familiar music triggered more activity in the dorsal striatum, a reward center in the brain, among high-empathy people, even when they listened to songs they said they hated.

Familiar music also activated parts of the lingual gyrus and occipital lobe, regions associated with visual processing, prompting the team to suggest that “empathic listeners may be more prone to visual imagery while listening to familiar music.”

In general, high-empathy people experienced more activity in brain regions associated with rewards and social interactions while listening to music than did low-empathy participants.

“This may indicate that music is being perceived weakly as a kind of social entity, as an imagined or virtual human presence,” said study author Zachary Wallmark, a professor at SiViU Meadows School of the Arts. “If music was not related to how we process the social world, then we likely would have seen no significant difference in the brain activation between high-empathy and low empathy people.”

We often conceptualize music as an abstract object for aesthetic contemplation, Wallmark said, but the new findings could help us reframe music as a way to connect others, and to our evolutionary past.

“If music can function something like a virtual “other,” then it might be capable of altering listeners’ views of real others, thus enabling it to play an ethically complex mediating role in the social discourse of music,” the team wrote.

Music, Empathy, and Cultural Understanding

Eric Clarke, Tia DeNora, and Jonna Vuoskoski

In the age of the internet and with the dramatic proliferation of mobile listening technologies, music has unprecedented global distribution and embeddedness in people’s lives. It is a source of intense experiences of both the most individual (personal stereos) and massively communal (large-scale live events, and global simulcasts) kind; and it increasingly brings together or exploits a huge range of cultures and histories, through developments in world music, sampling, the re-issue of historical recordings, and the explosion of informal and ‘bedroom’ music making that circulates via YouTube. For many people, involvement with music can be among the most powerful and potentially transforming experiences in their lives.

To what extent do these developments in music’s mediated and mediating presence facilitate contact and understanding, or perhaps division and distrust, between people? This project has pursued the idea that music affords insights into other consciousnesses and subjectivities, and that in doing so may have important potential for cultural understanding.

The project:

1) brings together and critically reviews a considerable body of research and scholarship, across disciplines ranging from the neuroscience and psychology of music to the sociology and anthropology of music, and cultural musicology, that has proposed or presented evidence for music’s power to promote empathy and social/cultural understanding through powerful affective, cognitive and social factors, and to explore ways in which to connect and make sense of this disparate evidence (and counter-evidence);

2) reports the outcome of an empirical study that tests one aspect of those claims demonstrating that ‘passive’ listening to the music of an unfamiliar culture can significantly change the cultural attitudes of listeners with high dispositional empathy.

Researchers and Project Partners

Eric Clarke, Faculty of Music, University of Oxford

Tia DeNora, Sociology, Philosophy & Anthropology, Exeter University

Jonna Vuoskoski, Faculty of Music, University of Oxford

Introduction

Music is a source of intense experiences of both the most individual (personal stereos, headphone listening) and massively communal (large-scale live events, and global simulcasts) kind; and it increasingly brings together or exploits an exceptional range of cultures and histories, through developments in ‘world music’, sampling, historical recording and hybridization. At a time when musicology, the social and cultural study of music, have become far more circumspect about essentializing and romanticizing claims, it is still not uncommon to find claims being made for music as a ‘universal language’ that can overcome (or even transcend) cultural difference, break down barriers of ethnicity, age, social class, ability/disability, and physical and psychological wellbeing.

There are widespread symptoms of this belief or claim, including the activities of the West-Eastern Divan Orchestra (founded by Edward Said and Daniel Barenboim, to bring together Israeli and Palestinian musicians); and the appointment by UNICEF of classical musicians to act as ‘goodwill ambassadors’, bringing their music to people in deprived, war-torn, or disaster-hit parts of the world so as to offer emotional support, solidarity, and a kind of communion.

An extract from the violinist Maxim Vengerov, who in 1997 was the first classical musician to be appointed a goodwill ambassador, reads: “1997, September: For Maxim Vengerov’s first official undertaking with UNICEF, he organized a musical exchange with children from Opus 118 a violin group from East Harlem, New York. The children of Opus 118, aged 6 to 13, came from three different elementary schools in this inner-city neighbourhood. This innovative programme has spurred a whole generation to learn ‘violin culture’. Along with the youths, Mr. Vengerov not only played Bach but also southern blues and tunes such as ‘Summertime’ and ‘We Shall Overcome’.”

And from the same webpage, beneath a picture showing the violinist in jeans and T-shirt playing as he leads a line of children in the manner of a latter-day Pied Piper is the caption: “In the remote village of Baan Nong Mon Tha, children from the Karen hill tribe ethnic group follow Maxim Vengerov, in a human chain, to a school run by a UNICEF-assisted NGO. Thailand, 2000.”

Similarly, the 1985 Live Aid, and 2005 Live 8, events were global pop music events intended not only to raise money (in the case of Live Aid) and popular pressure on politicians (in the case of Live 8) for the relief of famine and poverty, but also to galvanize a global consciousness and a united ‘voice’: as Bob Geldof, the prime mover of Live 8 put it: “These concerts are the start point for The Long Walk To Justice, the one way we can all make our voices heard in unison.”

And finally, the popular UK television series ‘The Choir’ (which has run to six series so far) documents the powerful ‘identity work’ and intense emotional experiences that accompany the formation of choirs in schools, workplaces, and military establishments out of groups of people who have had little or no previous formal musical experience, and who come from very varied walks of life (from bank executives to fire officers and military wives).

In all these very public examples of a much wider if less visible phenomenon, we see a complex mixture of implicit musical values, discourses about music’s ‘powers’, folk psychology and its sociological equivalent, and (in some cases) more or less grounded or unsupported claims about the impact of music on the brain (cf. Tame, 1984; Levitin, 2006). It would be easy to be hastily dismissive of some of these claims, but a considerable volume of research by highly regarded scientists and scholars, coming from disciplines that range from neuroscience and philosophy through psychology and sociology to anthropology and cultural studies has also made a significant case for the capacity of music and musicking (Small, 1998) to effect personal and social change (e.g. Becker 2004; DeNora 2013; Gabrielsson 2011; Herbert 2011). If music can effect change, and speak across barriers, it can also offer a means of intercultural understanding and identity work.

As Cook (1998: 129) puts it:

“If both music and musicology are ways of creating meaning rather than just of representing it, then we can see music as a means of gaining insight into the cultural or historical other. If music can communicate across gender differences, it can do so across other barriers as well. One example is music therapy… But the most obvious example is the way we listen to the music of other cultures (or, perhaps even more significantly, the music of subcultures within our own broader culture). We do this not just for the good sounds, though there is that, but in order to gain some insight into those (sub)cultures. And if we use music as a means of insight into other cultures, then equally we can see it as a means of negotiating cultural identity.”

In different ways, these (and other) claims seem to make use of a generalized notion of empathy. Empathy has recently seemed to gain considerable attention/currency in musicology, psychology of music, sociology of music and ethnomusicology as a way to conceptualize a whole range of affiliative, identity-forming, and ‘self-fashioning’ capacities in relation to music. But what is brought together or meant by the term ‘empathy’, and is it a useful and coherent way to think about music in relation to its individual and social effects?

Our project, and this report, arise from the disparate nature of the evidence for the claims about music’s transformative power, individually and socially, and the ‘scattering’ of the case across theories and findings in a huge disciplinary range: from research on music and mirror neurons (Overy and Molnar-Szakacs 2009) to the ethnomusicology of affect (Stokes 2010), the history of musical subjectivity (Butt 2010) and sociological studies of music and collective action (Eyerman and Jamieson 1998), the case has been made for different perspectives on music’s capacity to afford compassionate and empathetic insight and affiliation, and its consequent power to change social behaviour.

These diverse research strands all point to the crucial role that musicking plays in people’s lives, to its transformational capacity, and to the insights that it can afford. There is no single window onto ‘what it is like to be human’, but musicking seems to offer as rich, diverse, and globally distributed a perspective as any and one that engages people in a vast array of experiences located along dimensions of public and private, solitary and social, frenzied and reflective, technological and bodily, conceptual and immediate, calculated and improvised, instantaneous and timeless. The fact that music can be heard and experienced by large numbers of people simultaneously and in synchrony (orchestral concerts, stadium gigs, live simulcasts) means that the embodied experience of music can also be shared fostering entrainment and a sense of cosubjectivity. Indeed, some theories of the evolutionary significance of music highlight the importance of music’s empathy promoting aspects, suggesting that a fundamental adaptive characteristic of music is its capacity to promote group cohesion and affiliation (Cross & Morley, 2008).

While a whole range of studies has suggested that empathic interaction with other human beings is facilitated by musical engagement, the direct empirical evidence for this important possibility is scattered and disciplinarily disconnected. The aim of the project summarised in this report was to examine critically a substantial body of research evidence that relates to claims for music’s capacity to engender cultural understanding, primarily through the mediating construct of empathy; examine its consequences and significance, and provide a framework within which to connect its disparate elements and highlight points of interdisciplinary convergence and divergence; and carry out a focused empirical study that was designed to investigate a specific aspect of that complex case.

The report follows the general disciplinary outlines of the initial literature search, which revealed in excess of 300 items relating to the broad theme (‘Music, Empathy and Cultural Understanding’) of the project.

Empathy

The word empathy has had currency in English for little more than 100 years, listed by the Oxford English Dictionary as being first used by the psychologist Edward Titchener in 1909, and defined by the OED as:

“a. Psychol. and Aesthetics. The quality or power of projecting one’s personality into or mentally identifying oneself with an object of contemplation, and so fully understanding or appreciating it.

b. orig. Psychol. The ability to understand and appreciate another person’s feelings, experience, etc.”

Titchener’s ‘empathy’ was his attempt to translate the term Einfühlung, coined by the philosopher Robert Vischer (1873) in a book on visual aesthetics. But it was Theodor Lipps (1903) who really championed the concept of empathy, developing it from an essentially aesthetic category (the ability to ‘feel into’ an artwork) into a much more general psychological/philosophical concept to account for the human capacity to recognize one another as having minds. Laurence (2007) gives an important account of the origin and development of the idea of empathy, tracing a line back to Adam Smith’s (1759) The Theory of Moral Sentiments, and Smith’s appeal to a notion of sympathy and ‘fellow feeling’ as the basis for understanding and living a moral life that is based on imagining how we would feel in the circumstances of others. The distinction between imagining how we would feel and simply identifying with how another feels is crucial, since it places Smith’s notion of sympathy in the domain of imaginative reason rather than blind contagion, and makes clear the role of cultural artefacts (paintings, literature, drama, music) as a means of socially learning that sympathetic attitude.

Laurence also draws significantly on the work of Edith Stein (1917) a doctoral student of Edmund Husserl whose On the Problem of Empathy also engages with the problem of how it is that we can know or experience the mental states of others, whether this knowledge or experience is given in some direct and primordial sense, and Stein’s conclusion that empathy is dependent on the mediating role of similarity with the person (or even animal) with whom/which we attempt to empathize. Laurence ends up with definition of empathy that emphasizes empathy as both a process, and as a social and educable achievement:

“In empathizing, we, while retaining fully the sense of our own distinct consciousness, enter actively and imaginatively into others’ inner states to understand how they experience their world and how they are feeling, reaching out to what we perceive as similar while accepting difference, and experiencing upon reflection our own resulting feelings, appropriate to our own situation as empathic observer, which may be virtually the same feelings or different but sympathetic to theirs, within a context in which we care to respect and acknowledge their human dignity and our shared humanity.” (Laurence 2007: 24)

Finally, and in significant contrast to Laurence, Baron Cohen (2011) provides a wide ranging account of empathy that explicitly presents it as a psychometrically measurable trait, with a genetic and environmental basis, distributed in a particular network of brain regions, and manifested in seven ‘degrees’ ranging from the zero degrees of empathy of the psychopath or autistic person, to the six degrees of empathy of some ‘hyper empathic‘ individuals. Baron Cohen regards empathy as critically valuable human resource, and sees the erosion or loss of empathy as an issue of global importance that has the most serious consequences for social health at scales ranging from the family to international relations.

As this necessarily brief review has revealed, there is a significant range of perspectives on empathy, from which two in particular might be drawn. The first is the distinction between empathy as a skill or social achievement acquired, educable, and in some sense fundamentally collective; and empathy as a trait relatively fixed, individual, and with a genetic component. The second concerns the extent to which different perspectives emphasize the involuntary and inter subjective character of empathy (sometimes expressed through the metaphor of contagion), involving identification with the other and a loss of self; as opposed to a more cognitive and deliberate view in which empathy depends upon an imaginative projection into the circumstances of the other (closer to what Smith called sympathy).

These differences in perspective affect the scope and reach of the term empathy, and are an issue to which we return towards the end of this report in the specific context of music.

Music and Empathy across Different Fields

This section critically reviews the existing literature on music and empathy under a number of different conceptual and disciplinary headings.

1. Neuroscience

An increasing body of neuroscientific evidence indicates the very close coupling of perceptual and motor functions in the central nervous system, strongly suggesting that one way to account for the human capacity to adopt the perspective of another (sometimes referred to as ‘theory of mind’ or even ‘mind reading’) is on the basis of the way in which a person’s experience of their own actions is entangled with their perception of the actions of others. At the level of brain anatomy, it has long been recognized that there are suggestive parallels between the organization of sensory and motor cortices of the human brain and this might provide at least superficial evidence for the close relationship between perception and action.

More recently, however, and particularly in the wake of the discovery of mirror neurons in the early 1990s (e.g. Di Pellegrino, Fadiga, Fogassi, Gallese, and Rizzolatti G., 1992), there has been a surge of interest in the ways in which perception action relationships at the level of the central nervous system might provide a powerful way to explain a variety of intersubjective and empathic phenomena. Freedberg and Gallese (2007: 197) have argued that the activation of a variety of embodied neural mechanisms underlie a range of aesthetic responses, proposing that “a crucial element of esthetic response consists of the activation of embodied mechanisms encompassing the simulation of actions, emotions and corporeal sensation, and that these mechanisms are universal.” Freedberg and Gallese are primarily concerned with the embodied and empathic qualities of visual art, but Overy and co-authors (Molnar Szakacs & Overy 2006; Overy & Molnar Szakacs 2009; McGuiness & Overy 2011) have developed a persuasive model of how the embodied, emotive and empathic effects of music might be understood from a mirror neuron perspective.

(A mirror neuron is a neuron that fires both when an animal acts and when the animal observes the same action performed by another.
Thus, the neuron “mirrors” the behavior of the other, as though the observer were itself acting. Such neurons have been directly observed in primate species. Birds have been shown to have imitative resonance behaviors and neurological evidence suggests the presence of some form of mirroring system.
In humans, brain activity consistent with that of mirror neurons has been found in the premotor cortex, the supplementary motor area (SMA), the primary somatosensory cortex and the inferior parietal cortex.)

In simple terms, mirror neurons (or mirror systems as they are often called) are neurons in a motor area of the brain that become active when an individual merely observes an action of the kind that these neurons are usually responsible for controlling.

These ‘as if body loops’, as Damasio (1999) has called them, provide a direct identification with the actions of another, and constitute the fundamental building blocks of what Gallese (2001; 2003) has termed the ‘shared manifold’. The shared manifold is understood as a three-leveled mechanism for inter-subjective identification: i) a phenomenological level that is responsible for our sense of similarity with others which Gallese equates with an expanded notion of empathy; ii) a functional level characterized by models of self other interaction; and iii) a subpersonal level, instantiated by the activity of mirror matching neural circuits (Mirror Neuron Systems). The aim of the shared manifold hypothesis is to ground a sense of empathy and self other identity without suggesting that human experience and neuroscience can simply be collapsed into one another: hence the distinction between phenomenological, functional and subpersonal levels.

Gallese is also at pains to point out that self other identity is not all that there is to inter subjectivity: mirror systems do not allow us to experience others exactly as we experience ourselves, since to do so would (ironically) preclude the possibility of experiencing others as such at all. Our capacity to experience an external reality with content and behaviours that we can understand is made possible by “the presence of other subjects that are intelligible, while preserving their alterity character.” (Gallese 2003: 177)

At times the mirror neuron idea has been presented as if it were a hardwired feature of the brain that acted rather like a magic bullet. But as Heyes (2010) has argued, while one way to see mirror neurons is as an evolutionary adaptation (and therefore present at the species level), an alternative is to see the development of mirror systems as acquired through the operation of associative processes through the lifetime of individuals. From this perspective, mirror processes originate in sensorimotor experience, much of which is obtained through interaction with others. Thus, the mirror neuron system is a product of social interaction, as well as a process that enables and sustains social interaction. One rather specific example of this kind of plasticity is the finding by Bangert et al. (2006) that trained pianists listening to the sound of piano music showed significantly more neural activity in the motor areas of their brains than did a matched group of non-musicians.

2. Perception-action coupling, Empathy and Embodiment

Mirror systems are one way to understand inter-subjective interaction and identity, with direct relevance to music, at a neural level.

At the behavioural level there is another extensive literature that has revealed the significance of mimicry and synchronization in mediating human relationships in general, and music in particular. In a review of the extensive literature Chartrand and Dalton (2008; see also Chartrand & Bargh 1999) make the case for the importance of mimicry in social life, ranging from postural and facial to vocal and syntactic mimicry (people unconsciously mimicking one another’s accents and sentence structures) as both manifestations of existing social bonds and affiliations as well as the means by which such social bonds may be established (e.g. Inzlicht, Gutsell & Legault, 2012). As Heyes (2011) has argued such imitative behaviours may be automatic and insuppressible, and constitute a fundamental embodied basis for a critically important domain of human social interaction.

At a similarly general level, a number of authors (e.g. Valdesolo and DeSteno 2011) have demonstrated the power of synchronization in inducing altruistic and compassionate behaviours, this synchronization in many cases serving to entrain people’s behaviours upon one another.

With this general psychological literature in mind, it is easy to see that music powerfully affords these kinds of cooperative and affiliative engagements. Music has long been associated with socially coordinated work, worship and celebration, where its rhythmically entraining attributes and opportunities for controlled mimicry and complementation (such as in the ‘call and response’ character of many vernacular musical cultures) play a central role (e.g. Clayton, Sager and Will 2005).

Hove and Risen (2009) demonstrated with a tapping task that the degree of synchrony between individuals tapping together predicted how affiliated those individuals rated one another, and in a more directly musical context both Kirschner and Tomasello (2009) and Rabinowitch, Cross & Burnard (2012) have shown that over both shorter and longer timescales children involved in rhythmically synchronized music activities subsequently behaved more cooperatively and empathically than did children who were involved in an equivalent but not synchronized activity. Music is a powerfully multi-sensory, and particularly kinaesthetic (see Stuart 2012) phenomenon whose embodied character draws people into fluid and powerful social groups at a range of scales and degrees of (im)permanence, and in doing so helps to enact a kind of empathy.

3. Dispositional empathy and music

As discussed above, some authors (e.g. Baron-Cohen 2011) have understood empathy as a trait, arguing that since some people have a tendency to experience empathy more readily than others, being more or less empathic can be understood as a personality trait or a disposition.

In its broadest sense, dispositional empathy can be defined as an individual’s general responsiveness to the observed experiences of others, involving both perspective-taking capabilities or tendencies, and emotional reactivity (e.g., Davis, 1980).

Davis (1980) has suggested that dispositional empathy is a multidimensional construct comprising at least four components:

Perspective-taking (PT) can be understood as the ability as well as the tendency to shift perspectives (i.e., to see and understand things from another’s point of view)

Fantasy can be described as the tendency to identify oneself with fictional characters in books and films, for example. By contrast,

Empathic Concern (EC) taps into the tendency to experience feelings of compassion and concern for observed individuals, whereas

Personal Distress is associated with the individual’s own feelings of fear, apprehension and discomfort in response to the negative experiences of others.

Empathic Concern (EC) and Personal Distress are associated with the more emotional side of empathy.

Theories of music-induced emotions suggest that some form of empathy may be involved in the emotional responses induced by music (e.g., Scherer & Zentner, 2001; Juslin & vastfjall, 2008; Livingstone & Thompson, 2009). The proposed mechanisms range from pre-conscious ‘motor resonance’ with musical features that resemble vocal and motor expression of emotion (Molnar-Szakacs & Overy, 2006; Livingstone & Thompson, 2009) and emotional contagion (Juslin & Vastfjal, 2008) to empathizing with emotions and notions that are construed in the listener’s imagination (e.g., Scherer & Zentner, 2001). Indeed, empirical investigations have shown that people who have a tendency to be more empathic experience more intense emotions in response to music (Vuoskoski & Eerola, 2012; Ladinig & Schellenberg, 2011), providing indirect evidence for the role of empathy in music-induced emotions.

As people with high dispositional empathy are more susceptible to emotional contagion in general (Doherty, 1997), it may be that highly empathic people also experience emotional contagion from music more readily (Vuoskoski & Eerola, 2012). A complementary explanation is that empathic people may be more likely to engage in some form of reflective empathy during music listening, involving visual or narrative imagery, for example (e.g., Vuoskoski & Eerola, 2012; 2013).

Dispositional empathy has been associated with music-induced sadness in particular, as highly empathic people have been found to experience more intense sadness after listening to sad instrumental music (Vuoskoski & Eerola, 2012).

Interestingly, empathic individuals also tend to enjoy sad music more than non-empathic individuals, suggesting that empathically experienced negative emotions such as sadness can be enjoyable in the context of music (Vuoskoski et al., 2012; Garrido & Schubert, 2011).

Similar findings have been made in the context of films, where the experience of empathic distress while watching a tragic film has been associated with greater enjoyment of the film (De Wied et al., 1994).

It is not yet known what the mechanisms behind such enjoyment are, although the portrayal of more positive themes such as friendship, love, and human perseverance often present in tragic films have been proposed as one potential source (De Wied et al., 1994). However, it is not clear whether this explanation could also apply in the context of music. Nevertheless, these findings do suggest that there is something inherently enjoyable in empathic engagement in an aesthetic context even when the experienced emotions could be nominally characterized as negative.

4. Music as a virtual person, music and subjectivity

People tend to describe music in terms of attributes commonly used to describe psychological attributes of people (Watt & Ash, 1998). Indeed, it has been suggested that music is capable of creating a ‘virtual person’ of sorts (Watt & Ash, 1998; Livingstone & Thompson, 2009). The musical expression of emotion bears a close resemblance to human vocal and motor expression of emotion, involving similar auditory and gestural cues (for a review, see Juslin & Laukka, 2003), and it has been proposed that listeners may respond to music as they would to the perceived emotional state of a conspecific (e.g., Livingstone & Thompson, 2009). However, music’s capacity to represent a virtual person seems to go beyond acoustic and gestural cues that resemble vocal and motor expression of emotion.

An example is provided by studies that have investigated people’s reasons for listening to sad music when they already feel sad. These studies have found that some listeners can experience the music itself as providing empathy and understanding for the feelings that they are going through, functioning as a surrogate for an empathic friend (Lee, Andrade & Palmer, 2013; Van den Tol & Edwards, 2013).

The participants in Van den Tol and Edwards’s study felt that:

“The music was empathizing with their circumstances and feelings, supporting them, making them feel understood, or making them feel less alone in the way they were feeling” (Van den Tol & Edwards, 2013, p. 14).

Thus, it appears at least for some people that music is able to represent a virtual person with whom to empathize, and whom they can experience as empathizing with their felt emotions.

There has been considerable interest in the musicological literature in the relationship between music and human subjectivity (e.g. Cumming, 2000; McCIary, 2004), pursuing the idea that music has attributes either of an idealized person, or of an idealized collection or community of people. Lawrence Kramer (e.g. 2001; 2003) has written extensively about music as the instantiation of a kind of imagined subjectivity not associated specifically with the composer, performers, or anyone else explicitly and literally engaged with the making of the music, nor simply as the mirror of a listener’s own subjectivity, but in a more abstracted and generic manner. Likewise, the philosopher and violinist Naomi Cumming, in a paper that focuses on the violin introduction to the aria ‘Erbarme Dich’ from J. S. Bach’s St. Matthew Passion, writes of how the listener does not just find her or his own subjectivity passively reflected back, but reconfigured:

“The pathos of Bach’s introduction, and its elevated style, are quite unmistakable, and recognition promotes empathy. Once involved with the unfolding of the phrase’s subjectivity, the listener does not, however, find a simple reflection of his or her own expectancies. The music forms the listener’s experience, and in its unique negotiation of the tension between striving and grief, it creates a knowledge of something that has been formerly unknown, something that asks to be integrated in the mind of the hearer.” (Cumming, 1997: 17)

And in a still more explicitly psychological manner, DeNora (2000; 2003; 2013) has written of the ways in which music acts as a technology that affords a listener the opportunity to structure and organize their identity in long-term ways, and as a way of managing their immediate emotional states and sense of identity. Writing of one of her informants, ‘Lucy’, DeNora points out how she (Lucy) uses music as a medium in which she can draw a connection between the musical material, her own identity, and a kind of social ideal. As Lucy herself expresses it, she ‘finds herself’, the ‘me in life’ within musical materials, in a manner that allows her to reflect on who she is and how she would like to be, a process that DeNora points out is not just private and individual:

“Viewed from the perspective of how music is used to regulate and constitute the self, ‘solitary and individualistic’ practices may be re-viewed as part of a fundamentally social process of self-structuration, the constitution and maintenance of self. In this sense then, the ostensibly private sphere of music use is part and parcel of the cultural constitution of subjectivity, part of how individuals are involved in constituting themselves as social agents.” (DeNora, 2000: 47-8)

Music and musicking, then, can be viewed as a rich environment in which more or less active participants (listeners and makers) can engage with the real and virtual subjectivities of other real and virtual participants, and in doing so come to experience (and perhaps increasingly understand) the cultural perspective that those others (real or virtual) inhabit. Music is in this way both a medium for empathic (and antagonistic) engagement with others, and an environment in which to explore and experiment with a range of more or less projected, fantasized and genuinely discovered subject positions.

5. Sociological Perspectives

Turning from the rather individualistic accounts that have dominated the previous sections, towards understandings of music and empathy that take an explicitly social stance, sociological perspectives that enhance understanding of empathic processes derive from what may be termed the ‘new sociology of art’ (de la Fuente 2007). This sub-disciplinary paradigm investigates aesthetic materials for the ways that they may be seen to frame, shape or otherwise have an impact in social life. It is linked in turn to perspectives within sociology that cluster around the so-called, ‘strong’ program of cultural sociology (Alexander 2008) in which cultural materials are understood as active mediators of psycho-social and subjective processes and in which arts are not understood to be ‘about’ society or shaped ‘by’ society but rather ‘in’ society and constitutive of social relations (Hennion 2007).

These ‘new’ sociologies of art and culture are in turn linked to a ‘meso’ perspective in sociology devoted to groups of actors understood as networks of people, practices (conventions, operations, activities with histories of use) and things (Fine 2010). They focus on interaction orders (Fine 2012), or local actions that produce forms of ordering. The interaction order is the place where meanings are created, validated and reproduced in ways that travel to other networks.

Within this meso perspective there is no macro-micro divide since both macro and micro are mutually produced within scenes and settings of activity. The focus on this concerted activity in turn offers considerable scope for examining the question of just how cultural forms, including musical forms, actually enter into action and experience (DeNora 2003).

The impetus for these perspectives comes from various distinct but complementary developments in sociology since the middle 1980s that describe the ways that aesthetic and symbolic materials ‘anchor’ action (Swidler 2002) by presenting actors with orientational materials that can inform, focus and specify styles and trajectories of action in real time. The concern with how aesthetic materials ‘get into’ action (Acord and DeNora 2012) is one that has been associated with other developments in sociology, most notably the turn from a focus on the cognitive components of action, and models of social actors as calculating beings, to a focus on embodiment and feeling (Witkin 1994). These developments resonate well with, and are further illuminated by, developments in the philosophy of consciousness that begin with notions of the ‘extended mind’ (Clark and Chalmers 1998) and draw out that concept to embrace ‘the feeling body’ (Colombetti 2013) in which embodied conditions and sensations are understood both to take shape in relation to things outside of individuals and to inform cognitive appraisal.

Insofar as feeling and embodiment can be understood to take shape through encounters with aesthetic materials and can be understood to cultivate sensibilities or predispositions in favour of some social scenarios (and thus, contrarily, away from others), aesthetic materials have been highlighted within sociology as sources of social order. In this respect, the ‘new’ sociology of art harks back to Adam Smith’s ideas of sympathy and the capacity for fellow feeling discussed above, in which Smith suggests that the capacity for fellow feeling and being able to imagine the other is a lynchpin of mutual orientation and, thus, social stability. While Smith makes it clear that sympathy (the capacity to imagine the other) is not empathy (the capacity to feel what the other is feeling, literally to share their experience), Smith’s focus on the prerequisites for achieving sympathy highlight the importance of bodily processes. Specifically, Smith describes how, if sympathy is to be achieved, it is necessary for actors to moderate their passions (tamp down, raise up levels of intensity or ‘pitch’ as Smith calls it) so as to encourage mutual engagement through shared modalities of feeling (Smith 1759: I. I. 36-39). In this respect, Smith’s interest in mutual emotional calibration, understood as a prerequisite of mutual understanding, resonates with Alfred Schutz’s concept of attunement, understood as the prerequisite for ‘making music together’ (his example is the performance of a string quartet used as a case in point of social action writ large and the need for mutual orientation, entrainment, calibration and the gestalt to which they give rise, namely, shared feeling forms.

Classical sociology can, in short, be read as offering important leads for the study of empathy, understood as emotional and embodied mutual orientation, predisposition and preference, and in this sense it can also be read as offering an excellent basis for appreciating ‘art in action’ and the role of the arts in underwriting communicative action or how we bind ourselves together in time, whether in conversation, with its prosodic and timing patterns (Scollon 1982), or more generally, as Trevarthen puts it, as the dynamic sympathetic state of a human person that allows co-ordinated companionship to arise’ (cited in Ansdell et al 2010). As such the arts, and in the case of this project, music, can be conceptualised as offering materials for shaping up the feeling body from infancy to old age, in a wide range of roles and guises.

But if the arts and music more specifically ‘get into’ action, the question, as stated earlier, remains: how does this happen and can we trace that process? And in relation to empathy, this question can be posed in terms of how shared feeling states, sensibilities and predispositions come about, and how they can be cultivated and thus also how they may be more problematically controlled (Hesmondhalgh 2013; Born 2012; DeNora 2003). Within sociology the most fruitful paradigms have focused upon learning, mostly informal situated learning, among which the classic work on this topic is Howard S. Becker’s ‘Becoming a Marijuana User’ (1953).

Becker’s piece has been used by subsequent scholars to develop new (grounded) theories of how culture gets into action from comparisons of how one learns to respond to musical ‘highs’ (Gomart and Hennion 1999) to how one learns to feel and respond sexually (Jackson and Scott 2007; DeNora 1997) and how one learns to respond in various workplaces and forms of occupation (Pieslack 2009; DeNora 2013) and how one manages and modifies emotions and energy levels as part of everyday self-care (DeNora 2000; Batt-Rawden, DeNora and Ruud 2005; Skanland 2010) or in scene-specific settings such as retail outlets (DeNora 2000). Specifically these studies have followed the ways that individuals and groups engage in processes of modelling, adjustment, tutoring and directing and attempted alignment with musical materials in ways that draw out emotional and embodied sensation and experience in musically guided ways. This work helps to highlight just how deeply culture can come to penetrate embodied processes and experiences, and thus dovetails with more recent work on the culturally mediated experience of health and wellbeing.

6. Music Therapeutic and Wellbeing Perspectives

The focus on music, health and wellbeing is a growing area (Koen et al 2008; MacDonald et al 2012; MacDonald 2013). It encompasses music therapeutic perspectives, community music, psychotherapeutic perspectives and more overtly medical applications as well as the history of medicine and healing. At the level of the individual, and in overtly medical contexts, research in these areas has documented music’s potential for the management of pain (Edwards 2005; Hanser 2009), anxiety (Drahota et al 2012), palliative care (Aasgaard 2002; Archie et al 2013; DeNora 2012), and immunology (Fancourt et al 2013; Chandra and Levitin 2013) all of which emphasise mind-bodyculture interaction. At the broader level at which music connects with and can be seen to contribute to wellbeing, music has been described ecologically as part of salutogenic (health-promoting) space (DeNora 2013).

In all of this work, there are excellent resources for the study of empathy, in particular for investigating empathy understood as sensibility, perception and orientation as musically mediated. Specifically, the focus on the malleability of consciousness and selfperception (Clarke and Clarke 2011) points to a human capacity for entering into different modes of awareness, ones that are simultaneously sensitising (aesthetic) and desensitising (anaesthetic), and in so doing indicates the importance and power of the cultural technologies through which altered states can be achieved. The case of music and pain management illustrates many aspects of this theme.

As Hanser has described it, recent theoretical understandings of pain have moved toward a multi-dimensional conception of pain perception, one in which pain is not unmediated but rather comes to be experienced in relation to cultural and situated interventions, including music. In part, musical stimuli simply compete with neural pain messages. But more interestingly, music stimulates both oxytocin and embodied sympathetic responses (Grape 2002; Hurlemann et al 2010). Recent interdisciplinary perspectives highlight how the music, in tandem with other biographical and contextual factors, may lead a person in pain into alternative situations, ones in which she/he becomes sensitised to musically inspired associations and desensitised to the former situation of being in pain. Thus, music cannot necessarily address the cause of the pain but it can redirect the sensation of pain by capturing consciousness in ways that recalibrate it (DeNora 2013). So too, in the Bonny Method of Guided Imagery and Music (Bonde 2012) music may provide a grid or template against which knowledge-production (memory, self-and mutual understanding, historical accounts) can be elaborated and scaffolded in ways that can be used to diminish ‘negative’ emotions and associations, effectively recalibrating perception and, in this case, the self-perception of pain.

Methodologically, the music therapy index (Nordoff & Robbins 2007), a highly detailed real-time log of musical and para-musical action, can be used to display key or pivotal moments of musically instigated or musically guided action (movement, shifts in comportment, utterances). So too, the ‘musical event’ scheme can be used to track with some precision the ways in which the musical permeates the paramusical and vice versa across time and in keeping with the meso focus described earlier networks (DeNora 2003; Stige and Aara 2012).

More generally, and in ways that draw music therapy and music and conflict resolution into dialogue, musical engagement may be used to transform psycho-social situations, again leading the actor or actors away from the perception of distressing features of body/environment and toward more positive features and scenarios, and in ways that may also contribute to hope, patience and general mental wellbeing (Ansdell et al 2010; Ansdell 2014) as well as broader forms of cross-cultural and interactional accord, linked to music and guided imagery (Jordanger 2007). Community Music Therapy has perhaps most notably described music’s role in the production of communitas, through joint improvisation and as a means of generating proto-social capital (Procter 2012).

Within the growing field of music and conflict transformation studies (Laurence 2007), a key theme has focused on the importance of shared practice and actual grass-roots (bottomup) musicking as a prerequisite for enduring forms of change (Bergh 2011; 2010; Robertson 2010). In particular, as Bergh has described, if music is to contribute to enduringly altered practice, or altered consciousness of the other, that endurance requires continued and repeated practice, continued and repeated participation in musical activity. And as we have already indicated, music is by no means an unmitigated ‘good’ within the conflict transformation literature: as Bergh has observed (Bergh 2011), music can be and has been used to inculcate feelings of animosity, or for purposes of oppression and torture (Cusick 2008); and historically has been incorporated into military culture through drill, march music and, more recently, through psych-op motivational techniques (Gittoes 2004; Pieslack 2009). Indeed Laurence (2007: 33), even while writing of the potential for music in conflict resolution, argues that inculcating peaceful values is one of music’s rarest uses, and that “of music’s purposes, many and probably most, serve the ongoing ends of power relationships one way or another.”

7. Cross-cultural perspectives

The final category of literature that we consider in this report touches on the potentially vast question of cultural and cross-cultural understanding. Within the psychology of music there has been an interest in the relationship between possibly ‘universal’ and culturally specific aspects of musical communication dating back to the very beginnings of both the psychology of music and ethnomusicology in the work of Carl Stumpf (Stumpf & Trippett 1911/2012).

Among other more recent empirical studies, Balkwiil, Thompson, & Matsunaga (2004) have shown that music can successfully communicate emotional meanings across different cultures, but ethnomusicologists, perhaps rightly suspicious of simplistic notions of inter-cultural communication, have pointed to issues of representation, and of the incommensurability of concepts (or in this case emotional meanings) across cultural contexts as factors that might undermine the validity of a naively empirical approach (Stock 2014). A number of authors have recently proposed the value of a ‘relational musicology’ that might tackle issues of inter-cultural understanding, including Cook (2012: 196) who argues for relational musicology as “a means of addressing key personal, social and cultural work that is accomplished by music in today’s world.”

One specific kind of ‘cultural work’ that has recently been addressed in ethnomusicology that is of direct relevance to this project is the affective and social work that is accomplished by/within modern ‘sentimental’ cultures. Martin Stokes (2007; 2010) has provided vivid accounts of the emotional, intimate and affiliative character of contemporary sentimental musical cultures in Egypt and Turkey, and Butterworth (2014) in relation to Peruvian huayno music, in which something very much like empathy (though Stokes relates it more directly to a ‘Smithian’ as in Adam Smith notion of sympathy) is understood as a cultural construct or condition. In Stokes’s words (2010: 193), one might view “sentimentalism as a kind of civic project, a way of imagining affable relations of dependence on strangers in modern society.” This is a very different perspective on empathy one that sees it as a social achievement, rather than personality trait; a collective skill, rather than the expression of a circuit of ten interconnected brain regions (cf. Baron-Cohen 2011). As Cook (2012) argues in relation to the relational understanding of musical methods from one domain applied to another (Schenkerian analysis and Chinese music; Nineteenth century Western transcriptions of Indian melodies that were presented as ‘authentic Hindostannie airs’), such encounters conceived within an appropriate relational conceptual framework offer a domain of shared experience and cross-cuitural understanding.

Figure 1. Mean IAT scores (D-values) ±standard error of the mean, grouped by condition. Positive D-values indicate an unconscious preference for West African (relative to Indian) people, and negative values indicate an unconscious preference for Indian (relative to West African) people.

To investigate the effect of listening to Indian vs. West African music on participants’ Dvalues as well as the hypothesized moderating effect of dispositional empathy on the effects of music we conducted an ANCOVA with the Type of Music (Indian or West African) as a factor, and Dispositional Empathy (global IRI scores) as a covariate. We also included an interaction term of Type of Music and Dispositional Empathy in the model. There was no significant main effect of Type of Music; F(1,54) = 2.59, p = .11, although the trend was in the anticipated direction with participants exposed to Indian music displaying a slight preference for Indian (relative to West African) people, and participants exposed to West African music displaying no apparent preference.

The mean D-values of the two groups are displayed in Figure 1. As might have been expected, Dispositional Empathy was not significantly related to IAT scores when examined across the two conditions; F(1,54) = 0.20, p = .89. However, there was a significant interaction between Type of Music and Dispositional Empathy; F(1,54) = 5.51, p = .023, n(2/p) = .09, suggesting that dispositional empathy indeed moderated participants’ susceptibility to the musical manipulations. The relationship between dispositional empathy and D-values in the two groups is displayed in Figure 2. We also investigated the potential contributions of musical training, sex, and subjective responses to the music (ratings of liking and felt emotional impact) to the D-values, but no statistically significant relationships were found.

Figure 2. The relationship between dispositional empathy and IAT scores (D value), grouped by condition. Positive D values indicate an unconscious preference for West African (relative to Indian) people, and negative values indicate an unconscious preference for Indian (relative to West African) people.

2 Conclusions

The empirical study has provided preliminary evidence for the hypothesis that listening to music without any explicit semantic content (such as comprehensible lyrics) can evoke empathy and affiliation in listeners with high dispositional empathy. This interpretation is supported by the significant interaction between Type of Music and Dispositional Empathy, which revealed that people with high dispositional empathy scores were more likely to display an unconscious preference for the ethnic group to whose music they were exposed than those with low dispositional empathy scores. The fact that high dispositional empathy made participants more susceptible to the musical manipulations suggests that the observed findings cannot be explained in terms of priming or knowledge activation effects, such as those observed in the case of background music and purchasing decisions (e.g. North, Hargreaves & McKendrick, 1999). The lack of a statistically significant relationship between the IAT scores and liking ratings also indicates that our findings cannot be accounted for by a simple preference effect (cf., Nantais & Schellenberg, 1999).

Instead, we propose that the more empathic participants may have been more open to the music, and more likely to entrain with the music involving internal mimicry and emotional contagion; and may also have been more likely to engage in reflective empathy, in the form of visual and/or narrative imagery, and/or semantic elaboration. In the context of music, entrainment comprises both temporal as well as affective components (see e.g., Phillips-Silver & Keller, 2012), and in general imitation and entrainment have been found to both reflect and elicit affiliation (Chartrand & Bargh 1999; Hove & Risen 2009). Since people with high dispositional empathy have been found to exhibit stronger motor and sensory resonance to observed actions, and the pain of others (Gazzola, Aziz-Zadeh 8i Keysers, 2006; Avenanti et al., 2008), it is possible that empathic people are also more likely to resonate with the acoustic and gestural features of music. This stronger resonance could explain why empathic individuals are more susceptible to emotional contagion from music (cf. Vuoskoski & Eerola, 2012), and why they also appear to be more sensitive to the affiliation-inducing effects of music listening.

However, further investigation is required in order to better understand the phenomenon, and to distinguish between the potential contributions of pre-reflective motor and affective resonance, and the more reflective empathy involving imagery, perspective-taking, and other extra-musical associations. As dispositional empathy comprises both emotional reactivity and cognitive perspective-taking attributes, either or both of these components may contribute to the observed affiliation-inducing effects of music listening. A possible way to investigate this would be to implement a nondemanding distractor task during the music listening, which would limit participants’ capacity to conjure up imagery and other extra-musical associations. Furthermore, the failure to find a statistically significant main effect of Type of Music on participants’ implicit associations could either be due to the fact that the variation in participants’ pre-existing preferences for Indian vs. West African people was too great in relation to our sample size, or that the participants with low dispositional empathy were simply not affected by the music.

Future studies could attempt to investigate this issue by implementing pre as well as post-manipulation measures of implicit associations, although there may be other, more problematic issues associated with exposing participants to Indian and West African images prior to the musical manipulations.

5. General Discussion, Implications, Prospects

The result of our empirical study provides some evidence for the capacity of music even when encountered in arguably the most passive circumstances (solitary headphone listening in a ‘Iaboratory’ setting) to positively influence people’s unconscious attitudes towards cultural others. Specifically, people with higher dispositional empathy scores show more differentiated positive associations with images of people from two different cultural groups after listening to music explicitly belonging to that cultural group than do people with lower dispositional empathy scores.

This is a striking result, and provides what might be characterized as narrow but ‘hard-nosed’ evidence for music’s positive inter-cultural potential, and we have speculated on the broad psychological mechanisms (including entrainment, mimicry, emotional contagion, and semantic elaboration) that may be responsible.

But a number of notes of caution also need to be sounded. We have no evidence for the robustness or duration of the effects that we have observed: it may be that this is a very temporary shift that is easily disrupted, casting doubt on the practical efficacy of music as an agent of change in cultural understanding. And in the light of the interaction with dispositional empathy, the result suggests that any practical efficacy might be confined to those individuals who are already predisposed to be empathic towards others arguably those people who are (to put it simplistically) the least urgent cases.

Are we then forced to conclude that music has little or no power to change attitudes among those people who are most resistant? Perhaps more seriously, music as we have already indicated is arguably as capable of distinguishing (Bourdieu 1984/1979), dividing and alienating people as it is of bringing them together. Hesmondhalgh (2013: 85) points out that “Music can reinforce defensive and even aggressive forms of identity that narrow down opportunities for flourishing in the lives of those individuals who adhere to such forms of identification”, and provides a vivid anecdotal example of just such a defensive/aggressive encounter with or through music. He describes a Friday night out with friends at a pub where an Elvis impersonator is performing. Having at first dreaded the performance, Hesmondhalgh and his friends, along with a large number of strangers who are also in the pub for a night out, are quickly won over and join with one another, and the performer, with increasing intensity. The chorus of the final song “elicits an ecstasy of collective singing, women and men, all at the top of our voices. There are smiles and laughter, but there’s melancholy too. It seems that bittersweet lines from the Elvis repertory are invoking thoughts about relationships, past and present… [We] stagger out of the pub feeling we’ve had a great night, and that the working week has been obliterated by laughter and bittersweet emotion. Unwittingly, I brush against a man’s drink as I’m leaving, and he follows me out demanding an apology for his spilt beer… The power of Elvis’s music, it seems, has brought strangers and acquaintances together, and with a formidable intensity. But my pursuer has reminded me unpleasantly that there are those who feel excluded from such collective pleasures. If music-based gatherings answer to our need for sociality and attachment, and combat loneliness, might they also evoke envy when others miss out?” (Hesmondhalgh 2013: 103-4)

Are we to regard music’s affiliative and divisive attributes as two sides of the same coin, or as a more fundamental incompatibility between emancipatory and oppressive qualities? Indeed, rather than considering how music might help to make a bridge between apparently pre-existent cultural ghettos, should we not be asking in what ways music is already implicated in the establishment and maintenance of those very ghettos in the first place? These are significant challenges to the potentially starry-eyed representation of music that an uncritical attitude might project; but as Hesmondhalgh, again, puts it: “Music’s ability to enrich people’s lives [and expand their empathic understanding] is fragile, but I believe it can be defended better if we understand that fragility, and do not pretend it floats free of the profound problems we face in our inner lives, and in our attempts to live together.” (Hesmondhalgh 2013: 171)

Part of understanding that ‘fragility’ is considering what, if anything, is special about music as a force for (compromised) cultural benefit. Why not football, or food, both of which can lay claim to mass engagement and global reach? Is there anything about music that affords either particular, or particularly powerful or efficacious kinds of intercultural engagement? One way to tackle these questions is consider what the mechanisms for empathy and cultural understanding might be, and in what ways those mechanisms are engaged by different cultural manifestations whether those are music, food or football. As our critical review of the literature reveals, this is a fascinating but considerable challenge, and one that turns in part on how broad or narrow a conception of empathy is entertained.

One approach might be to admit a considerable range of inter-subjective engagements as occupying different positions on an empathy spectrum, from conditions of seIf-other identity in the context of what might be called ‘deep intersubjectivity’ (perhaps emblematically represented by that pre-Oedipal oneness between mother and infant); through powerful experiences of compassionate fellow-feeling; to the operation of much more controlled and deliberate rational, imaginative projection into the circumstances of others. Some (such as Adam Smith, Felicity Laurence and Colwyn Trevarthen) would want to make firm distinctions between, say, empathy and sympathy. But an alternative might be to agree on an umbrella term (and empathy might do), and then focus on what distinguishes different positions under the umbrella, and what the implications (practical, functional, conceptual) of those differences might be.

A common thread that runs through most of these positions is the central role of embodiment in empathy. From the most neuroscientifically reductionist approach (e.g. a ‘fundamentalist’ mirror neuron perspective) to the position of Smith or Stokes, a capacity to feel the situation of another underpins the inter-subjective character of empathy/feIlow-feeling/sympathy. And arguably it is in this respect that music has ‘special properties’ properties of enactment, of synchronization and entrainment in situations ranging from a single individual alone with their music (the solitary headphone listener ‘Lost in music’ (Clarke 2014) to massively social contexts (pop festivals, simulcasts) where enormous numbers of peopie can participate in collective, synchronized, embodied engagement.

As others have pointed out (e.g. Cross 2012), music is a uniquely widespread, emotionally and physically engaging, social, participatory and fluidly communicative cultural achievement, a powerful (cultural) ecological niche that affords extraordinary possibilities for participants, and which both complements and in certain respects surpasses those other global cultural achievements in which human beings participate (language, religion, visual culture, craft). There is little, perhaps, to be gained by attempting to set any one of these up on a uniquely high pedestal but equally it is important not to flatten the terrain by failing to recognize music’s particular combination of affordances in this rich cultural mix: cognitive and emotional complexity, from solitary to mass-social engagement, compelling embodiment, floating intentionality (Cross 2012), synchronization/entrainment, flexible mimicry, temporal and ambient character, and digitaI-analog mix.

As our critical review of the literature has revealed, the empathy-affording character of this mix of affordances has been explored and theorized across an astonishing range of disciplines invoking mechanisms that range from mirror neurons to semiotics and the cultural history of sentimentalism. Are these kinds of explanation in any way compatible with one another, and is there a way to avoid a simplistic and potentially reductionist ‘layers of an onion’ approach in which supposedly ‘fundamental’ biological attributes (whether those are genetic in the case of a narrowly ‘trait’ perspective on empathy; or neurological in the case of sensorimotor contingency theory) underpin progressively more ramified and arbitrary cultural constructs? We have already seen (e.g. Heyes 2010) that from within the scientific literature itself, as well as from outside it, there is ample evidence for the plasticity of so-called fundamental properties, and for the reciprocal relationship between biology and culture. Mirror neurons may be as much a consequence of a culture of inter-subjective engagement as they are a foundation for it. But it clearly remains a considerable challenge to develop in detail the more flexible and relational approach that we point towards in this report.

Finally, there is the question of the utility of the concept or term ‘empathy’ itself. Perhaps rather like the word ‘meaning’, it both enables and suffers from the capacity to bring together a wide range of phenomena, which critics may find unhelpful in its heterogeneity. We share the concern not to confuse chalk with cheese, but against a drive to compart-mentalize (sic) we are persuaded of the long-term value of sticking with a word and its associated conceptual field which, although still just a century old, offers a rich and powerful way to try to understand a central element of human sociality. The debates about whether to understand empathy as a genetic predisposition, a personality trait, an emergent attribute of perception-action coupling, a skill, or a social achievement are symptomatic of the conceptual reach of the term.

Engelen and Rottger-Rossler (2012), in a brief overview of a speciai issue of the journal Emotion Review devoted to empathy, declare in their first sentence that “there is no accepted standard definition of empathy, either among the sciences and humanities or in the specific disciplines”, but nonetheless emphatically endorse the importance of continuing to develop better understandings of that fundamentally social capacity to “feel one’s way into others, to take part in the other’s affective situation, and adopt the other’s perspective“ to grasp the other’s intentions and thus to engage in meaningful social interaction.”

We, too, are committed to the value of that enterprise, and to the specific role that music may play in understanding empathy, and as itself a ‘medium’ for empathy. In addressing the complex network of relationships between neighbouring terms (sympathy, compassion, contagion, entrainment, ‘theory of mind‘, attunement…) we see the prospect of a more nuanced and differentiated understanding of what Baron Cohen (2011: 107) has characterized as “the most valuable resource in our world” and “an important global issue related to the health of our communities.”

Current Disciplinary and Interdisciplinary Debates on Empathy

Eva-Maria Engelen, Birgitt Röttger-Rössler, University of Konstanz, Department of Philosophy & Freie Universitat Berlin, Social and Cultural Anthropology

Almost anybody writing in the field would declare that there is no accepted standard definition of empathy, either among the sciences and humanities or in the specific disciplines. However, even when accepting that there can be no all time and universally valid definition, one can still try to clarify some aspects and establish a few landmarks that will help to ensure that the phenomenon with which various researchers are dealing is the same or has at least important features in common.

Although there is no established concept, several topics and discussions have proved to be crucial for the phenomenon that was once given this specially made up label empathy by Edward Titchner who introduced this word into English at the beginning of the 20th century in order to translate the German term Einfühlung.

The idea behind this special issue on empathy is to present a range of the currently most lively topics and discussions to be found not only within several disciplines but also across several disciplinary boundaries. This makes it interdisciplinary. Authors from different disciplines were asked to contribute to the field in a style that would be accessible for a broader range of interested readers. These contributions come from the following disciplines in which empathy is either an ongoing or an upcoming topic of academic interest: neuropsychology, developmental psychology, philosophy, literary studies, and anthropology. The commentators giving their views on the articles are sometimes experts on empathy from the same discipline as the authors and sometimes from adjoining ones. We tried as far as possible to introduce crossovers, but these did not always fit.

Points of Discussion and Open Questions

Roughly speaking, there are two pathways when it comes to understanding each other: thinking or mind reading and feeling or empathy. Nonetheless, one of the ongoing debates in psychology and philosophy concerns the question whether these two abilities, namely, understanding what the other is thinking and “understanding“ what the other is feeling, are separate or not.

Other debates refer to the best theoretical model for empathy and ask whether it makes sense to assume just one kind of empathy or whether one should differentiate between at least two kinds: cognitive and affective.

Further questions are: Does a living being have to be able to make a self-other distinction in order to be empathic? How far do emotional contagion or sympathy and pity differ from empathy? Is empathy necessarily an affective ability and does it have to be conscious? Does it occur in face to face relationships between two persons or more? And can it also occur between a reader and a fictive character in a novel (Coplan 2004)?

These are just some of the questions currently being discussed. But before addressing them in detail in the following six articles and twelve commentaries, we shall survey the different definitions of empathy presented and defended in this special issue.

A Starting Point for the Discussions

We start off with the concept of empathy in the social cognitive neurosciences. The major growth of interest in empathy is largely due to a recent debate in this field. Previously, in the late nineteenth and first half to middle of the twentieth century, it was an important term in psychology, hermeneutics, and phenomenology. Later on, interest in the concept spread to developmental psychology as well. But the currently ongoing debate received its initial impetus from the question how far mind reading and empathizing are different faculties and how far they may not be completely separable (Singer 2006).

Basically speaking, both faculties are about understanding the other, either cognitively or emotionally. What are the intentions of the other? What are his or her wishes, beliefs, or deductions? These questions belong to the mind reading side, whereas understanding the other‘s emotional state belongs to the other side: the capacity of empathy.

Nonetheless, despite these clear cut definitions, there are also concepts such as the affective theory of mind that is also called cognitive empathy. The rationale for this distinction is that empathy is based on understanding the affective states of others.

Another question that one might consider before reading the assembled articles on empathy is whether empathy has to be a process leading to a conscious state. We advise the reader to bring to mind the definition of empathy in his or her own research perspective before reading the articles presented here. Whether one agrees or disagrees with many of the arguments exchanged and discussed in the following articles and commentaries will depend on which definition of empathy one already has in mind. Hence, a reflection on one’s own implicit or explicit definition might lead one to reconsider one’s initial assumptions. Whatever the case, it will certainly help one to understand how different disciplines take divergent approaches to the subject.

One might also bear in mind that the notions of understanding and empathy to be found in the long lasting philosophical hermeneutic tradition have been used to differentiate between the sciences and the humanities. Explaining was considered to be the method of the sciences, whereas understanding and empathy were the methods of the humanities. This involves the assumption of a deep dualism, and one should be cautious about claiming a particular term for one or the other discipline and tradition without thoughtful reflection if one wishes to avoid stepping into the footprints of such dualisms.

Empathy as Embodied Capacity for Social Orientation

Coming from the humanities, we propose the following definition for empathy:

Empathy is a social feeling that consists in feelingly grasping or retracing the present, future, or past emotional state of the other; thus empathy is also called a vicarious emotion. (Vicarious: experienced in the imagination through the feelings or actions of another person.)

As a social feeling empathy is always shaped through cultural codes, which differently emphasize, modulate and train the capacity to “feel into“ another person’s emotions. The main function of this feelingly grasping is, we assume. orientation in social contexts. This can mean taking part in the precise emotional state that the other is in at a certain moment, namely: being happy when she is happy, scared when she is scared. and so forth.

But this does not have to be the case. Grasping the other’s emotional state, that is. adopting the other‘s emotional perspective, could also produce a different feeling or emotion in me than the one currently being experienced in the other. And even when the empathic adoption of the other’s perspective produces in me the same emotion as the other is having (or is fictively experiencing) at that very moment, it would not be the same emotion, because the self-other differentiation has not been overcome.

We want to make sure that we do not take empathy to mean the same as sympathy or pity. Both are, in our opinion, special forms of empathy that cover only a certain aspect of empathic processes. Whereas pity is the mode of feeling sorry for the other, sympathy is the mode of being in favor of the other. Both these feelings are ways of adopting an emotional perspective (as empathy is), but they cover only a special form of emotional perspective taking that is structured by the social bond or relation between the persons involved. Thus in social life, pity and sympathy are most likely to occur toward persons one is related to or who belong to one’s own ingroup, but less often toward outgroup members who are mostly perceived as being totally different, strange, or even malevolent, in short, as persons one can scarcely identify with.

Pity and compassion as particular kinds of empathy are deeply connected to social attachment. Frans de Waal (2009) conceives empathy as an evolved concern for others that is triggered through identification with these others. “Empathy’s chief portal is identification,” he argues, meaning that close social bonds increase, in a quasi-automatic way, the emotional responsiveness to others and thus the readiness to help and support fellow beings (de Waal. 2009, 2l3).

Continuing his line of argument, he stresses that empathy also needs a “turn off switch,” a mechanism to override and regulate automatic empathic responses. He considers that what constitutes this turn off switch of empathic processes is a lack of identification. What becomes evident here is that de Waal is implicitly equating pity and compassion with empathy, or he is conceiving them as the evolutionary basis of empathy. lf fellow beings harm or violate each other, as it is often the case in social reality, they must, according to de Waal’s model, have switched off their empathic capacity.

We deliberately take another position here: We conceive empathy as an evolutionarily grounded capacity to adopt an emotional perspective, to implicitly “feel into” the other regardless of the behavioral outcome. This may be directed toward ingroup members and be prosocial and supporting, or toward outgroup members and be destructive and harming.

We make a point of affectively grasping the emotional state of another, but that does not mean to draw a definite line between cognitive understanding and emotional grasping. There are good reasons to stick to a narrower notion when it comes to defining empathy as a “feelingly grasping” if one wants to make sense of notions such as vicarious emotion or of the history of the notion that started with Einfühlung (feeling into). However, the specific conceptual perspective one takes depends very strongly on one’s research traditions and research interest.

When it comes to the relation between empathic perspective taking and the cognitive perspective taking that is related to theory of mind (TOM), we cannot judge the discussions amongst neuropsychologists regarding whether or not these are completely different kinds of perspective taking, and whether or not these processes take place in different brain areas. However, defining the term according to an established tradition, we take empathy to be the emotional perspective taking; and mind reading (in TOM), to be the cognitive perspective taking. Nonetheless, on a purely conceptual level, one might have to admit that the two faculties cannot be separated altogether, because in cognitive perspective taking, the subject who is taking the perspective of another being has to be at least interested in the other being, and that means to care for the other in some way. First, you have to consider the other as an equal in a certain way, as a fellow human being, for instance, or at least as a creature able to feel. Second. you have to consider the other and the other‘s actions as relevant to yourself. You have to be somehow interested in order to be either emotionally involved or curious about the other’s intentions. Therefore, both cases, empathy and Tom, start with the same precondition:

You have to consider the other as being the same as you and of being your counterpart in a particular situation; there has to be a tacit analogy between the subject adopting the other‘s perspective and the other whose perspective is being taken, be it emotional or cognitive.

When specifying what we meant by empathy, we wrote of feelingly grasping or feelingly retracing something; this already suggests that the processes of feeling and of comprehending cannot always be separated clearly. And this makes empathic acts particularly interesting, because they resist the artificial dualisms in the philosophy of mind that still emboss philosophical, scientific, and everyday speech.

To recap briefly, empathy, as the embodied (or bodily grounded) capacity to feel one‘s way into others, to take part in the other’s affective situation, and adopt the other‘s perspective, is a fundamentally social capacity. It allows one to grasp the other’s intentions and thus to engage in meaningful social interaction. Empathy is a crucial means of social communication. It is not just an emotional contagiousness: in which one remains concentrated on oneself.

However, this definition of empathy fails to specify whether this comprehension involves a kind of simulation or imitation of the minds of others. In many of the following contributions, we shall see what important role simulation plays in the debates on a theoretical model of empathy.

Outline of the Contributions

The following six articles are written by distinguished scholars on empathy who come from five different disciplines. Each contribution presents recent research findings and theoretical reflections about the phenomenon of empathy within the respective discipline and simultaneously gives an insight into some currently ongoing debates on the subject within as well as across disciplinary boundaries. The following outline might already give a first impression about this.

Social Cognitive Neuroscience: Cognitive and Affective Empathy

The neuropsychologist Henrik Walter (2012) places his accent on understanding the emotional or affective states of another human being. Furthermore, he views understanding as a purely cognitive concept in this context that suggests making deductions and reasoning. Because Walter concentrates on this approach to understanding the affective states of others, conceptions such as affective theory of mind or cognitive empathy are also highly relevant for his ideas on the capacities for understanding other human beings. Whether this empathy is due to a cognitive faculty or an affective one is not the focus of this distinction. Empathy is, in this case, defined only by the understanding of the emotional state of the other and not by whether the process of understanding is either an affective one or a cognitive one. If it is a cognitive one, it is called cognitive empathy or affective theory of mind; if it is an affective one, it is called affective empathy.

Walter presents this conceptual analysis before linking it both to findings in empirical research investigating the neural basis of empathy and to data on the possible neurogenetic basis of empathy. The tradition followed by Walter when differentiating between TOM, cognitive empathy, and affective empathy is one developed in psychology since the late 1950s. It defined empathy as an emotional or affective phenomenon, and introduced the notion of cognitive empathy as a cognitive faculty or “intellectual or imaginative apprehension of another‘s condition or state of mind” (Hogan, 1969, 308). The main topic within this research tradition is the accuracy of our ability to conceive the other’s condition. Cognitive empathy is not defined in terms of shared emotions but in terms of knowing another’s state of mind by inferential processing (Ickes, 1997).

Social Cognitive Neuroscience again: Neural Overlap and Self-Other Overlap Stephanie Preston and Alicia Hofelich’s contribution (2012) comes from one of the most rapidly growing research fields on empathy, namely, the social neuroscience of empathy. Preston and Frans de Waal (2002) are well known in this field for having developed the perception-aclion model of empathy. This proposes that observing an emotion in someone else generates that emotion in the observer. Preston and Hofelich use this model to argue in favor of a neural overlap in the early stages of processing all cases of social understanding such as cognitive empathy, empathic accuracy, emolion contagion, sympathy. and helping behavior. The self-other overlap in empathy occurs only at a later state of processing. They offer some criteria for differentiating between neural overlap. subjeclive resonance, and personal distress. Because the self-other overlap is crucial for the definition of empathy. this represents an important attempt to seek empirical support for a theoretical differentiation. In addition, it offers a taxonomy of the different cases of social understanding that are supposed to be highlighted by a biological view of empathy.

The academic challenge of this undertaking lies not least in the attempt to show that there is some such thing as a self-other overlap on the neural level, and that it is not just to be found on the subjective level on which the conceptual capacities of a human being are already“at work.”

In order to engage in an empathic process, the empathic subject has to be able to differentiate between his or her own affective states and those of the being he or she is being empathic with, be this a conscious process, as is quite often the case on the subjective level, or a subconscious process on the neural level. This is also a necessary precondition for cognitive empathy and sympathy, but not for emotional contagion. Scientific research on the subjective overlap, that is, the sharing of an emotion, is the task of psychology. But in order to grasp this point on a biological level one has to avoid the subjective perspective. This is done by defining the self-other overlap via the notion of the activation of a personal representation in order to experience an observed state or action, and not via the notion of the activation of a personal representation when acting oneself or being in the state oneself. The overlap in representation on the neural level has to be reflected by a spatial overlap of brain activation between imitation and observation of facial emotional expression (on the subjective level, one is speaking about “sharing another’s emotional or intentional state”).

The process of observing or imagining someone else in a situation might therefore be crucial for determining whether a neural representation of an emotion is the representation of the emotion in somebody else, and therefore an empathic reaction, or whether it is the neural representation of one‘s own emotional process.

Developmental Psychology: The Self-Other Distinction

The developmental psychologist Doris Bischof Kohler (20l2) concentrates on the subjective level of empathy. She defines empathy as understanding and sharing the emotional state of another person. This definition implies not only that an empathic capacity is linked strongly to cognitive capacities, but also that the self-other distinction is crucial for the notion of empathy.

Bischof Kohler’s investigations on empathy are therefore related to her research on the symbolic representation of the self in imagination (self recognition). Her findings reveal that only children who are able to recognize themselves exhibit empathic behavior. This does not imply that self recognition leads to empathic behavior, but that it is a necessary precondition for empathy. And as her data show, this mode of self recognition does not have to be a kind of metarepresentation or conscious self reflection that the theory of mind predicts to first emerge only in 4 year olds. This can explain not only why empathy is already observable in 2 year old children but also why the mere recognition of a mark on one’s cheek while looking in a mirror is a transitional state to self recognition that is not linked to empathy. Her conclusion from these results is that “the capacity to empathize is an effect of maturation rather than socialization.”

Philosophy: Empathy and Simulation Theory

The philosopher Karsten Stueber (20l2) presents a model of the cognitive and afective understanding and knowledge of another human being’s mind, and demonstrates the importance of empathy for social cognition. He is well known as a representative of simulation Iheory-an approach that fits quite well with empirically based theories on empathy. In this article, he extends this basic approach by replying to some narrativist criticism. His main focus is on the cognitive mechanisms that allow us to gain knowledge of other minds and therefore on social cognition and on our understanding of individual agency. One challenge for such an approach is to give a theoretical account of resonance phenomena and projection mechanisms that does not presuppose some kind of Canesian subject who remains in a solitary state of skepticism about the existence of other minds. While insisting on the imponance of our sensitivity to differences between ourselves and other human beings, he introduces the importance of the other on the two levels distinguished in the simulation approach. The first level is the basic level of neuronal resonance phenomena. It is activated automatically by observation of the bodily activities and the accompanying bodily and facial expressions of other beings (basic empathy). The second level is the more developed stage, namely, the re enactment of the thoughts and reasonings of another human being as a rational agent (re enactive empathy). On this level, Stueber admits that in order to understand the actions of another person, we do not necessarily have to appeal to his or her beliefs and desires, but that the knowledge of the other‘s character traits or the other’s role in various social contexts could be equally important. By accepting this possibility, he opens up his model not only to some narrativist proposals for understanding the actions of others but also to the social, historical, or cultural contexts that one might have to consider in order to understand the actions of another human being. He insists, however, that this information would make neither the re enactment nor the simulation superfluous, because pretend beliefs and pretend desires are at the core of the imaginative perspective taking that is necessary for empathy.

Anthropology: The Cultural Embedednass of Empathy

The opening up of simulation theory toward an integration of personal, historical, and cultural information makes a philosophical approach like Stueber‘s attractive for a cultural and social anthropologist such as Douglas Hollan (2012). He takes up the distinction between basic empathy and re enactive empathy, although calling the latter complex empathy instead. This allows him not only to accept embodied forms of imitation and attunement as biologically evolved capacities, but also to concentrate on the more language bound evaluations and adjustments that have evolved culturally and historically. Hollan emphasizes that one has to be acquainted with the latter and with the personal background of a person in order to understand why he or she is in a certain emotional state. And, as he points out, this is necessary in order to be able to be empathic, because one has to understand not only that a person is in a certain emotional state but also why. In other words, one needs to have a cenain amount of knowledge about the normative and moral standards of a culture or society before one can evaluate the meaning of social situations and forms of behavior and comprehend another’s feeling state within the context of social circumstances. In short, empathic processes cannot be detached from the social and cultural contexts in which they are embedded. One way to narrow down the range of the meaning of the definition of empathy is to delete the need to understand why the person is in the state from the definition, leaving only the understanding that a person is in a certain emotional state.

The heuristic differentiation between basic empathy and complex empathy is in line with the ability to determine that another person is in a cenain emotional state and to understand the experience of the other. By reporting important research results on empathy in social anthropology, Douglas Hollan demonstrates not only how far some of the main features of empathy seem to be, by some means, universal, but also how far the studies on empathy need to be refined in light of some findings from anthropological research.

Intercultural findings on empathy reveal that the blending of feelingly perspective taking and cognitive perspective taking is one of the constant features of empathy. whereas the differentiation into “me” and “the other“ seems to be less distinct in empathic like responses in many non Western societies. Another finding of Hollan‘s research is that in the Pacific region, empathy is not a neutral engagement in the understanding of the emotional state of the other, but more like a sympathy that is linked very frequently to a positive attunement with that other person. And this positive attunement is expressed as an active doing rather than a passive experience.

Alongside these research results, he has noticed another, rather opposite tendency: a widespread fear that an empathic like knowledge could be used to harm others. This is why in many parts of the world-from the lndo Pacific to Latin America or Nonhem Canadapeople try to mask their faces. that is, to not express their inner feelings and thoughts but always show a “bright” face and not disclose their vulnerabilities. This phenomenon points to the fact discussed above that empathy is not linked automatically to compassion and helping attitudes, but might also be used by enemies or individual psychopaths as a way to find out how to harm the other.

Among the most challenging research desiderata that result from anthropological findings is the call for more studies on the complex interrelationship between the culture specific moral and situational contexts mediating the expression of empathy on the one side and the dispositions (or traits) that individuals develop to experience and display empathy on the other. Put succinctly, all cultures have some people who are likely to empathize more and others who are likely to empathize less. Hollan considers one of the most demanding tasks facing future research is to investigate how far personality traits interact with the culturally different modes of conceptualizing empathy.

Literary Studies: A Three-Step Model of Human Empathy

The findings on empathy filters introduced by the ethologist and primatologist Frans de Waal might well have been one of the starting points for the theory on empathy proposed by Fritz Breithaupt (2012), a scholar of German studies. As already mentioned. de Waal (2009, 213) has argued that “empathy needs both a filter that makes us select what we react to, and a turn off switch.” Breithaupt shares the hidden agenda for this approach, namely, that human beings are hyperempalhic, without equating pity and compassion with empathy. He has developed a three step model of human empathy that should account for the individual and cultural variety in empathy that also interests Douglas Hollan. According to Breithaupt’s theory, individual and cultural diferences are due to the control functions of blocking and channeling empathy.

These blucking mechanisms are important for a hyperempathic being (Step I) because of the costs accompanying such a social hyperactivity. As well as requiring energy, the danger of self loss might be another cost of empathy in this approach. This possibly ongoing activity therefore needs to be blocked (Step 2). Neurobiologists such as Marco lacobini (2008) have therefore proposed some kind of “super mirror neurons“ that control the mirror neurons. But, because Breithaupt is dealing with more conscious processes, he is hinting at cultural techniques and learning without excluding the possible existence of evolutionarily evolved mechanisms as well. Once the blocking mechanisms are in action, a third step is needed in order to be able to experience empathy at all (Step 3). This step consists in the techniques to circumvent the blocking mechanisms.

The technique to unblock the empathy inhibition on which Breithaupt is concentrating is side raking in a three person setting of empathy. The reason why he turns to a three person instead of a two person model is linked to the observation that hyperempathy in human beings goes hand in hand with hypersociabiliry, and a two person model might be too narrow to encompass this. The side taking process is deliberate: A person decides who’s side to take. After making this decision, empathy emerges (or returns), and it maintains and strengthens the initial choice, because empathy allows emotions to be released that confirm the decision. Breithaupt points out explicitly that the side taking is not involved in empathy itself (as it is in sympathy), but that it is rather “external” to it. The advantage of this model lies in the ability to combine cognitive elements in perspective taking with a caring attitude that might evolve when the side taking decision is followed by empathy.

The ambition of this special issue with its six articles from several disciplines is to give an overview on recent research on empathy. The twelve commentaries not only contribute greatly to achieving this aim but also help significantly to identify the hotspots in ongoing disciplinary and interdisciplinary debates.

Neurophysiological Effects of Trait Empathy in Music Listening

Zachary Wallmark, Choi Deblieck and Marco Iacaboni.

The social cognitive basis of music processing has long been noted, and recent research has shown that trait empathy is linked to musical preferences and listening style.

Does empathy modulate neural responses to musical sounds?

We designed two functional magnetic resonance imaging (fMRI) experiments to address this question. In Experiment 1, subjects listened to brief isolated musical timbres while being scanned. In Experiment 2, subjects listened to excerpts of music in four conditions (familiar liked (FL)/disliked (FD) and unfamiliar liked (UL)/disliked (UD).

For both types of musical stimuli, emotional and cognitive forms of trait empathy modulated activity in sensorimotor and cognitive areas: in the first experiment, empathy was primarily correlated with activity in Supplementary motor area (SMA),

Inferior frontal gyrus (IFG)

and Insula;

In Experiment 2, empathy was mainly correlated wth activity in prefrontal,

temporo-parietal

and reward areas, Taken together. these findings reveal the interactions between bottom-up and top-down mechanisms of empathy in response to musical sounds, in line with recent findings from other cognitive domains.

INTRODUCTION

Music is a portal into the interior lives of others. By disclosing the affective and cognitive states of actual or imagined human actors, musical engagement can function as a mediated form of social encounter, even when listening by ourselves. It is commonplace for us to imagine music as a kind of virtual “persona,” with intentions and emotions of its own: we resonate with certain songs just as we would with other people, while we struggle to identify with other music.

Arguing from an evolutionary perspective, it has been proposed that the efficacy of music as a technology of social affiliation and bonding may have contributed to its adaptive value, As Leman indicates: “Music can be conceived as a Virtual social agent… listening to music can be seen as a socializing activity in the sense that it may train the listener’s self in social attuning and empathic relationships.” In short, musical experience and empathy are psychological neighbors.

The concept of empathy has generated sustained interest in recent years among researchers seeking to better account for the social and affective valence of musical experience; it is also a popular topic of research in social neuroscience. However, the precise neurophysiological relationship between music processing and empathy remains unexplored. Individual differences in trait empathy modulate how we process social stimuli, does empathy modulate music processing as well?

(Valence, as used in psychology, especially in discussing emotions, means the intrinsic attractiveness/”good”-ness (positive valence) or averseness/”bad”-ness (negative valence) of an event, object, or situation. The term also characterizes and categorize specific emotions. For example, emotions popularly referred to as “negative”, such as anger and fear, have negative valence. Joy has positive valence. Positively valenced emotions are evoked by positively valenced events, objects, or situations. The term is also used to describe the hedonic tone of feelings, affect, certain behaviors (for example, approach and avoidance), goal attainment or nonattainment, and conformity with or violation of norms. Ambivalence can be viewed as conflict between positive and negative valence carriers.)

If we consider music through a social psychological lens, it is plausible that individuals with a greater dispositional capacity to empathize with others might also respond to music’s social stimulus differently on a neurophysiological level by preferentially engaging brain networks previously found to be involved in trait empathy.

In this article, we test this hypothesis in two experiments using functional magnetic resonance imaging (fMRI). In Experiment 1, we explore the neural correlates of trait empathy (as measured using the Interpersonal Reactivity Index) as participants listened to isolated instrument and vocal tones. In Experiment 2. excerpts of music in four conditions (familiar liked/disliked. unfamiliar liked/disliked) were used as stimuli. allowmg us to examine correlations of neural activity with trait empathy in naturalistic listening contexts.

Measuring Trait Empathy

Trait empathy refers to the capacity for empathic reactions as a stable feature of personality. Individual differences in trait empathy have been shown to correlate with prosocial behavior and situational “state” empathic reactions to others.

Trait empathy is commonly divided into two components: emotional empathy is the often unconscious tendency to share the emotions of others, while cognitive empathy is the ability to consciously detect and understand the internal states of others.

There are a number of scales to measure individual differences in trait empathy currently in use. including the Toronto Empathy Questionnaire (TEQ). Balanced Emotional Empathy Scale (BEES). Empathy Quotient (EQ). Questionnaire of Cognitive and Affective Empathy (QCAE) and Interpersonal Reactivity INDEX (IRI). Here we use the IRI, which is the oldest and most widely validated of these scales and frequently used in neurophysiological studies of empathy.

The IRI consists of 28 statements evaluated on a 5 point Likert scale (from “does not describe me well” to “describes me very well”). It is subdivided into four subscales meant to tap different dimensions of self reported emotional and cognitive empathy. Emotional empathy is represented by two subscales: the empathic concern scale (hereafter EC) assesses trait level “other oriented” sympathy towards misfortunate others. and the personal distress scale (PD) measures “self oriented” anxiety and distress towards misfortunate others. The two cognitive empathy subscales «most of perspedive taking (PT). or the tendency to see oneself from another’s perspective, and fantasy (PS). the tendency to imaginatively project oneself into the situations of fictional characters.

Music and Empathy

Theories of empathy have long resonated with the arts. The father of the modern concept of empathy, philosopher Theodor Lipps originally devised the notion of Emfühlung (“feeling into”) in order to explain aesthetic experience. Contemporary psychological accounts have invoked mirror neurons as a possible substrate supporting Lipps’s “inner imitation” theory of the visual and performing arts. However. the incorporation of psychological models of empathy in empirical music research is still in its early stages, Empathy remains an ambiguous concept in general. but applications to music can appear doubly vexed in an influential formulation.

Esenherg et al (1991) define empathy as. “an emotional response that stems from another’s emotional state or condition and is congruent with the other’s emotional state or condition.” Aspects of this definition. though. might seem incongruous when applied to music. which is inanimate and not capable of possessing an emotional “state”. To connect music processing to trait empathy. therefore. it is first necessary to determine the extent to which music comprises a social stimulus, who or what do we empathize with when listening to music?

Scherer and Lentner proposed that empathy toward music is often achieved via identification and sympathy with the lived experiences and expressive intentions of composers and performers. Corroborating this view, in a large web based experiment Egermann and McAdams found that “empathy for the musician” moderated between recognized and induced emotions in music: the greater the empathy. the more likely an individual was to exhibit a strong affective response when listening.

In a related study Wollner presented participants with video of a string quartet performance in three conditions audio/visual, visual only. and audio only and reported a significant correlation between trait empathy measures and perceived expressiveness in both visual conditions (music only condition was non significant), leading him to conclude: “since music is the audible outcome of actions, empathic responses to the performer‘s movements may enhance the enjoyment of music.“ Similarly, Taruiti et al found correlations between the EC and FS scales of the IRI and accuracy in emotion recognition relative to musicians’ self reported expressive encodings in an audio only task.

A music specific manifestation of trait empathy was proposed by Kreutz et al, who defined “music empathizmg“ as a cognitive style of processmg music that privileges emotional recognition and experience over the tendency to analyze and predict the rules of musical structure (or. “music systematizing”). Garrido and Schubert compared this “music empathy” scale alongside the IRI EC subscale in a study exploring individual differences in preference for sad music. They found that people who tend towards music empathizing are more likely to enjoy sad music; however. high trait empathy was not significantly correlated with enjoyment of sad music. This would seem to suggest that the music empathizing cognitive style differs from general trait empathy,

A number of other studies have investigated the relationship between trait empathy and enjoyment of sad music using the IRI. In a series of experiments. Vuoskoski and Eerola reported statistically significant correlations between EC and FS subscales and self reported liking for sad and tender music. Similarly, Kawakami and Katahora found that FS and PT were associated with preference for and intensity of emotional reactions to sad music among children.

There is evidence that musical affect is often achieved through mechanisms of emotional empathy. According to this theory, composers and performers encode affective gestures into the musical signal, and listeners decode that signal by way of mimetic, mirroring processes; musical expression is conveyed transparently as affective bodily motions are internally reenacted in the listening process. Shubert, in his Common Coding Model of Prosocial Behavior Processing, suggests that musical and social processing draw upon shared neural resources: music. in this account, is a social stimulus capable of recruiting empathy systems, including the core cingulate paracingulate supplementary motor area (SMA) insula network, along with possible sensorimotor, paralimbic and limbic representations. The cognitive empathy component, which can be minimal, is involved primarily in detecting the aesthetic context of listening, enabling the listener to consciously bracket the experience apart from the purely social. This model may help account for the perceived “visuality” of musical experience, whereby music is commonly heard as manifesting the presence of an imagined other.

In sum, trait empathy appears to modulate self reported affective reactions to music. There is also peripheral psychophysiological evidence that primed situational empathy may increase emotional reactivity to music. It is plausible that such a relationship is supported by shared social cognitive mechanisms that enable us to process music as a social stimulus; however, this hypothesis has not yet been explicitly tested at the neurophysiological level.

Neural Correlates of Trait Empathy

Corroborating the bipartite structure of trait empathy that appears in many behavioral models of empathy, two interrelated but distinct neural “routes” to empathy have been proposed, one associated with emotional contagion and the other with cognitive perspective taking. Emotional empathy is conceived as a bottom up process that enables “feeling with someone else” through perception action coupling of affective cues. Such simulation or “mirroring” models maintain that empathy is subserved by the activation of similar sensorimotor, paralimbic and limbic representations both when one observes another and experiences the same action and emotional state oneself. This proposed mechanism is generally considered to be pre reflective and phylogenetically ancient; it has also been linked behaviorally to emotional contagion, or the propensity to “catch” others’ feeling states and unconsciously co experience them. For example. several imaging studies have found evidence for shared representation of observed/experienced pain in anterior cingulate and anterior insula, as well as somatosensory cortex. Similarly, disgust for smells and tastes has been shown to recruit the insula during both perception and action, and insula has been proposed as a relay between a sensorimotor fronto parietal circuit with mirror properties and the amygdala in observation and imitation of emotional facial expressions. There is also evidence that insula functions similarly in music induced emotions, particularly involving negative valence.

In contrast to emotional empathy, trait cognitive empathy has been conceived as a deliberative tendency to engage in top down, imaginative transpositions of the self into the “other’s shoes,” with concomitant reliance upon areas of the brain associated with theory-of-mind, executive control, and contextual appraisal, including medial, ventral and orbital parts of the prefrontal cortex; somatomotor areas; temporoparietal junction; and precuneus/postenor cingulate. As implied in the functional overlap between certain emotional and cognitive empathy circuits, some have argued that the two routes are neither hierarchical nor mutually exclusive: cognitive perspective taking is premised upon emotional empathy, though it may, in turn, exert top down control over contagion circuits, modifying emotional reactivity in light of contextual cues and more complex social appraisals.

Brain studies have converged upon the importance of the human mirror neuron system in action understanding, imitation and empathy, and has been demonstrated in multiple sensorimotor domains, including the perception of action sounds. Mirror properties were initially reported in the inferior frontal gyrus (IFG) and the inferior parietal lobule (IPL); consistent with simulation theories of trait empathy. Moreover, activity in these and other sensorimotor mirror circuits has been found to correlate with IRI scales in a variety of experimental tasks, including viewing emotional facial expressions; and video of hands injected with a needle. That is, high empathy people tend to exhibit greater activation in mirror regions during the observation of others. Simulation mechanisms also appear to underpin prosocial decision making.

Implication of inferior frontal and inferior parietal mirror neuron areas is not a universal finding in the empathy literature, and some have suggested that it may reflect specific socially relevant tasks or stimulus types, not empathy in and of itself. However, evidence for mirror properties in single cells of the primate brain now exists in medial frontal and medial temporal cortex, dorsal premotor and primary motor cortex, lateral intraparietal area, and ventral intraparietal area. This means that in brain imaging data the activity of multiple brain areas may potentially be driven by cells with mirror properties.

In addition to studies using visual tasks, auditory studies have revealed correlations between mirror neuron activity and trait empathy. Gazzola et al, for instance, reported increased premotor and somatosensory activity associated with PT during a manual action sound listening task. A similar link was observed between IFG and PD scores while participants listened to emotional speech prosody. To date, however, no studies have investigated whether individual differences in empathy modulate processing of more socially complex auditory stimuli, such as music.

Study Aim

To investigate the neural substrates underlying the relationship between trait empathy and music. we carried out two experiments using fMRI.

In Experiment 1, we focused on a Single low level attribute of musical sound timbre, or “tone color”, to investigate the effects of empathy on how listeners process isolated vocal and instrumental sounds outside of musical context.

We tested two main hypotheses:

First, we anticipated that trait empathy (measured with the IRI) would be correlated with increased recruitment of empathy circuits even when listening to brief isolated sounds out of musical context (Gazzola et al).

Second, following an embodied cognitive view of timbre perception (Wallmark et al), we hypothesized that subjectively and acoustically ”noisy” timbral qualities would preferentially engage the emotional empathy system among higher empathy listeners. Abrasive. noisy acoustic features in human and many non human mammal vocalizations are often signs of distress, pain, or aggression (Isai et al): such state cues may elicit heighted responses among people with higher levels of trait EC.

To explore the relationship between trait empathy and music processing, in Experiment 2 participants passively listened to excerpts of self selected and experimenter selected “liked” and “disliked” music in familiar and unfamiliar conditions while being scanned. Musical preference and familiarity have been shown to modulate neural response. Extending previous research on the neural mechanisms of empathy, we predicted that music processing would involve circuitry shared with empathic response in non musical contexts (Schubert).

Unlike Experiment 1, we had no a priori hypotheses regarding modulatory effects of empathy specific to each of the four music conditions However, we predicted in both experiments that emotional empathy scales (EC and FD) would be associated with regions of the emotional empathy system in music listening, including sensorimotor. paralimbic and limbic areas, while cognitive empathy scales (PT and FS) would primarily be correlated With activity in prefrontal areas implicated in previous cognitive empathy studies (Singer and Lamm).

Results

Experiment 1 demonstrated that trait empathy is correlated With Increased activation of circuitry often associated with emotional contagion, including sensorimotor areas and insula, in the perception of isolated musical timbres. FS and EC also appear to be sensitive to the affective connotations of the stimuli. Timbre is arguably the most basic and quickly processed building block of music. Though sufficient to recruit empathy areas, these brief stimuli do not, however, constitute “music” per sci

In Experiment 2, we turned our focus to more naturalistic stimuli including excerpts of music selected in advance by participants in order to explore the effect of trait empathy on the processing of music.

DISCUSSION

The present study demonstrates that trait empathy is correlated with neurophysiological differences in music processing. Music has long been conceived as a social stimulus. Supporting this view, our study offers novel evidence that neural circuitry involved in trait empathy is active to a greater degree in empathic individuals during perception of both simple musical tones and full musical excerpts. Individual variances in empathy are reflected in differential recruitment of core empathy networks during music listening; specifically. IRI subscales were found to correlate with activity in regions associated with both emotional (e.g.. sensorimotor regions, insular and cingulate cortex) and cognitive empathy (cg, PFC. TPI) during passive listening tasks

Our main hypotheses were continued, though with an unexpected twist regarding the two putative empathy types (at least as structured by the MU), Both experiments seem to suggest interactions between bottom up and top down processes (indexed in our study by both IRI scores and activity in neural systems) in empathy modulated music listening. This is in line with recent findings in prosocial decision making studies. Stimulus type, however, seems associated with different patterns of neural systems engagement.

In Experiment 1, sensorimotor areas were more frequently modulated by trait empathy in the processing of musical timbre: conversely. in Experiment 2, cognitive areas were more frequently modulated by trait empathy in the processmg of (famillar) music. Together this suggests that, contrary to our initial hypothesis for Experiment 2, modulation of neural activity by empathy was driven more by stimulus type than by empathy type; that is. the emotional empathy subscale (BC) was no more selective to emotional contagion circuitry than cognitive empathy scales (PT and FS), and vice versa (the PD scale did not reveal any significant correlations with brain activity. In what follows, we interpret these results and discuss their implications.

Empathy-Modulated Sensorimotor Engagement in Timbre Processing

Using isolated 2-s instrument and vocal tones as stimuli, Experiment 1 found that the four IRI subscales modulated response to timbre. First, we found that cognitive perspective was correlated with activity in motor areas SMA for A0: and SI and anterior cingulate (ACC).

This finding is in line with numerous studies suggesting a role for ACC and SI in emotional empathy; it also replicates a result of Gazzola et al 2006. who reported a correlation of somatomotor activity and PT scores in an action sound listening task. Activity in these regions may suggest a sensorimotor simulation process whereby high PT individuals imitate internally some aspect of the production of these sounds, This result could be explained in light of Cox’s 2016 “mimetic hypothesis,” according to which music is understood by way of covert or overt motor reenactments of sound producing physical gestures. It is quite conceivable that people who are inclined to imagine themselves from others’ perspectives also tend to take up the physical actions implied by others’ musical sounds, whether a smooth and gentle voice, a growled saxophone, or any other musical sound reflecting human actions.

It is intriguing, however, that PT was not implicated in the processing of positive or negative valence. One might assume that perspective takers possess a neural preference for “good“ sounds: for example, one study reported activation of larynx control areas in the Rolandic operculum while subjects listened to pleasant music (but not unpleasant), suggesting subvocalization only to positively valenced music (K elsch et al) Our results, however. indicate that PT is not selective to valence in these sensorimotor areas.

FS also revealed motor involvement (SMA) in the task > baseline contrast. Unlike PT, FS appeared to be sensitive to both positive and negative valence of timbres: we found activity in left TH and Broca‘s area of the IFG associated with positively valenced timbres, and temporal, parietal and prefrontal activations associated with disliked timbres. TPI is an important structure for theory of mind. Together with Broca‘s area, a well studied language and voice specific motor region that has been implicated in emotional empathy. It is plausible to suggest that individuals who are prone to fantasizing may exhibit a greater tendency to attribute mental states to the virtual human agents responsible for making musical sounds, and that this attribution would be more pronounced for positively valenced stimuli.

As hypothesized. EC was correlated with activation in a range of areas previously implicated in empathy studies, including IPL, IPG and SMA, along With SI, STG. cerebellum and AIC. It was also sensitive to negative valence: noisy timbres were processed with greater involvement from SMA in individuals with higher EC. EC is an “other oriented” emotional scale measuring sympathy or compassion towards the misfortune of others. Since noisy, distorted qualities of vocal timbre are an index of generally high arousal, negatively valenced affective states, we theorize that individuals with higher trait EC exhibited greater motor attunement owing to the ecological urgency typically signaled by such sound events.

In short, we usually deploy harsh vocal timbres when distressed or endangered (e.g., screaming or shouting), not during affectively positive or neutral low arousal states, and high empathy people are more likely to pick up on and simulate the affective motor implications of others in distress. Though our sensitivity to the human voice is especially acute, researchers have hypothesized that instrumental timbre can similarly function as a “superexpressive voice” via acoustic similarities to emotional vocal expression. Our result would seem to support this theory, as motor response appears to encode the combined effects of noisy tones, both vocal and instrumental.

It is also worth noting, as might be expected given the above, that noisy voice produced a unique signature of activation among high FS and EC participants relative to the normal vocal stimuli: FS modulated processing of the noisy voice in SII and IPL, while EC was selective to noisy vocal sounds in the SMA and primary motor cortex. This result appears to be at odds with other studies of vocal affect sensitivity that report motor mimetic selectivity for pleasant vocalizations. It is likely that individual variances in empathy (plus other mediating factors) predispose listeners to differing orientations towards others’ affective vocalizations, with empathic listeners more likely to “catch” the motor affective implications of aversive sounds than low empathy people, who might only respond to sounds they find pleasant while tuning out negatively valenced vocalizations.

Cox (2016) theorizes that music can afford listeners an “invitation” for motor engagement, which they may choose to accept or decline, Seen from this perspective, it is likely that individual differences in empathy play an important role in determining how we choose to respond to music’s motor invitations.

Regarding motor engagement across IRI subscales it is apparent that SMA is the most prominent sensorimotor area involved in empathy modulated processing of timbre. SMA is a frequently reported yet undertheorized part of the core empathy network; it has also been implicated in internally generated movement and coordination of action sequences, and has been shown in a single neuron study to possess mirror properties. Most relevant to the present study, moreover, SMA contributes to the vividness of auditory imagery, including imagery for timbre. Halpern et al and Lima et al attributed SMA activity in an auditory imagery task in part to subvocalization of timbral attributes, and the present study would seem to partially corroborate this explanation. We interpret this result as a possible instance of sensorimotor integration: SMA activity could reflect a basic propensity to link sounds with their associated actions, which are internally mirrored while listening. In accordance with this view, we would argue that people do not just passively listen to different qualities of musical timbre, they enact some of the underlying physical determinants of sound production, whether through subvocalization, biography specific act sound associations.

To summarize, sensorimotor areas have been implicated in many previous studies of emotional empathy, including IFG and IPL; “pain circuit” areas in AIC and ACC; and somatomotor regions. Interestingly. these precise regions dominated results of the Experiment 1 timbre listening task. This is true, moreover, for both emotional and cognitive scales: PT and FS, though often implicated in cognitive tasks, were found in this experiment to modulate SMA, SI, primary motor cortex, IPL, MC and IFG, well documented motor affective AREAS. We theorize that the contextual impoverishment and short duration of the timbre listening task (2-s isolated tones) may have largely precluded any genuine perspective taking or fantasizing from occurring, it is much harder to put oneself in the “shoes” of an single isolated voice or instrument, of course, than it is an affectively rich piece of actual music. However, even in the absence of conscious cognitive empathizing, which presumably would have been reflected in engagement of the cognitive empathy system, individuals with high trait PT and FS still showed selective activations of sensorimotor and affective relay circuits typically associated with emotional empathy. This could be interpreted to suggest that the two “routes” to empathy are not dissociated in music listening: although conscious PT in response to abbreviated auditory cues is unlikely, people who frequently imagine themselves in the positions of others also exhibit a tendency toward motor resonance in this basic listening task, even when musical context is missing.

Prefrontal and Reward Activation During Music Listening

Experiment 2 used 16-s excerpts of self and experimenter selected music to explore the effect of dispositional empathy on the processing of music in four conditions. familiar liked (FL), familiar disliked (FD), unfamiliar liked (UL), and unfamiliar disliked (UD). Participants consisted of individuals who reported regularly experiencing intense emotional reactions while listening to music. Musical liking is associated at the group level (ie. no IRI covariates), with left basal ganglia reward areas, and disliking with activity in right AIC, primary auditory cortex and prefrontal areas (OFC and VLPFC). Musical familiarity is associated with activation across a broad region of the cortex, subcortical areas, and cerebellum, including IPL. premotor cortex and the core empathy network, while unfamiliarity recruits only the SFG.

This robust familiarity effect is even more acute among high empathy listeners: after adding empathy covariates to our analysis, there were no regions that demonstrated an affect specific response after controlling for familiarity. This result is consistent with the literature in showing a large neurophysiological effect of familiarity on musical liking; it appears that trait empathy, as well, modulates responses to familiar music to a greater degree than unfamiliar music.

Contrary to expectations, activation in regions primarily associated with emotional empathy (e.g., sensorimotor areas, ACC, AIC) was not a major component in empathy modulated music processing. Instead. the most prominent activation sites for PT and EC scales were prefrontal, including medial, lateral, and orbital portions of the cortex, as well as TPJ. These regions are involved in executive control, regulation of emotions, mentalizing, contextual appraisal, and “enactment imagination”, and have figured prominently in many studies on the neurophysiology of cognitive empathy. Additionally, FS and EC results were characterized by dorsal striatum when participants listened to familiar music. This basal ganglia structure has been frequently reported in empathy studies but not often discussed; it has also long been associated with musical pleasure.

basal ganglia

Replicating this association, our results suggest that empathic people experience a higher degree of reward and motivation when listening to familiar music compared to lower empathy people.

PT was associated with left TPI in the task > baseline contrast. Activation of this region among perspective takers is consistent with studies implicating TPI in theory of mind and the merging of self and other (Lawrence et a1, 2006). The TPI was joined by posterior cingulate, cerebellum and superior prefrontal areas when listening to familiar liked music (FL > FD), the former two of which were also identified in a study on the neural bases of perspective taking. Interestingly, these results differ substantially from the PT correlations in Experiment 1, which were entirely sensorimotor. In the context of isolated musical sounds, PT results were interpreted as a reflection of covert imitation (or, enactive perspective taking): in contrast. however, it appears here that PT may reflect a more cognitively mediated, mental form of perspective taking, which conceivably extends beyond action perception coupling of musicians‘ affective motor cues to encompass contextual appraisal, assessments of the affective intent embodied in the music, and other executive functions.

In contrast to the prominent TPI and prefrontal activation associated with PT, FS results revealed activation of dorsal striatum (caudaie and putamen) and limbic areas (thalamus, hippocampus and amygdala). Activation of reward and emotion centers may suggest that fantasizers also tend to exhibit heightened positive emotional reactions to familiar music. Indeed, we found a moderate correlation between FS and preference ratings for familiar liked music, which may tentatively corroborate this claim. Moreover, structural brain studies have found that FS is associated with increased gray matter volume in hippocampus, an important memory area, perhaps also indicating enhanced encoding of familiar liked music among fantasizers.

The contrast in activation between the two IRI cognitive empathy scales (PT and FS) is notable, and may be attributed to the different aspects of empathy they were designed to assess. PT taps the tendency to imagine oneself in other people’s shoes, whereas FS captures the tendency to imagine oneself from the perspective of fictional characters. With this distinction in mind, one could surmise that the two scales also tap different views regarding the ontology of the musical agent: in this reading, people with high trait PT are more likely to take music as a social stimulus, i.e., as if it was a real or virtual human presence (with theory of mind, goals, beliefs), while high FS listeners are more likely to hear it as “fictional” from a social perspective, i.e., as a rewarding sensory stimulus with an attenuated grip on actual social cognition. Further research is called for to explore possible explanations for the differences in cognitive scales as reflected in music listening.

Turning finally to emotional empathy, we found that EC recruits prefrontal, reward and sensorimotor affective areas in music listening, and is likewise quite sensitive to familiarity. In the Familiar > Unfamiliar contrast, we found activation of cerebellum, IPL, DLPFC, IFG, DMPFC, amygdala, anterior paracingulate, dorsal striatum, OFC and lingual gyrus, and a variation on this general pattern for the Familiar liked > Unfamiliar liked and interaction contrasts. Activation of bilateral IPL and IFG is consistent with mirror accounts of empathy. Furthermore, the ACC, paracingulate, and areas that extend dorsally (SMA, DMPFC) have been proposed as the core of the empathy network: our result would seem to extend support for the primacy of this region using an experimental task that is not explicitly social in the manner of most empathy studies. Lastly, DLPFC is an important executive control area in cognitive empathy, and has been implicated in emotional regulation. Activation of this region may reflect top down control over affective responses to familiar music, both in terms of up regulation to liked music and down regulation to disliked (or possibly up regulation to negative stimuli, as Open minded empathic listeners try to “see something positive” in the disliked music), In further research, connectivity analysis between DLPFC and limbic/reward areas may help to specify the neurophysiological mechanisms underlying empathy modulated emotional regulation during music listening.

In addition to motor, cingulate and prefrontal activity, we found the recruitment of emotion and reward processing areas as a function of EC and musical familiarity: dorsal striatum (the whole extent of the caudate nucleus, plus thalamus) may reflect increased pleasure in response to familiar music among empathic listeners. It is not surprising that the reward system would show preferential activation to familiar music, as confirmed in the basic group Liked > Disliked contrast.

Prevalence of basal ganglia for both EC and FS suggests that trait empathy may effectively sensitize people to the music they already know. This even appears to be the case for disliked music, which showed dorsal striatum activation (along with OFC) in the Familiar disliked > Unfamiliar disliked contrast. This could be interpreted to indicate that empathic people may experience heightened musical pleasure even when listening to the music they self select as “hating,” provided it is familiar. By way of contrast. no striatum activation was found for any of the unfamiliar music conditions.

In concert with limbic circuitry, then, it is apparent that musical familiarity recruits a broad region of the affect reward system in high EC listeners.

Activation of inferior parts of the lingual gyrus and occipital lobe was another novel finding, and may also be linked to musical affect. These areas are associated with visual processing, including perception and recognition of familiar sights and emotional facial expressions, as well as visual imagery. It is reasonable to think that empathic listeners may be more prone to visual imagery while listening to familiar music. Visual responses are an important mechanism of musical affect more generally, and are a fairly reliable index of musical engagement and attention.

If high EC people are more susceptible to musical affect, as suggested by our results, they may also show a greater tendency towards visual imagery in music listening.

To be clear, we did not explicitly operationalize visual imagery in this study: in the future, it would be interesting to follow up on this result by comparing visual imagery and music listening tasks using the EC scale as a covariate.

The behavioral data resonate in interesting and sometimes contradictory ways with these imaging findings. We found that EC is strongly associated with preference for liked music and unfamiliar music, and negative responses to familiar disliked music. Results suggest that high EC people are more responsive to the affective components of music, as reflected in polarity of preference responses. EC was also associated with open mindedness to new music (i,e.. higher ratings for unfamiliar music), though imaging results for this contrast did not reach significance, and might appear to be contradicted by the clear familiarity effect discussed previously.

We must be cautious in the interpretation of these findings owing to the small sample size, but this resonance between behavioral and imaging evidence is nonetheless suggestive in demonstrating a role for EC in affective responsiveness to familiar music. This conclusion is broadly consistent With previous behavioral studies, especially regarding pleasurable responses to sad music.

In sum, the present results provide complementary neural evidence that involvement of prefrontal areas and limbic/basal ganglia in music listening covaries with individual trait differences in empathy, with sensorimotor engagement playing a smaller role.

How do we account for the prominence of cognitive, prefrontal areas in music listening but not musical timbre in isolation? It must be noted that a broad swath of the emotional empathy system was involved in the basic task > baseline contrast (used to mask all IRI covariates): in other words, it is clear that music in aggregate is processed with some level of sensorimotor, paralimbic, and limbic involvement, regardless the empathy level of the listeners or the valence/familiarity of the music. However, our results seem to suggest that empathic people tend to be more attuned to the attribution of human agency and affective intention in the musical signal. as indicated by preferential engagement of cognitive empathy networks including PFC (MPF and DLPFC) and TP), as well as reward areas.

In other words, what seems to best characterize the high empathy response to musical stimuli is the tendency to take an extra cognitive step towards identification with some agentive quality of the music, over and above the work of emotional contagion mechanisms alone.

Thus while patterns of neural resonance consistent with emotional contagion appear to be common to most experiences of music and were also found among high empathy participants in Experiment 1, activation of prefrontal cognitive empathy systems for the PT and EC scales may indicate the tendency of empathic listeners to try to “get into the heads” of composers, performers, and/or the virtual persona of the music. This top down process is effortful, imaginative, and self aware, in contrast to the automatic and pre reflective mechanisms undergirding emotional contagion. Accordingly, as suggested by Schubert, the involvement of cognitive systems may not strictly speaking be required for affective musical response, which can largely be accounted for by emotional contagion circuitry alone.

A number of studies have shown that mental imagery may be supported by sensorimotor and affective components without the contribution of prefrontal areas. Nevertheless, they could betoken a more social cognitive mode of listening, a deliberative attempt on the part of listeners to project themselves into the lived experience of the musical agent. This imaginative projection is more intense, understandably, for music that empathic people already know, and also appears to interact with musical preference.

General Implications

The present study has a number of implications for social and affective neuroscience, music psychology, and musicology. For neuroscientific empathy research, we demonstrate the involvement of the core empathy network and mirror neuron system outside of tasks that are explicitly social cognitive. Most studies use transparently social experimental tasks and stimuli to assess neural correlates of state and trait empathy; for example, viewing pictures or videos of other people.

This study demonstrates that musical sound. which is perhaps not an obvious social stimulus, can elicit neural responses consistent with theories of empathy. By domg so, this study highlights the potential value of operationalizing artistic and aesthetic experience as a window into social cognitive and affective processing, a perspective that is arguably the historical progenitor of contemporary empathy research.

For music psychology, this research has at least three main implications.

First, this study demonstrates that trait empathy may modulate the neurophysiology of music listening. Although there is mounting behavioral and psychophysiological evidence pointing to this conclusion, this is the first study to investigate the effects of empathy on the musical brain.

Second, this study confirms and extends empirical claims that music cognition is inextricably linked to social cognition. Our results suggest that aspects of affective music processing can be viewed as a specialized subprocess of general social affective perception and cognition. This may begin to explain the neural bases for how music can function as a “virtual social agent”.

Third, in demonstrating neural differences in music processing as a function of empathy, we highlight the possible significance of looking at other trait features when assessing the functional neural correlates of musical tasks and stimuli. Many neurophysiological music studies take only a few trait features into account in sampling procedures and analysis, most notably sex, age, and musical training: the latter has been well explored, but other factors such as personality factors and mood are not frequently addressed. Individual differences in music processing may relate to dispositional characteristics that can be captured by psychosocial questionnaires, indirect observational techniques, or other methods. Exploring the role of such trait variables in musical behaviors and brain processing could provide a more detailed and granular account of music cognition,

Finally, these results enrich the humanistic study of music in providing a plausible psychobiological account for the social valence of musical experience observed in diverse cultural and historical settings. As music theorist Clifton claims, “the ‘other’ need not be a person: it can be music.”

In a very rough sense, this study provides empirical support for this statement: areas implicated in trait empathy and social cognition also appear to be involved in music processing, and to a significantly greater degree for individuals with high trait empathy.

If music can function something like a virtual ”other,” then it might be capable of altering listeners‘ views of real others, thus enabling it to play an ethically complex mediating role in the social discourse of music. Indeed, musicologists have historically documented moments of tense cultural encounter wherein music played an instrumental role in helping one group to realize the other’s shared humanity.

Recent research would seem to provide behavioral ballast for this view: using an implicit association task,Vuoskoski et a showed that listening to the music of another culture could positively modulate attitudes towards members of that culture among empathic listeners. Though we do not in this study explicitly address whether music can alter empathic brain circuits, it is suggestive that certain attitudes toward musical sound may have behavioral and neural bases in individual differences in trait empathy.

Limitations

A few important limitations must be considered in interpreting these results, First, this study was correlational: no causative links can thus be determined in the relationship between music and trait empathy. In the future, it would be interesting to use an empathy priming paradigm in an MRI context to compare neurophysiological correlates of trait empathy with primed “state” empathy in music listening; this could provide a powerful method for disentangling possible differences in processing between dispositional attributes of empathy and contextual factors (e.g., socially conditioned attitudes about a performer, mood when listening).

As a corollary to the above, moreover, this study does not address whether our results are specific to music listening: perhaps high empathy people utilize more of these areas when performing other non musical yet not explicitly social tasks as well (eg. viewing abstract art). Additionally. we do not explore whether there could be other mediating trait factors in music processing besides empathy and sex: personality and temperament, for instance, have been shown to modulate responses to music.

Finally, this study will need to be replicated with a larger sample size, and with participants who do not self select based on strong emotional reactions to music, in order to strengthen the statistical power and generalizability of the results.

CONCLUSION

In two experiments using fMRI, this article demonstrates that trait empathy modulates music processing. Replicating previous findings in the social neuroscience literature, isolated musical timbres are related to sensorimotor and paralimbic activation; in actual MUSIC listening, however, empathy is primarily associated with activity in prefrontal and reward areas. Empathic participants were found to be particularly sensitive to abrasive, “noisy” qualities of musical timbre, showing preferential activation of the SMA, possibly reflecting heightened motor mimetic susceptibility to sounds signaling high arousal, low valence affective states.

In the music listening task. empathic subjects demonstrated enhanced responsiveness to familiar music, with musical preference playing a mediating role. Taken together, these results confirm and extend recent research on the link between music and empathy, and may help bring us closer to understanding the social cognitive basis for music perception and cognition.

INTERPERSONAL REACTIVITY INDEX (IRI)

Reference:

Davis, M. H. (1980). A multidimensional approach to individual differences in empathy. JSAS Catalog of Selected Documents in Psychology, 10, 85.

Description of Measure:

Defines empathy as the “reactions of one individual to the observed experiences of another (Davis, 1983).”

28 items answered on a 5 point Likert scale ranging from “Does not describe me well” to “Describes me very well”. The measure has 4 subscales, each made up of 7 different items. These subscales are (taken directly from Davis, 1983):

Perspective Taking, the tendency to spontaneously adopt the psychological point of view of others.

Fantasy taps respondents‘ tendencies to transpose themselves imaginatively into the feelings and actions of fictitious characters in books, movies, and plays

Empathic Concern assesses “other-oriented” feelings of sympathy and concern for unfortunate others

Personal Distress measures “self oriented” feelings of personal anxiety and unease in tense interpersonal settings

Abstracts of Selected Related Articles:

Davis, M. H. (1983). Measuring individual differences in empathy: Evidence for a multidimensional approach. Journal of Personality and Social Psychology, 44, 113126.

The past decade has seen growing movement toward a view of empathy as a multidimensional construct. The Interpersonal Reactivity Index (IRI; Davis, 1980), which taps four separate aspects of empathy, is described, and its relationships with measures of social functioning, self esteem, emotionality, and sensitivity to others is assessed. As expected, each of the four subscales displays a distinctive and predictable pattern of relationships with these measures, as well as with previous unidimensional empathy measures. These findings, coupled with the theoretically important relationships existing among the four subscales themselves, provide considerable evidence for a multidimensional approach to empathy in general and for the use of the IRI in particular.

Pulos, S., Elison, J ,, & Lennon, R. (2004). Hierarchical structure of the Interpersonal Reactivity Index. Social Behavior and Personality, 32, 355 360.

The hierarchical factor structure of the Interpersonal Reactivity Index (IRI) (Davis, 1980) inventory was investigated with the Schmid Leiman orthogonalization procedure (Schmid & Leiman, 1957). The sample consisted of 409 college students. The analysis found that the IRI could be factored into four first order factors, corresponding to the four scales of the IRI. and two second order orthogonal factors, a general empathy factor and an emotional control factor.

INTERPERSONAL REACTIVITY INDEX

The following statements inquire about your thoughts and feelings in a variety of situations. For each item, indicate how well it describes you by choosing the appropriate letter on the scale at the top of the page: A, B, C, D, or E.

When you have decided on your answer, fill in the letter next to the item number.

READ EACH ITEM CAREFULLY BEFORE RESPONDING. Answer as honestly as you can. Thank you.

ANSWER SCALE:

A DOES NOT DESCRIBE ME WELL

B

C

D

E DESCRIBES ME VERY WELL

1. I daydream and fantasize, with some regularity, about things that might happen to me. (FS)

2. I often have tender, concerned feelings for people less fortunate than me. (EC)

3. I sometimes find it difficult to see things from the “other guy’s” point of View. (PT) (-)

4. Sometimes I don’t feel very sorry for other people when they are having problems. (EC) (-)

5. I really get involved with the feelings of the characters in a novel. (FS)

6. In emergency situations, I feel apprehensive and ill at ease. (PD)

7. I am usually objective when I watch a movie or play, and I don’t often get completely caught up in it. (FS) (-)

8. I try to look at everybody’s side of a disagreement before I make a decision. (PT)

9. When I see someone being taken advantage of, I feel kind of protective towards them. (EC)

10. I sometimes feel helpless when I am in the middle of a very emotional situation. (PD)

11. I sometimes try to understand my friends better by imagining how things look from their perspective. (PT)

12. Becoming extremely involved in a good book or movie is somewhat rare for me. (FS) (-)

13. When I see someone get hurt, I tend to remain calm. (PD) (-)

14. Other people’s misfortunes do not usually disturb me a great deal. (EC) (-)

15. If I‘m sure I’m right about something, I don’t waste much time listening to other people’s arguments. (PT) (-)

16. After seeing a play or movie, I have felt as though I were one of the characters. (FS)

17. Being in a tense emotional situation scares me. (PD)

18. When I see someone being treated unfairly, I sometimes don’t feel very much pity for them. (EC) (-)

19. I am usually pretty effective in dealing with emergencies. (PD) (-)

20. I am often quite touched by things that I see happen. (EC)

21. I believe that there are two sides to every question and try to look at them both. (PT)

22. I would describe myself as a pretty soft hearted person. (EC)

23. When I watch a good movie, I can very easily put myself in the place of a leading character. (FS)

24. I tend to lose control during emergencies. (PD)

25. When I’m upset at someone, I usually try to “put myself in his shoes” for a while. (PT)

26. When I am reading an interesting story or novel, I imagine how I would feel if the events in the story were happening to me. (FS)

27. When I see someone who badly needs help in an emergency, I go to pieces. (PD)

28. Before criticizing somebody, I try to imagine how I would feel if I were in their place. (PT)

See also:

Music and the Mind

by Anthony Storr

Inequality breeds stress and anxiety. No wonder so many Britons are suffering – Richard Wilkinson and Kate Pickett.

Studies of people who are most into our consumerist culture have found that they are the least happy, the most insecure and often suffer poor mental health.

Understanding inequality means recognising that it increases school shootings, bullying, anxiety levels, mental illness and consumerism because it threatens feelings of self-worth.

In equal societies, citizens trust each other and contribute to their community. This goes into reverse in countries like ours.

The gap between image and reality yawns ever wider. Our rich society is full of people presenting happy smiling faces both in person and online, but when the Mental Health Foundation commissioned a large survey last year, it found that 74% of adults were so stressed they felt overwhelmed or unable to cope. Almost a third had had suicidal thoughts and 16% had selfharmed at some time in their lives. The figures were higher for women than men, and substantially higher for young adults than for older age groups. And rather than getting better, the long-term trends in anxiety and mental illness are upwards.

For a society that believes happiness is a product of high incomes and consumption, these figures are baffling. However, studies of people who are most into our consumerist culture have found that they are the least happy, the most insecure and often suffer poor mental health.

An important part of the explanation involves the psychological effects of inequality. The greater the material differences between us, the more important status and money become. They are increasingly seen as if they were a measure of a person’s inner worth. And, as research shows, the result is that the more unequal the society, the more people feel anxiety about status and how they are seen and judged. These effects are seen across all income groups from the poorest to the richest tenth of the population.

Inequality increases our insecurities about selfworth because it emphasises status and strengthens the idea that some people are worth much more than others. People at the top appear supremely important, almost as superior beings, while others are made to feel as if they are of little or no value. A study of how people experience low social status in different countries found, predictably, that people felt they were failures. They felt a strong sense of shame and despised themselves for failing. Whether they lived in countries as rich as the UK and Norway, or as poor as Uganda and Pakistan, made very little difference to what it felt like to be near the bottom of the social ladder.

Studies have shown that conspicuous consumption is intensified by inequality. If you live in a more unequal area, you are more likely to spend money on a flashy car and shop for status goods. The strength of this effect on consumption can be seen in the tendency for inequality to drive up levels of personal debt as people try to enhance their status.

But it is not just that inequality increases status anxiety. For many, it would be nearer to the truth to say that it is an assault on their feeling of self-worth. It increases what psychologists have called the “social evaluative threat”, where social contact becomes increasingly stressful. The result for some is low self-esteem and a collapse of self-confidence. For them, social gatherings become an ordeal to be avoided. As they withdraw from social life they suffer higher levels of anxiety and depression.

Others react quite differently to the greater ego threat of invidious social comparisons. They react by trying to boost the impression they give to others. Instead of being modest about achievements and abilities, they flaunt them.

Rising narcissism is part of the increased concern with impression management. A study of what has been called “self-enhancement” asked people in different countries how they rated themselves relative to others. Rather like the tell-tale finding that 90% of the population think they are better drivers than average, more people in more unequal countries rated themselves above average on a number of different dimensions. They claimed, for example, that they were cleverer and more attractive than most people.

Nor does the damage stop there. Psychological research has shown that a number of mental illnesses and personality disorders are linked to issues of dominance and subordination exacerbated by inequality. Some, like depression, are related to an acceptance of inferiority, others relate to an endless attempt to defend yourself from being looked down on and disrespected. Still others are borne of the assumption of superiority or to an endless struggle for it. Confirming the picture, the international data shows not only that mental illness as a whole is more common in more unequal societies, but specifically that depression, schizophrenia and psychoses are all more common in those societies.

What is perhaps saddest about this picture is that good social relationships and involvement in community life have been shown repeatedly to be powerful determinants of health and happiness. But it is exactly here that great inequality throws another spanner in the works. By making class and status divisions more powerful, it leads to a decline in community life, a reduction in social mobility, an increase in residential segregation and fewer inter-class marriages.

More equal societies are marked by strong community life, high levels of trust, a greater willingness to help others, and low levels of violence. As inequality rises, all this goes into reverse. Community life atrophies, people cease to trust each other, and homicide rates are higher.

In the most unequal societies, like Mexico and South Africa, the damage has gone further: citizens have become afraid of each other. Houses are barricaded with bars on windows and doors, razor wire atop walls and fences.

And as inequality increases, a higher proportion of a country’s labour force is employed in what has been called “guard labour” the security staff, prison officers and police we use to protect ourselves from each other.

Understanding inequality means recognising that it increases school shootings, bullying, anxiety levels, mental illness and consumerism because it threatens feelings of self-worth.

Richard Wilkinson and Kate Pickett are the authors of The Inner Level: How More Equal Societies Reduce Stress, Restore Sanity and Improve Everyone’s Wellbeing

Life after Severe Childhood Trauma. I Think I’ll Make It. A True Story of Lost and Found – Kat Hurley.

Had I known I should have been squirreling away memories as precious keepsakes, I would have scavenged for more smiles, clung to each note of contagious laughter and lingered steadfast in every embrace.

Memory is funny like that: futile facts and infinitesimal details are fixed in time, yet things you miss, things you wish you paid fuller attention to, you may never see again.

“I learned this, at least, by my experiment: that if one advances confidently in the direction of his dreams, and endeavors to live the life which he has imagined, he will meet with a success unexpected in common hours.”

Henry David Thoreau, Walden: Or, Life in the Woods

To write this book, I relied heavily on archived emails and journals, researched facts when I thought necessary, consulted with some of the people who appear in the book, and called upon my own memory, which has a habitual tendency to embellish, but as it turns out, there wasn’t much need for that here. Events in this book may be out of sequence, a handful of locations were changed to protect privacy, many conversations and emails were re-created, and a few names and identifying characteristics have been changed.

It was hardly a secret growing up that psychologists predicted I would never lead a truly happy and normal life. Whether those words were intended for my ears or not seemed of little concern, given the lack of disclaimer to follow. There was no telling what exceedingly honest bits of information would slip through the cracks of our family’s filtration system of poor Roman Catholic communication. I mean, we spoke all the time but rarely talked. On the issues at least, silence seemed to suit us best, yet surprising morsels of un-sugarcoated facts would either fly straight out of the horse’s mouth or trickle their way down through the boys until they hit me, the baby.

I was five when I went to therapy. Twice. On the second visit, the dumb lady asked me to draw what I felt on a piece of plain construction paper. I stared at the few crayons next to the page when I told her politely that I’d rather not. We made small talk instead, until the end of the hour when she finally stood up, walked to the door and invited my grandma in. They whispered some before she smiled at me and waved. I smiled back, even if she was still dumb. I’m sure it had been suggested that I go see her anyway, because truth be known, psychologists were a “bunch of quacks,” according to my grandma. When I said I didn’t want to go back, nobody so much as batted an eye.

And that was the end of that.

When I draw up some of my earliest most vivid memories, what I see reminds me of an old slide projector, screening crooked, fuzzy images at random. in the earliest scenes, I am lopsidedly pigtailed, grass stained, clothes painfully clashing. In one frame I am ready for my first day of preschool in my bright red, pill-bottomed bathing suit, standing at the bottom of the stairs where my mom has met me to explain, through her contained laughter, that a carpool isn’t anything near as fun as it sounds. In another, I am in the living room, turning down the volume on my mom’s Richard Simmons tape so I can show her that, all on my own yet only with a side-puckered face, I’d learned how to snap. In one scene, I’m crouched down in the closet playing hide-and-seek, recycling my own hot Cheerio breath, patiently waiting to be found, picking my toes. Soon Mom would come home and together we’d realize that the boys weren’t seeking (babysitting) me at all, they’d simply gone down the street to play with friends.

I replay footage of the boys, Ben and Jack, pushing me in the driveway, albeit unintentionally, toward the busy road on my first day with no training wheels, and (don’t worry, I tattled) intentionally using me as the crash-test dummy when they sent me flying down the stairs in a laundry basket. I have the scene of us playing ice hockey in the driveway after a big ice storm hit, me proudly dropping the puck while my brothers Stanley Cup serious faced off.

I call up the image of me cross-legged on my parents’ bed, and my mom’s horrified face when she found me scissors in hand thrilled with what she referred to as my new “hacked” do. That same bed, in another scene, gets hauled into my room when it was no longer my parents’, and my mom, I presume, couldn’t stand to look at it any longer. I can still see the worry on her face in those days and the disgust on his. I see the aftermaths of the few fights they couldn’t help but have us witness.

Most of the scenes are of our house at the top of the hill on McClintock Drive, but a few are of Dad’s townhouse in Rockville, near the roller rink. I remember his girlfriend, Amy, and how stupid I thought she was. I remember our Atari set and all our cool new stuff over there. And, of course, I remember Dad’s really annoying crack-of-dawn routine of “Rise and Shine!”

I was my daddy’s darling, and my mommy’s little angel.

Then without warning I wasn’t.

Had I known I should have been squirreling away memories as precious keepsakes, I would have scavenged for more smiles, clung to each note of contagious laughter and lingered steadfast in every embrace. Memory is funny like that: futile facts and infinitesimal details are fixed in time, yet things you miss, things you wish you paid fuller attention to, you may never see again.

I was just a regular kid before I was ever really asked to “remember.” Up until then, I’d been safe in my own little world: every boo-boo kissed, every bogeyman chased away. And for a small voice that had never been cool enough, clever enough, or captivating enough, it was finally my turn. There was no other choice; I was the only witness.

“Tell us everything you know, Katie. It is very important that you try to remember everything you saw.”

August 11, 1983

I am five. I’ll be in kindergarten this year, Ben is going to third grade, Jack will be in seventh. I’m not sure where the boys are today; all I know is that I’m glad it’s just me and Mom. We’re in the car, driving in our Ford wagon, me bouncing unbuckled in the way back. We sing over the radio like we always do. We’re on our way to my dad’s office, for the fivehundredth time. Not sure why, again, except that “they have to talk.” They always have to talk. Ever since Dad left and got his new townhouse with his new girlfriend, all they do is talk.

Mom pulls into a space in front of the office. The parking lot for some reason is practically empty. His cleaning business is all the way in the back of this long, lonely stretch of warehouse offices, all boring beige and ugly brown, with big garage doors and small window fronts.

“You can stay here, sweetie pie I won’t be long.”

I have some of my favorite coloring books and a giant box of crayons; I’ll be fine.

Time passes in terms of works of art. Goofy, Mickey, and Donald are all colored to perfection be fore I even think to look up. I am very fond of my artistic abilities; my paint by numbers are exquisite, and my papier-maché, as far as I’m concerned, has real promise for five. All of my works are fridge-worthy; even my mom thinks so. My special notes and handmade cards litter her nightstand, dresser, and bathroom counter.

I hear a scream. Like one I’d never heard before, except on TV. Was that her? I sit still for a second, wait for another clue. That wasn’t her. But something tells me to check anyway just in case.

I scramble out from the way back, over the seat, and try to open the door, but I’m locked in why would she look me in? I tug at the lock and let myself out. With the car door still open, I scurry to the front window of my dad’s shop, and on my tiptoes, ten fingers to the ledge, I can see inside. The cage with the snakes is there, the desk and chairs are there, the cabinets and files are there, everything looks normal like the last time I was inside. Where are they?

Then through the window, I see my mom. At the end of the hall, I can see her through the doorway. But just her feet. Well, her feet and part of her legs. They are there, on the floor her sandals still on. I can make out the tip of his shoe too, at her thigh, like he’s sitting on top of her. She is still. I don’t get it. Why are they on the floor? I try to open the door, but it’s locked. I don’t recall knocking; maybe I did. I do know that I didn’t yell to be let in, call for help, or demand that I know what was going on.

It wasn’t her. It sounded like it came from down the street, I tell myself. Maybe it wasn’t a scream scream, anyway. Someone was probably just playing, I convince myself. I get back in the car. I close the door behind me and color some more.

Only two pages are colored in this time. Not Mickey and friends, Snow White now. Fairy tales. My dad knocks on the window, startling me, smiling. “Hey, princess. Your mom is on the phone with Aunt Jeannie, so you’ll just see her Monday. You’re coming with me, kiddo. We have to go get your brother.”

Everything I’ve seen is forgotten. My dad’s convincing smile, tender voice, and earnest eyes make all my fright disappear. He told me she was on the phone, and I believed him. How was I supposed to know that dads could lie?

Two days later, my brothers and I were at the beach on a job with Dad when our grandparents surprised us with the news. “Your mother is missing.” And it was only then, when I sensed the fear they tried so intently to wash from their faces, that the realization struck me as stark panic, that l was brought back to the scene for the first time and heard the scream I understood was really her.

My testimony would later become the turning point in the case, reason enough to convict my father, who in his cowardice had covered all his traces. Even after his conviction, it would be three more years until he fully confessed to the crime. I was eight when I stood, uncomfortable, in a stiff dress at her grave for the second time more flowers, same priest, same prayers.

To say I grew up quickly, though, as people have always suspected, would be a stretch. Certainly, I was more aware, but the shades of darkness were graced with laughter and lullabies and being a kid and building forts, and later, learning about my period from my crazy grandma.

I honestly don’t remember being treated any differently, from Grandma Kate at least. If I got any special attention, I didn’t know it. Life went on. Time was supposed to heal all wounds. My few memories of mom, despite my every attempt, faded with each passing holiday.

I was in Mrs. Dunne’s third grade class when my dad finally confessed. We faced a whole ’nother wave of reporters, news crews, and commotion. They replayed the footage on every channel: me, five years old again, clad in overalls, with my Care Bear, walking into the courtroom. And just like before, my grandpa taped all the news reels. “So we never forget,” he said.

For our final TV interview, my grandparents, the boys, and I sat in our church clothes in the front room to answer the reporter’s questions. I shifted around on Grandma Kate’s lap in my neatly pressed striped Easter dress. Everybody had a turn to talk. I was last. “Katie, now that the case is closed, do you think you will be able to move on?”

I’m not sure how I knew it then, especially when so many years of uncertainty were still to come, but I was confident: “Yeah.” I grinned. “I think I’ll make it.”

Chapter One

TEACHING MOMENT

“Well, I just called to tell you I’ve made up my mind.” Silence “I will not be returning to school next year.”

Silence “I don’t know where I’m going or what I’m going to do I just know I cannot come back.”

Barbara, my faculty chair, on the other end of the line, fumed. I could hear it in each syllable of Catholic guilt she spat back at me. We’d ended a face-to-face meeting the day before with, “I’ll call you tomorrow with my decision,” as we agreed to disagree on the fact that the students were more important than my mental health and well-being.

“What will they do without you? You know how much they love you. We created this new position for you, and now you’re just going to leave? Who will teach the class? It’s August!” she agonized.

God, she was good. She had this guilt thing down pat. An ex-nun, obviously an expert, and this was the first I’d been on her bad side, a whole year’s worth of smiles, waves and high-fives in the hallways seemed to get clapped out with the erasers.

It was true; I loved the kids and didn’t want to do this so abruptly, like this is August. This was not my idea of a resume builder. Nevertheless, as each bit of honesty rose from my lips, I felt freer and freer and more true to myself than I’d felt in, well, a long frickin’ time. A sense of relief washed through me in a kind of cathartic baptism, cleansing me of the guilt. I stopped pacing. A warm breeze swept over the grass on the hill in front of our condo then over me. I stood on the sidewalk still nervous, sweating, smiling, teary-eyed. I can’t believe I just did that.

St. Anne’s was a very liberal Catholic school, which ironically, had given me a new faith in the closeminded. The building housed a great energy of love and family. I felt right at home walking through its doors even at new-teacher orientation, despite it having been a while since I needed to be shown the ropes. I’d already been teaching for six years in a position where I’d been mentoring, writing curriculum and leading administrative teams. I normally didn’t do very well on the bottom rung of the totem pole, but more pay with less responsibility had its merit.

It was definitely different, but a good different. I felt newly challenged in a bigger school, looked forward to the many programs already in place and the diversity of the staff and student body. The ceremonies performed in the religion-based setting seemed foreign at first, yet witnessing the conviction of our resident nuns and tenured faculty restored a respect I had lost over the years. They were the hymns that I recognized, the verses I used to recite, the prayers I was surprised I still remembered, the responses I thought I’d never say again.

The first time we had Mass together as an entire school, I was nearly brought to tears. I got goose bumps when the notes from the piano reverberated off the backboards on the court the gym-turned-place-of-worship hardly seemed the place to recommit. Yet, hearing the harmony of our award-winning gospel choir and witnessing the level of participation from the students, faculty, and administration, I was taken aback. The maturity of devotion in the room was something I had never experienced in any of my churches growing up. Students, lip-synching their words, distracted and bored, still displayed more enthusiasm than the lumps hunched at my old parishes.

It was during that first Mass that I realized there was only one person who could have gotten me there to a place she would have been so proud to tell her bridge club I was working. She would have been thrilled for me to find God here. The God she knew, her Catholic God the one who had listened to her rosary, day after day, her pleas for her family’s health and well-being, her pleas for her own peace and forgiveness. Gma had orchestrated it all. I was certain.

As that realization unfolded, I saw a glimpse of her endearing eyes, her tender smile before me, and with that my body got hot, my lashes heavy, soaked with a teary mist. Although it would be months till I stumbled upon a glimpse of what some might call God, it was here, at St. Anne’s, where I gained a tradition I had lost, a perspective I had thought impossible, a familiarity that let me feel a part of something, and a trust that may have ultimately led me straight out the door.

Our kitchen, growing up, reeked of canned beans and burnt edges. Grandma Kate knew of only one way to cook meat, crispy. On most nights, the fire alarm let us know that dinner was ready. The table was always set before I’d come running in, at the sound of her call, breathless from playing, to scrub the dirt from my fingernails. She was a diligent housewife, though at times she played the part of something far more independent. The matriarch, we called her the gel to the whole damn bunch of us: her six, or five rather, and us three.

She responded to Grandma Kate, or just Kate, or Kitty, as her friends from St. Cecelia’s called her, or Catherine, as she generally introduced herself, or Gma, as I later deemed her all names necessary to do and be everything that she was to all of us.

She and I had our moments through my adolescence where the chasm of generations between us was more evident than we’d bother to address. They’d sold their five-bedroom home in Manor Club when it was just she and Grandpa left alone inside the walls baring all their memories. The house had character worn into its beams by years of raising six children and consequently taking the abuse of the (then) eleven grandchildren like a docile Golden Retriever.

It wasn’t long after my grandpa died that I moved back in with Gma. At fifteen, it was just she and I in their new two-bedroom condo like college roommates, bickering at each other’s annoying habits, ridiculing each other’s guests, and sharing intimate details about each other’s lives when all guards were off and each other was all we had.

Despite our differences, her narratives always fascinated me. I had grown up on Gma’s tales and adventures of her youth. In most of her stories, she depicted the trials of the Depression and conversely, the joys of simplicity. She encouraged any craft that didn’t involve sitting in front of the television. She believed in hard work, and despite her dyslexia, was the first woman to graduate from Catholic University’s Architectural School in the mid-1940s. “Of course,” she said. “There was no such thing as dyslexia in my day. Those nuns damn near had me convinced I was just plain dumb.”

She was a trained painter and teacher, a fine quilter, gardener, and proud lefty. She had more sides to her than a rainbow-scattering prism. When we were young and curious, flooding her with questions, we’d “look it up” together. When we had ideas, no matter how silly, she’d figure out a plan to somehow help us make it happen. All of us grandkids had ongoing special projects at any given time: whether it was building in the garage, sewing in the living room, painting in the basement, or taking long, often lost, “adventures” that brought us closer to her past.

She was from Washington DC, so subway rides from Silver Spring into the city were a regular episode. We spent so many hours in the Museum of Natural History I might attribute one of my cavities to its famous astronaut ice cream. We also went to see the cherry blossoms when they were in bloom each year, visited the National Zoo and toured the Washington Monument as well as several of the surviving parks and canal trails from her childhood.

It was on these journeys that she and I would discuss life, politics, war, religion, and whatever else came to mind. She was a woman of many words, so silences were few and far between. I got to know her opinion on just about everything because nothing was typically left unsaid, nothing.

By the time I was in high school and college, the only music we could agree on in the car was the Sister Act soundtrack. On our longer jaunts when conversation dripped to a minimum, I would toss in the tape before the banter went sour, which was a given with our opposite views on nearly everything. I’d slide back the sunroof, and we’d sing till our hearts were content.

“Hail mother of mercy and of love. Oh, Maria!”

She played the grouchy old nun, while I was Whoopi, trying to change her stubborn ways.

Gma and I both loved musicals, but while I was off scalping tickets to see Rent on Broadway, which she would have found too loud and too crude (God knows she would have had a thing or two to say about the “fairy” drag queen), she was content with her video of Fiddler on the Roof.

As I sat in the theater recently for the Broadway performance of Lion King, I couldn’t help but picture her sitting there beside me, her big, brown eyes shifted right with her good ear turned to the stage; it was a show we would have both agreed on.

For the theater, she would have wetted down her short gray wispy hair and parted it to the side and then patted it down just so with both hands. A blouse and a skirt would have already been picked out, lying on the bed. The blouse would get tucked in and the belt fastened not too far below her bra line. Then she’d unroll her knee highs from the toes and slip on some open toe sandals, depending on the season; she didn’t mind if the hose showed. Some clip-on earrings might have made their way to her virgin lobes, if she remembered, and she would have puckered up in the hallway mirror with a tube of Clairol’s light pink lipstick from her pocketbook before announcing that she was ready.

Gma would have loved the costumes, the music, the precision in each detail. And in the car ride home, I can hear her now, yelling over the drone of the car’s engine because her hearing aid had remained in the dresser drawer since the day she brought it home. “There wasn’t but one white fella’ in the whole gosh dern show. Every last one of ’em was black as the day is long, but boy could they sing. God, what beautiful voices they had, and even as deaf as I am I could understand what they were saying. They were all so well spoken.”

Rarely does a day go by that I don’t smile at one of her idioms or imagine one of her crazy shenanigans, her backward lessons, or silly songs. I used to feel guilty about the proportion I spent missing her over the amount I did my own mother. I guess it makes sense, though, to miss what I knew for far longer, and I suppose I had been swimming laps in the gaping void I housed for my mom.

Over the years, I often thought if I truly searched for my mom she would give me a sign, but where would I even look? Or would I even dare? Gma believed in those kinds of things, and despite having long lost my religion, she made me believe.

She told me a story once, without even looking up from the quilt she mended, about a dark angel who sat in a chair by the window in the corner of the room, accompanying her in the hospital as her mother lay on her deathbed gripped by cancer. She said the angel’s presence alone had been enough to give her peace. I had watched her get mistyeyed while she brought herself back to the scene, still pushing the thimble to the fabric. Another time, she continued, she sat on the front step of their first house on Pine Hill in hysterics as she’d just gotten word of her three-year-old daughter’s cancer diagnosis; she’d felt a hand on her shoulder enough to calm her. She knew then she wasn’t alone.

These conversations became typical when it was just us. When she cried, so did I. We wore each other’s pain like thick costume makeup, nothing a good cry and some heavy cold cream couldn’t take off. She shared with me her brinks of meltdowns after losing my mother, and I grew up knowing that she had far more depth than her overt simplicity echoed.

It wasn’t until my latter college years, though, when we had become so close we were able to overlook most of our differences. By then, I wanted all the time I spent running away back; I wanted my high school bad attitude and disrespect erased; I wanted the smell of my cigarette smoke in her station wagon to finally go away. She was my history. She was my companion. She was home to me.

In the last few years, we shared our haunts, our fears, our regrets. Yet, we laughed a lot. She never minded being the butt of any good joke. She got crazier and goofier in her old age, shedding more of her crossbred New England proper and Southern Belle style. One of my favorite memories was of the time my college roommate, Kathleen, and I taught her how to play “Asshole” at our Bethany, Delaware, beach house.

Gma had said, “The kids were all down here whoopin’ it up the other night playing a game, havin’ a good ol’ time, hootin’ and hollerin’. I would like to learn that game. They kept shouting some curse word what’s it called again?”

“Asshole?” I had said.

“Yup, that must be it. Asshole sounds right. Think you can teach this old bird?”

Kathleen and I nearly fell over at the request but were obliged to widen Gma’s eyes to the awesome college beer-drinking game full of presidents, assholes, and beer bitches. And she loved it, quite possibly a little tipsy after a few rounds. We didn’t typically play Asshole with Jacob’s Creek chardonnay.

Throughout the course of several conversations, Gma assured me that she’d had a good life and when the time came, she’d be ready. In those last few years, if I stood in her condo and so much as mentioned the slightest gesture of admiration toward anything she owned, she’d say, “Write your name on the back.” She’d have the Scotch tape and a Sharpie out before I could even reconsider.

It was 2003, a year into my teaching career, when Gma finally expressed how proud she was of me. She said that my mom had always wanted to be a teacher, that she was surely proud of me, too. I’ll never forget waking up to my brother’s phone call, his voice solemn. I was devastated.

It was my mom and Gma who helped Brooke and I get our house, I always said. I had signed a contract to start at St. Anne’s in the fall, so we needed a home outside the city that would make my new commute toward DC more bearable. Three years after Gma died, since I wasn’t speaking to God much in those days, I asked Mom and Gma to help us out if they could. Brooke, who only knew Gma through my incessant stories, was just as kooky as I was when it came to talking to the dead so she never batted an eye at the references I made to the china cabinet.

Gma’s old antique china cabinet green until she stripped, sanded and painted it maroon the year she moved to her condo sat in the dining room of our rented row house in Baltimore. (The smell of turpentine will always remind me of her leathered hands.) Sometimes, for no good reason, the door would fall slightly ajar, and each time it did, I swore she was trying to tell me something. While dating a girl I imagine Gma was not particularly fond of, I eventually had to put a matchbook in the door just to keep the damn thing closed it creeped me out in the mornings when I’d wake up to the glass door gaping.

The exact night Brooke and I put the contract in on our house, we mentioned something to Gma before going to bed, kissing our hands and casually patting the side of the paint-chipped cabinet. The next morning wide open. Two days later contract accepted. I was elated; I’d never had such a good feeling about anything.

I felt so close to my team of guardian angels then. Everything seemed to be in its delightfully divine order, and I thanked them immensely from the moment we began the purchasing process until the time we moved in, displaying my gratitude thereafter with each stroke of my paintbrush and each rock pulled from the garden. I adored the home we were blessed with, our cute little cobblestone accented condo, our very first house. Even though we knew it wasn’t a forever home, it was ours to make our own for now. And we did or we started to.

So when the fairy tale began to fall apart, just a little over a year later, I couldn’t help but question everything, intentions, meaning. There was no sign from the china cabinet. None of it made sense, the reason behind it all, I mean. Sure, I had always known growing up that everything has its reason. I have lived by that motto, but I could make no sense of this. It’s one thing for a relationship to fall apart, but to have gone all this way, with the house to tie us even further? I was beside myself.

Needless to say, my bits of gratitude tapered off as I felt like I had less and less to be thankful for. I still talked to Mom and Gma, but not without first asking, “Why?” And something, quite possibly the silence that made the question seem rhetorical told me I was going to have to get through this on my own. Perhaps it was a test of independence or a sudden stroke of bad karma for all the years spent being an obnoxious teenager, ungrateful, untrustworthy. Either way I was screwed; of that much I was certain.

I had always wanted to leave. To go away, I mean. Study abroad or go live in another state and explore. I had traveled a little in college but nowhere extensively. So, as all the boxes moved into our brand new house were unpacked and making their way into storage, the reality of being bound started creeping into my dreams through suffocation. I was faintly torn. Not enough to dampen the mood, because I imagined that somehow all that other stuff, my writing, my passions, would come later. It would all fall into place somehow. I guess I trusted even in the slightest possibility, although I knew that with each year of teaching, the job that was supposed to give me time off to be creative, I felt more and more comfortable and lackadaisical about pursuing my dreams.

I took a writing course online that drove in some discipline, only to drop it midway when things got complicated. Brooke often entertained the idea of moving to California, which kept me content, although I knew with the look of things that was only getting further and further from practical. But since being honest with myself wasn’t my strong suit, I ignored my intuition, and looking back, ignored a lot of signs that might have politely escorted me out the door rather than having it slammed in my face.

Chapter Two

SEX IN PLURALISTIC SOCIETY

I took a course, Sex in a Pluralistic Society, in my last semester of college. Somehow I thought it was going to be a lecture on the sociology of gender. Keep in mind this was the same semester I tried to cram in all my last requirements, registering for other such gems as Plagues and People; Death, Dying and Bereavement; and History of Theology.

Yes, the sex class was the lighter side to my schedule, but my prude Catholic upbringing made a sex journal, “Or, if you don’t have a partner, make it a self-love journal,” a really difficult assignment. Plus, the guy who taught the class just creeped me out. The videos he made us watch, I’m still traumatized. A classmate and I thought to complain, on several occasions, but it was both of our last semesters so it’s fair to say that, like me, she left that sort of tenacity to the underclassmen.

Despite the dildos, the pornography, and the daylong discussion on G-spots, I did take away one valuable lesson from that loony old perv. It was toward the end of the semester when the concept of love was finally introduced. By then, I had done my fair share of heart breaking and had tasted the bitter side of breakup a few times myself. I was sure I knew everything he had to say.

Instead, I was surprised to find myself taking notes when he broke down the Greeks’ take on the four different kinds of love: agape, eros, philia, storge. We discussed unconditional love versus conditional love. Yeah, yeah; I knew all that. He went on to describe eros as manic love, obsessive love, desperate love.

“This is the kind of love movies are based on. It’s high energy, high drama, requires no sleep, is built on attraction, jealousy runs rampant; it comes in like a storm and subsides often as quickly as it came in.” I cringed when he said, “It’s immature love.”

And here, I thought, this is what it was all about. All lesbian love, at least all those wonderful, electrifying things! Eros it even sounds erroneous.

It was when I was dating the most confident and beautiful, twinkly-eyed woman I’d ever laid my hands on, some four years later, that I was brought back to that lecture. Despite our good intentions and valiant attempts at maturity, Brooke and I had a relationship built on many of those very erroneous virtues. It was movie-worthy high passion infused with depths that felt like coming down from a rock star kind of party.

Perhaps it’s because it began all wrong. She was fresh out of college. I was already teaching, working weekends at a chick bar in Baltimore at the time, Coconuts, our very own Coyote Ugly. One night, a friend of hers (she admitted later) noticed me, in my finest wicker cowboy hat and cut-off shirt, slinging beers and lining up shots between stolen, flirtatious moments on the dance floor. A week later, Brooke and I were fixed up at a party. We were both in other relationships that we needed excuses to get out of, so why not? She was beautiful (did I say that already?), tall, caramel skin and hazel eyes, tomboy cute when she was feeling sporty, simply stunning when dressed to the nines. She even fell into her dad’s Brazilian accent after a few cocktails, which sealed it for me; I was enamored. Plus, she was a bona fide lesbian (a first for me), and we wore the same size shoe. What more do you need?

We did everything together: tennis, basketball, squash. She’d patiently sit on the beach while I surfed. I always said yes to her shopping trips. We even peed with the door open so as to not interrupt conversation. And I’m almost certain I slept right on top of her for at least a solid year, I’d never been considered a “peanut” before. In fact, I don’t think we separated at all for the first couple of years we dated, now that I think about it. Maybe for an odd trip, but it didn’t go without feeling like we’d lost a limb, I swear. We’d always say, “No more than five days,” as if we wouldn’t have been able to breathe on day six.

When we first started dating, I went to Japan for nine days to visit my brother Jack who had been stationed at Atsugi. I was pretty pathetic. It was my first time traveling alone, so when I stepped off the plane on foreign soil and my family wasn’t at the gate ready to collect me, I quickly reverted to my inner child, the sweeping panic stretched from my tippy toes to my fingertips.

It was the same feeling I used to get in Kmart when I’d look up from the shelf to tug at the skirt of the lady standing beside me, only to be both mortified and petrified when I realized that face and body didn’t belong to my Gma. I’m not sure who was supposed to be keeping track of whom, but whoever it was did so poorly. Hence the reason why I developed a system: I’d go sit in the back of our station wagon where I knew it would be impossible for me to be forgotten among the dusty racks of stiff clothes. The first time I put this system into place, unbeknownst to anyone, I resurfaced from the car when the two police cars arrived, to see what all the hubbub was about. Boy, were they glad to see me when I strolled back through the automatic sliding doors, unaware of all the excitement I had started.

Thank God my sister-in-law found me in Tokyo after I’d already figured out how to work the phones and had dialed home. Brooke had calmed me down by talking me through the basics: I wasn’t lost; I was just on the brink of being found, she assured me. I’d hung up and collected myself by the time Jill and the kids arrived.

Every evening in Japan, I slid away from the family and hid in my room where I clumsily punched hundreds of calling card numbers into the phone just so I could hear Brooke’s voice before bed. And like me, she was dying inside at the distance between us.

Sure, there were some caution signs, some red flags being waved, but all the good seemed to outweigh the bad, and who’s perfect, really? I thought some of my ideologies about love were too lofty and maybe, just maybe, I had to accept that I would never have all that I desired from a relationship, like say, trust. Plus, people grow, they mature, relationships mature; surely we’d be the growing kind. We liked self-help books. We had a shelf where they sat, most of them at least half-read.

Her family loved me, and I adored them. Yes, it took a while for them to get used to the idea of me being more than just Brooke’s “roommate.” Thankfully, the week Brooke came out to her family, a close family friend, battling breast cancer, took a turn for the worse. Brooke came back at her parents’ retorts with, “Well, at least I don’t have cancer.” And to that, well they had to agree.

Brooke and I traveled together. We loved the beach. We loved food and cute, quaint little restaurants. We loved playing house and raising a puppy. We loved talking about our future and a big fat gay wedding, and most of all we loved being loved. We bought each other flowers and little presents and surprised each other with dinner and trips and concert tickets. I’ll never forget the anniversary when she had me get all dressed up just to trick me into a beautiful candlelit dinner at home. I could have sat at that table forever, staring into her shimmering, smiling eyes, or let her hold me for just as long as we danced among the rose petals she’d scattered at our feet.

It was for all those reasons that the darkness never outweighed the light, the screaming matches, the silent treatments, the distrust, the jealousy. All those things seemed part of our short past when we began shopping for our first home. It was a blank slate, a new beginning signing the paperwork, picking out furniture, remodeling our kitchen.

God, we danced so much in that kitchen.

We laughed at our goofy dog, Porter. We cried on our couch, watching movies. We supported each other in our few separate endeavors. We shared chores and “mom” duty and bills and credit cards. And I think it was under the weight of all the things of which we were once so proud that it all began to crumble. “Do you have to slam the cabinets like that?” as if I were picking up new habits to purposefully push her away. “I hate fighting like this in front of him!” she’d say, pointing at Porter. “Look, we’re making him nervous.”

She sobbed and sobbed, and her big beautiful eyes remained bloodshot for at least six months as I watched her slip away from me. I begged her to tell me what she needed, and even that she couldn’t do.

Brooke finally had a social life that I supported wholeheartedly, but that social life seemed to echo more and more of what was wrong with us. During the day things appeared fine and good and normal, but at night her cold shoulder sent me shivering further and further to the opposite side of the bed until I eventually moved into the spare bedroom.

I didn’t get it. I said that I did, that I understood, but I didn’t.

She spent an awful lot of time with a “friend.” Julie, a mutual friend, or so I thought. We all hung out together, thus I didn’t think to question anything until it became more and more blatant. I would beg, “Just tell me what’s going on with the two of you. I’m a big girl. I’ll just walk away. But I can’t just sit around here feeling batty while you deny what I can see with my own two eyes!”

She wouldn’t admit to it. “Nothing is going on.” She said she just needed time to figure herself out.

In the meantime, I was still her home. I was still her best friend and even at the furthest distance she’d pushed me to, I was the one who calmed her when the weight of it all made her come unhinged.

I was the one who rubbed her back and kissed her forehead.

She wanted me to be an asshole, so she’d have an excuse. She wanted me to get pissed to lessen her compounding guilt. I’m not sure if it was that I couldn’t or that I wouldn’t do either of those things. I still hung onto what I’d promised with that sparkly little ring I’d given her, not the real thing, but a big promise. I had taken it all very seriously. “In sickness and in health.” And here she was before me, as far as I could see it, sick.

Well, sick was the only diagnosis that wouldn’t allow me to hate her as she inhabited our home with me, a platonic roommate, sometimes cold and aloof and other times recognizable and warm. I felt like we had somehow been dragged into the drama of a bad after-school special without the happy commercials of sugary cereals and toys that will never break or end up like the Velveteen Rabbit, who ironically, I was really starting to resemble in the confines of our condo with its walls caving in.

While the final days of summer strode past in their lengthy hour, the honest words, “I want to take a break,” were inescapably spoken. I felt sick, stunned by the syllables as they fell from her lips. We’d been at the beach for the weekend where I naively thought we might be able to spend some time all to ourselves, mending the stacks of broken things between us. I knew this had to do with Julie, but still nobody had the guts to admit it. I was infuriated. So much so, that I reduced myself to checking cell phone logs and sleuthing around my own home. I hated myself for the lengths I allowed her to push me.

There was no way I could return to school as my signed contract promised. I couldn’t imagine focusing on my students while I was so busy focusing on my failing relationship. Although the last thing I wanted to do was uproot myself, I had finally begun to gather the pebbles of self-respect that would eventually become its new foundation. I had to go.

And with the phone call to my faculty chair, I did exactly what I never imagined I would do. I resigned. I had never been so excited to throw in the towel well, except for that one awful restaurant where I was too much of a coward to quit so I faxed in my resignation an hour before my shift that time felt good too. But this was different. I didn’t chicken out. I stood up to Barbara’s crucifix-firing cannon and prevailed.

When Brooke and I weren’t fighting or walking on eggshells around each other, she dove into my arms expressing her undying love for me, and I held the stranger I no longer connected with, consoling her. I didn’t know what to make of all the mixed emotions. I had taken my accusations to Julie herself to try to get some answers, but she laughed at my arguments, claiming Brooke was “too confused” to be dating anyone right now. Julie was older, with graying wisps, loafers and pleated pants. To look at her anymore made me sick. And, after all, Brooke still wore the ring I’d given her. Still, after nine months, none of it made any sense.

The night she woke me, cross-legged on the floor at my bed because she couldn’t sleep and it was driving her crazy, she looked desperate. I held her and stroked her hair, calming her with my patient voice, exuding every ounce of love that could look past my own pain to reduce hers. Healthy? Probably not. But that was the only way I knew how to love her. To put everything of me aside. Everything.

I have always wanted a family. From the time I was little I knew I would be a mom. At eight, I thought marrying a rich man and becoming a housewife was the golden ticket to true happiness, along with becoming the president, a monkey trainer, and a marine biologist. My pending future changed with the weather, but rich was almost always a constant. A valid measure of success at eight, I suppose. A family, and its entire construct, was very important to me: the house, the dog, the hus or now the wife, all of it.

And that’s what Brooke and I had, or we talked like we did. Raising our puppy from ten weeks to his “man”hood and buying household goods on joint credit cards. We were all grown up like a real family. With our names linked on more than just the dog’s birth certificate, “taking a break” was really a separation and anything beyond that was really a divorce. I hadn’t reached that logic in my head, perhaps because I still refused to believe that all I imagined was disintegrating before me, where I stood, clenching fistfuls of hopeless dust.

Chapter Three

ON THE GOOD FOOT

I toyed with the idea of California, as I had always talked about. No reason to stay here. Seriously, with no excuses holding me back, I searched tirelessly for jobs on craigslist day in and day out. And there was an edge of excitement in taking control, or that’s what I convinced myself was going on. I applied for a few teaching jobs in California, Colorado, British Columbia, and even New York. I was intrigued by the schools that touted their outdoor education programs and offered classes like rock climbing and snowboarding. I reasoned with myself: teaching can’t be all that bad with a mountain backdrop and class cancelations for white-water rafting.

*

from

I Think I’ll Make It. A True Story of Lost and Found

by Kat Hurley

get it at Amazon.com

The Handbook Of Solitude. Psychological Perspectives on Social Isolation, Social Withdrawal, and Being Alone.

Some might believe that it is not fear that guides the behaviors of some of these solitary individuals. Instead, it might be proposed that some of these noninteracting individuals have a biological orientation that leads them to prefer a solitary existence.

I am quite certain that what the reader will come away with after having completed the chapters included herein is that solitude has many faces.

On Solitude, Withdrawal, and Social Isolation

Kenneth H. Rubin

As I sit in my office pondering what it is that I should be writing in the Foreword to this extraordinary compendium, I am alone. With the door closed, I am protected against possible interruptions and am reminded of the positive features of solitude, there is no one around, it is quiet, and I can concentrate on the duties at hand. Indeed, several contributors to this volume have written about the pleasantries associated with solitude; frankly, I must agree with this perspective, but do so with a number of significant provisos. I will offer a listing of these provisos in the following text. However, before so doing, I would like to suggest a thought experiment or two.

A Science Fiction Thought Experiment

Why must one understand the significance of solitude, withdrawal, and social isolation? Let’s begin with a little thought experiment. Imagine, for at least one millisecond, that we have arrived on a planet populated by billions of people. Never mind how these people came into existence. Let’s just assume that they happen to be on the planet and that we know not how they came to be. Imagine too that there is no interpersonal magnetism, that these people never come together, there are no interactions, there is no crashing together or colliding of these individuals. All we can see are solitary entities walking aimlessly, perhaps occasionally observing each other. In short, we are left with many individuals who produce, collectively, an enormous social void. From an Earthly perspective, we might find the entire enterprise to be rather intriguing or boring or frightening and would likely predict that prospects for the future of this planet are dim.

Given that this is a supposed “thought exercise,” please allow me to humor myself and replace the aforementioned noun “people” with “atoms” or their intrinsic properties of electrons, protons, and neutrons. By so doing, one might have to contemplate such topics as magnetism and collision and the products of these actions. This would immediately give rise to thoughts of mass, electricity, and excitement. Without magnetism (attraction), electricity, and excitement, whatever would we be left with? As I move more forcefully into this exercise, I find myself in increasingly unfamiliar territory I may study pretense, but I am not a pretender at least insofar as suggesting to anyone willing to listen (or read) that l have “real” knowledge about anything pertaining to physics. In fact, I am ever so happy to leave the study of the Higgs boson to that group of scholars engaged in research at CERN’s Large Hadron Collider.

For the time being, I will escape from any contemplation of physics and swiftly return to thinking about a planet on which people appear to exist without laws of attraction. If the “people” who inhabit the planet do not collide, we are left with the inevitability of what solitude would eventually predict, a nothingness, an emptiness, a void. If “people” did not collide, did not interact, there would be no “us.” Relationships would not exist; there would be no human groups, no communities, no cultures. There would be no sense of values, norms, rules, laws. Social hierarchies would not exist; there would be no need to think about mindreading, perspective taking, interpersonal problemsolving. Liking, loving, accepting, rejecting, excluding, victimizing none of these significant constructs would be relevant. Social comparison, self-appraisal, felt security, loneliness, rejection sensitivity topics that tend to appear regularly in the Developmental, Social, Personality, Cognitive, and Clinical Psychology literatures would be irrelevant. From my admittedly limited perspective, as a Developmental Scientist (and thankfully not as a Physicist), there would be nothing to write, think, feel, or be about.

Thank goodness for those nuclear researchers at CERN. They have taught us that magnetism matters, that interactions matter, that clusters matter (and may collide to produce new entities). These folks are not pondering what happens with people, they are thinking at the subatomic level. I, on the other hand, have spent the past 40-some years thinking about people, their individual characteristics, their interactions and collisions with one another, the relationships that are formed on the basis of their interactions, and the groups, communities, and cultures within which these individuals and relationships can be found. Indeed, I have collected more than a fair share of data on these topics. In so doing, I am left with the conclusion that solitude, isolation, and social withdrawal can be ruinous. It ain’t science fiction.

A Second Thought Experience

Let’s move to a rather different thought experience. Imagine that the community within which we live teaches its inhabitants, from early childhood, that normative sociocultural expectations involve helping, sharing, and caring with and for each other; teaching each other about that which defines the “good, bad, and ugly”; communicating with each other about norms and what may happen when one conforms to or violates them. Imagine too, that in such a community within which interaction, cooperation, and relationships matter, there are some individuals who, for whatever reason, do not interact with their confreres. One might suppose that the remaining members of the community could ponder why it is that these solitary individuals behave as they do. And several suggestions may be offered for their solitude.

For example, it may be suggested that some of these noninteracting individuals have some biological or perhaps some genetic orientation that leads them to feel uncomfortable in the presence of others. Perhaps members of the community may have read something about a gene that is associated with diminished 5-HTT transcription and reduced serotonin uptake. Some in the community may have read somewhere that without the regulating effects of serotonin, the amygdala and hypothalamic-pituitary-adrenal (HPA) system can become overactive, leading to the physiological profile of a fearful or anxious individual.

Fear may be a guiding force for these solitary individuals fear of what may happen if they approach others in the community; fear of what may happen if they attempt to develop a nonfamilial relationship with another in the community; fear of leaving a negative impression on those who may judge their actions, thoughts, emotions, and behaviors.

Or perhaps, some might believe that it is not fear that guides the behaviors of some of these solitary individuals. Instead, it might be proposed that some of these noninteracting individuals have a biological orientation that leads them to prefer a solitary existence. These individuals may feel more positively inclined when in the company of inanimate objects things.

At this point, our second thought experience leaves us with the identification of two “types” of solitary individuals:

1. Those who are motivated by fear, the prospects of social appraisal, and heightened sensitivity to the possibility of rejection;

2. Those who have a distinct preference for solitude.

Regardless of the epidemiological “causes” of solitary behavior, in a society that has strong beliefs in the importance of cooperation, collaboration, and caregiving, it is likely that the majority of individuals who adhere to the cultural ethos would begin to think unpleasant thoughts about the noninteracting minority. They may think of solitary individuals as displaying unacceptable, discomfiting behavior; they may begin to feel negatively about them; they may discuss among themselves the need to exclude these noninteractors or to alter the behavior of these nonconforming individuals. Indeed, from the extant research, it is known that those who display behaviors considered to be inappropriate or abhorrent to the majority may be isolated by the group-at-large.

And so now we have a third group of solitary individuals those who have been isolated by the social group.

But how would these hypothetical community responses affect the nonsocial, nonconforming individual? What kinds of interactive/noninteractive cycles would be generated? And what would the solitary individuals think and feel about the larger community responses to them?

The Point

The preceding verbiage brings me to the singular message that I am attempting to convey. From “all of the above,” I am willing to step out on a limb to suggest, straight-out, that solitude can be punishing, humbling, debilitating, and destructive.

I do admit that it would be foolish to ignore the perspectives of those who have sung the praises of solitude. This would include several authors of chapters in this compendium. It would also include the many beloved and respected authors, poets, painters, philosophers, spiritualists, and scientists who have suggested that their best work or their deepest thoughts derive from those moments when they are able to escape the madding crowd. Here are a few examples:

1 “You do not need to leave your room. Remain sitting at your table and listen. Do not even listen, simply wait, be quiet still and solitary. The world will freely offer itself to you to be unmasked, it has no choice, it will roll in ecstasy at your feet.” Franz Kafka

2 “How much better is silence; the coffee cup, the table. How much better to sit by myself like the solitary seabird that opens its wings on the stake. Let me sit here forever with bare things, this coffee cup, this knife, this fork, things in themselves, myself being myself.” Virginia Woolf

I could offer hundreds of quotations about the glories of solitude from rather well known people. Nevertheless, from my perhaps distorted, limited, and ego-centered perspective, I find it difficult to believe that one can lead a productive and happy life locked in a closet, a cave, a tent, a room. Virginia Woolf committed suicide; Kafka had documented psychological difficulties vis-a-vis his inability to develop and maintain positive and supportive relationships with others.

One may prefer solitude and many of us require solitude for contemplation, exploration, problem solving, introspection, and the escape of pressures elicited by the social/academic/employment/political communities. As I noted in the opening paragraph, solitude may be an entirely acceptable pursuit. But this statement comes with several provisos.

The “ifs”

If one spends time alone voluntarily, and if one can join a social group when one wants to, and if one can regulate one’s emotions (e.g., social fears and anger) effectively, and if one can initiate and maintain positive, supportive relationships with significant others, then the solitary experience can be productive.

But the provisos that I have appended to the solitary experience are rather significant. I am quite certain that what the reader will come away with after having completed the chapters included herein is that solitude has many faces. These faces have varied developmental beginnings, concomitants, and courses. And these faces may be interpreted in different ways in different contexts, communities, and cultures. And perhaps most importantly, the provisos offered previously must be kept in mind regardless of context, community, and culture. Frankly, if one fails to be mindful of these provisos, one can return to the introductory thought experiment and be assured that the failure of individuals to “collide” with one another will result in unpleasant consequences.

People do need to collide, or better put, interact with others. Of course, these interactions must be viewed by both partners as acceptable, positive, and productive. These interactions must be need fulfilling. Drawing from the wisdom of others who have written of the significance of such interactions (e.g., John Bowlby and Robert Hinde), one might expect that a product of these interactive experiences is the expectation of the nature of future interactions with the same partners. Furthermore, from this perspective, one might expect that each partner is likely to develop a set of expectations about the nature of future interactions with unknown others. If the interactions experienced are pleasant and productive, then positive dyadic relationships may result. if, however, the interactions experienced are unpleasant or agonistic, the partners may avoid each other. And in some cases, if a particular individual comes to expect that all interactions will eventually prove negative, withdrawal from the social community may result.

A Final Comment: Annus horribilis

During the first six months of 2012, I “lived” in a hospital after having endured a heart transplant and numerous health complications. Although I was surrounded by medical staff and had many regular visitors, I was literally isolated from the “outside world.” For the first two months of my hospitalization, my mind and body were at the river’s edge. But when the neurons began firing somewhat normally (beginning March 2012), and when I was able to converse with hospital staff and visitors, I nevertheless felt totally alone. It did not help that when visitors (and medical staff) met with me, they were required to wear masks, gloves, and medical gowns of one sort or another.

Eventually, it struck me that I was living at the extreme edge of what I had been studying for most of my professional career. And just as I had found through the use of questionnaires, interviews, rating scales, and observations (with samples of children and adolescents, and their parents, peers, and friends), solitude brought with it intrapersonal feelings of loneliness, sadness, anxiety, helplessness, and hopelessness. I felt disconnected from my personal and professional communities. Despite visitors’ generosity and kindness, I was miserable. Of course, when I was able to read and use my laptop, I could have taken the opportunity to play with ideas and data; my solitude could have been productive. But negative affect (emotion dysregulation) got in the way.

Upon return home, I rehabilitated and received visitors family, friends, colleagues, students, former golf and hockey “buddies.” I welcomed news about family (I was especially grateful to be reunited with my grandchildren!), friends, academe, and the world at large. I began to catch up on the various projects that my lab was involved in. Within a matter of weeks, I was coauthoring manuscripts and preparing abstracts for submission to various conferences. Although physically weak and incapable of taking lengthy walks or lifting anything heavier than a few pounds, my spirits were greatly improving, I was no longer alone! And finally, by August, when I returned to campus for the first time, I felt reconnected and valued!

The bottom line is that my personal solitude, especially given that it was experienced for a lengthy period of time and “enforced” externally and involuntarily, resulted in unpleasant consequences. The good news is that I have come to believe that the data my colleagues and I have collected over the years are actually meaningful beyond the halls of academe! Spending an inordinate time alone; feeling disconnected, rejected, and lonely; being excluded and perhaps victimized by others; being unable to competently converse with and relate to others (which may well result from solitude) can create a life of misery and malcontent; in some cases, this combination of factors may result in attempts at self-harm; in other cases it may result in attempts to harm others. Think for a moment about how often perpetrators of violence (e.g., Columbine, Virginia Tech, Newton High School, and the Boston Marathon bombings) have been described as loners, withdrawn, victimized, isolated, and friendless. Indeed, think about how some of the perpetrators have described themselves.

As I write this last sentence, my mind drifts to the lyricist/songwriting team of Eddie Vedder and Jeff Ament. Their evocative song “Jeremy” is based, in part, on the description of the death of Jeremy Wade Delle, a 15-year-old high school student in Richardson, Texas. Jeremy is portrayed as a quiet, sad adolescent who “spoke in class today” by committing suicide (by gunshot) in the presence of his classmates. The lyrics also suggest that the Jeremy in the song suffered parental abuse and/or neglect. In the music video, Jeremy appears to be rejected, excluded, and isolated by his peers. The words “harmless,” “peers,” and “problem” appear throughout the video. And in interviews about the “meanings” of the lyrics, Vedder has suggested that he was attempting to draw attention to one possible consequence of difficulties that can be produced by familial and peer disruptions. More importantly, he argued that one must gather one’s strength to fight against the seeming inevitability of the negative consequences of isolation, solitude, and rejection. I would suggest that the central message is that family members, peers, school personnel, and community leaders should be aware of the signs that presage intra and interpersonal desolation.

Of course, not all people described as “solitary” or “isolated” have intra or interpersonal problems. As noted previously, solitude and social withdrawal are not “necessarily evil.” We all need time alone to energize and re-energize, to mull, to produce this-and-that without interruption. But our species is a social species. So much is gained when people interact, collaborate, help, and care for others, develop relationships, and become active members of groups and communities. However, when combined with dysregulated emotions, social incompetence, and a lack of supportive relationships, solitude, much like many other behavioral constructs studied by psychologists, can induce miserable consequences. The “trick” is to know if, when, and how to intervene within the family, peer group, and community.

In closing, it is with pleasure and pride that two of my former students (and current colleagues and close friends) have done such a wonderful job in putting together this compendium on solitude. After all, I do believe that once upon a time, I may have introduced the constructs of social withdrawal and solitude to Rob Coplan and Julie Bowker! Somehow, I doubt that I instructed or commandeered Rob and Julie to study solitude, isolation, and aloneness. If memory serves me correct, they were each interested in things social. All I happened to do was provide them with a personal, historical (perhaps hysterical) note about how and why I became interested in the research I was doing. Of course, I could never claim to have played a role in the thoughts and research of those who have examined solitude from the perspectives of anthropology, biology, computer science, divinity, neuroscience, political science, primatology, psychoanalysis, sociology, and those tracks of psychology that focus primarily on personality, the environment, autism, and adult relationships. Therein lies the beauty of this compendium.

Editors Coplan and Bowker have cleverly taken a twisty turn that curves beyond their own comfort zones of Developmental Science. By so doing, they have left me absolutely delighted. Coplan and Bowker have clearly attempted to move the reader into multiple zones of cognitive disequilibration and to appreciate that if we are to truly understand any given phenomenon, we must look well beyond the silos within which we are typically reinforced to reside.

You now hold in your hands a selection of readings that describe a variety of perspectives on solitude. You will read what solitude looks like; why it is that people spend time alone; why it is that solitude can be a necessary experience; how it feels and what one thinks about when one spends a good deal of time avoiding others or being rejected and excluded by one’s social community. There is no compendium quite like the one that you are handling. I applaud the editors’ efforts, and I do hope that the reader does herself/himself justice by closely examining chapters that move well beyond their own self-defined areas of expertise and intrapersonal comfort tunnels.

1 All Alone

Multiple Perspectives on the Study of Solitude

Robert J. Coplan, Department of Psychology, Carleton University, Ottawa, Canada

Julie C. Bowker, Department of Psychology, University at Buffalo, USA


Seems I’m not alone in being alone. Gordon Matthew Sumner (1979)

The experience of solitude is a ubiquitous phenomenon. Historically, solitude has been considered both a boon and a curse, with artists, poets, musicians, and philosophers both lauding and lamenting being alone. Over the course of the lifespan, humans experience solitude for many different reasons and subjectively respond to solitude with a wide range of reactions and consequences. Some people may retreat to solitude as a respite from the stresses of life, for quiet contemplation, to foster creative impulses, or to commune with nature. Others may suffer the pain and loneliness of social isolation, withdrawing or being forcefully excluded from social interactions. Indeed, we all have and will experience different types of solitude in our lives.

The complex relationship we have with solitude and its multifaceted nature is reflected in our everyday language and culture. We can be alone in a crowd, alone with nature, or alone with our thoughts. Solitude can be differentially characterized along the full range of a continuum from a form of punishment (e.g., timeouts for children, solitary confinement for prisoners) to a less than ideal context (e.g., no man is an island, one is the loneliest number, misery loves company), all the way to a desirable state (e.g., taking time for oneself, needing your space or alone time).

In this Handbook, we explore the many different faces of solitude, from perspectives inside and outside of psychology. In this introductory chapter, we consider some emergent themes in the historical study of solitude (see Figure 1.1) and provide an overview of the contents of this volume.

Figure 1.1 Emergent themes in the psychological study of solitude.

Emergent Themes

The study of solitude cuts across virtually all psychology subdisciplines and has been explored from multiple and diverse theoretical perspectives across the lifespan. Accordingly, it is not surprising that there remains competing hypotheses regarding the nature of solitude and its implications for well-being. Indeed, from our view, these fundamentally opposed differential characterizations of solitude represent the most pervasive theme in the historical study of solitude as a psychological construct.

In essence, this ongoing debate about the nature of solitude can be distilled down to an analysis of its costs versus benefits.

Solitude is bad

Social affiliations are relationships that have long been considered to be adaptive to the survival of the human species. Indeed, social groups offer several well-documented evolutionary advantages: e.g., protection against predators, cooperative hunting, and food sharing. The notion that solitude may have negative consequences has a long history and can literally be traced back to biblical times: Genesis 2:18, And the LORD God said “It is not good for the man to be alone”.

Within the field of psychology, Triplett (1898) demonstrated in one of the earliest psychology experiments that children performed a simple task (pulling back a fishing reel) more slowly when alone than when paired with other children performing the same task. Thus, at the turn of the century, it was clear that certain types of performance were hindered by solitude.

Developmental psychologists have also long suggested that excessive solitude during childhood can cause psychological pain and suffering, damage critically important family relationships, impede the development of the self-system, and prevent children from learning from their peers. The profound psychological impairments caused by extreme cases of social isolation in childhood, in cases such as Victor (Lane, 1976) or Genie (Curtiss, 1977), have emphasized that human contact is a basic necessity of development.

Social psychologists have also long considered the need for affiliation to be a basic human need. Early social psychology studies on small group dynamics, such as the Robbers Cave experiments, further highlighted the ways in which intergroup conflict can emerge and how out-group members can become quickly perceived negatively and in a stereotypical fashion and become mistreated. More recently, the need to belong theory has suggested that we all have a fundamental need to belong or be accepted and to maintain positive relationships with others, and that the failure to fulfill such needs can lead to significant physical and psychological distress. Relatedly, social neuroscientists now suggest that loneliness and social isolation can be bad not only for our psychological functioning and well-being but also for our physical health.

Finally, from the perspective of clinical psychology, social isolation has been traditionally viewed as a target criterion for intervention. In the first edition of the Diagnostic statistical manual of mental disorders, people who failed to relate effectively to others could be classified as suffering from either a psychotic disorder, such as schizophrenia; a psychoneurotic disorder, such as anxiety; or a personality disorder, such as an inadequate personality, characterized by inadaptability, ineptness, poor judgment, lack of physical and emotional stamina, and social incompatibility.

Schizoid personality disorder is described as another personality disorder characterized by social difficulties, specifically social avoidance. Interestingly, children with schizoid personalities are described as quiet, shy, and sensitive; adolescents were described as withdrawn, introverted, unsociable, and as shut-ins.

Solitude can be good

In stark contrast, and from a very different historical tradition, many theorists and researchers have long called attention to the benefits of being alone.

For example, a central question for ancient Greek and Roman philosophers was the role of the group in society and the extent to which the individual should be a part of and separate from the group in order to achieve wisdom, excellence, and happiness. Later, Montaigne acknowledged the difficulties of attaining solitude but argued that individuals should strive for experiences of solitude to escape pressures, dogma, conventional ways of thinking and being, vices, and the power of the group. For Montaigne, the fullest experiences of solitude could not be guaranteed by physical separation from others; instead, solitude involved a state of natural personal experience that could be accomplished both alone and in the company of others.

Related ideas can be found in religious writings and theology. For example, Thomas Merton, a Trappist monk who spent many years in solitude, passionately argued in several books and essays that solitude offered unique experiences for contemplation and prayer and that solitary retreats are necessary to achieve authentic connections with others.

Ideas about the benefits of solitude can also be found in the writings of Winnicott (1958). For Winnicott, solitude was an experience of aloneness afforded by a good enough facilitating environment and was a necessary precondition during infancy and childhood for later psychological maturity and self-discovery and self-realization.

In adulthood, spending time alone and away from others has also long been argued by philosophers, authors, and poets to be necessary for imaginative, creative, and artistic enterprises (e.g., Thoreau, 1854). In these perspectives, solitary experiences provide benefits when the individual chooses to be alone. However, personal stories of several accomplished authors, such as Beatrix Potter and Emily Dickinson, suggest that creativity and artistic talents may also develop in response to long periods of painful social isolation and rejection (Middleton, 1935; Storr, 1988).

Underlying mechanisms of solitude

Although the costs versus benefits debate regarding solitude is somewhat all-encompassing, nested within this broader distinction is a theme pertaining to the different mechanisms that may underlie our experiences of solitude. To begin with, it is important to distinguish between instances when solitude is other imposed versus sought after. Rubin (1982) was one of the first psychologists to describe these different processes as distinguishing between social isolation, where the individual is excluded, rejected, or ostracized by their peer group, and social withdrawal, where the individual removes themselves from opportunities for social interaction.

As we have previously discussed, there are long-studied negative consequences that accompany being socially isolated from one’s group of peers. Thus, we turn now to a consideration of varying views regarding why individuals might chose to withdraw into solitude.

Within the psychological literature, researchers have highlighted several different reasons why individuals may seek out solitude, including a desire for privacy (Pedersen, 1979), the pursuance of religious experiences (Hay & Morisey, 1978), the simple enjoyment of leisure activities (Purcell & Keller, 1989), and seeking solace from or avoiding upsetting situations (Larson, 1990).

Biological and neurophysiological processes have also been considered as putative sources of solitary behaviors. For example, the ancient Greeks and Romans argued that biologically based individual differences in character help to determine mood (such as fear and anxiety) and social behavioral patterns (such as the tendency to be sociable or not), ideas which were precursors to the contemporary study of child temperament (Kagan & Fox, 2006). As well, recent interest in the specific neural systems that may be involved in social behaviors can be traced to the late 1800s with the case of Phineas Gage, who injured his orbitofrontal cortex in a railroad construction accident and afterwards was reported to no longer adhere to social norms or to be able to sustain positive relationships (Macmillan, 2000).

Finally, there is also a notable history of research pertaining to motivations for social contact (e.g., Murphy, 1954; Murray, 1938), which has been construed as a primary substrate of human personality (Eysenck, 1947). An important distinction was made between social approach and social avoidance motivations (Lewinsky, 1941; Mehrabian & Ksionzky, 1970). It has since been argued that individual differences in these social motivations further discriminate different reasons why individuals might withdraw from social interactions. For example, a low social approach motivation, or solitropic orientation, is construed as a non-fearful preference for solitude in adults (Burger, 1995; Cheek & Buss, 1981; Leary, Herbst, & McCrary, 2001) and children (Asendorpf, 1990; Coplan, Rubin, Fox, Calkins, & Stewart, 1994). In contrast, the conflict between competing social approach and social avoidance motivations (i.e., approach-avoidance conflict) is thought to lead to shyness and social anxiety (Cheek & Melchior, 1990; Jones, Briggs, & Smith, 1986).

Developmental timing effects of solitude

Our final theme has to do with developmental timing or when (or at what age/developmental period) experiences of solitude occur. The costs of solitude are often assumed to be greater during childhood than in adolescence or adulthood given the now widely held notion that the young developing child requires a significant amount of positive peer interaction for healthy social, emotional, and social-cognitive development and well-being (Rubin, Bukowski, & Parker, 2006). This pervasive belief may explain, in part, why considerably more developmental research on the concomitants of social withdrawal has focused on children as compared to adolescents. In addition, it is during adolescence that increasing needs for and enjoyment of privacy and solitude are thought to emerge (Larson, 1990). For this reason, it has been posited that some of the negative peer consequences often associated with social withdrawal during childhood, such as peer rejection and peer victimization, may diminish during the adolescent developmental period (Bowker, Rubin, & Coplan, 2012). However, it has also long been argued that solitude at any age can foster loneliness and psychological angst, particularly if it is other-imposed.

As mentioned previously, social needs are thought to exist in individuals of all ages, with several social and developmental theories suggesting that psychological well-being is determined by whether social needs are satisfied. For example, Sullivan (1953) posited that all individuals have social needs but that with development, the nature of the social needs change (e.g., with puberty, needs for sexual relations emerge), as well as the type of relationship required to fulfill the needs (e.g., relationships with parents might satisfy early needs for tenderness; same-sex chumships or best friendships might satisfy needs for intimacy that emerge in early adolescence). Regardless of the developmental changes, however, Sullivan argued that if social needs were not fulfilled, significant negative self-system and psychological consequences would ensue. Consistent with these latter ideas are research findings that have identified loneliness, at any age, as one of the strongest risk factors for psychological illbeing (Heinrich & Gullone, 2006).

The debate as to when in development solitude might carry the greatest costs is yet to be resolved. However, it must also be acknowledged that the very nature of solitary experiences likely changes with age. For example, young children may retreat to their rooms, engage in solitary play in the company of peers, or find themselves forced to the periphery of social groups. Although other-imposed solitude might be manifested similarly at older ages (e.g., adolescents being forced to eat alone at lunchtime, adults being left out of afterwork gatherings), adolescents and adults have greater control over and increased opportunities for selfselected solitary experiences relative to children. For example, adolescents are sometimes left alone without parental supervision in their homes or able to take themselves to places of their choosing. Adults can also choose to travel alone, can engage in meditative and religious retreats, and can select relatively solitary occupations and ways to spend their free time. In contrast, there may come a time in the life of an older adult where they are significantly impeded in their ability to actively seek out social contacts. It remains to be seen how these potential differences in agency pertaining to solitude across the lifespan speak to the relation between solitude and well-being.

Final Comments: Solitude…Together?

It is somewhat ironic that the future study of solitude will likely be pursued within the context of an everexpanding and increasingly connected global social community. The chapter authors in this Handbook span 13 countries and represent only the very tip of the iceberg in terms of cross-cultural research in this area. There is growing evidence to suggest that both the meaning and impact of (different types of) solitude differ substantively across cultures (e.g., Chen & French, 2008). Accordingly, it is critically important to embed this psychological research within a larger cultural context.

Moreover, as evidenced by the chapters in the final section of this volume, psychologists have much to learn about the study of solitude from our colleagues in other disciplines. Indeed, we should expect interdisciplinary collaboration to eventually become the norm in these (and other) research areas. Such collaborations will allow us to further explore both the depth and breadth of our experiences of solitude and perhaps help to resolve some of the great debates in theory and research on solitude, such as when and why solitude causes harm or brings benefits.

Finally, rapidly evolving technological advances intend to connect all of us all of the time to social and informational networks. This inevitably leads to the question as to whether any of us will ever truly be alone in the future. It is certain that our relationship with solitude will necessarily evolve in the digital age. In this regard, it remains to be seen if the experience of solitude is itself doomed to become an archaic remnant of a past era.

*

from

The Handbook Of Solitude. Psychological Perspectives on Social Isolation, Social Withdrawal, and Being Alone.

get it at Amazon.com

Mental Illness, Why Some and not Others? Gene-Environment Interaction and Differential Susceptibility – Scott Barry Kaufman * Gene-Environment Interaction in Psychological Traits and Disorders – Danielle M. Dick * Differential Susceptibility to Environmental Influences – Jay Belsky.

“Whether your story is about having met with emotional pain or physical pain, the important thing is to take the lid off of those feelings. When you keep your emotions repressed, that’s when the body starts to try to get your attention. Because you aren’t paying attention. Our childhood is stored up in our bodies, and one day, the body will present its bill.”

Bernie Siegel MD


In recent years numerous studies show the importance of gene-environment interactions in psychological development, but here’s the thing: we’re not just finding that the environment matters in determining whether mental illness exists. What we’re discovering is far more interesting and nuanced: Some of the very same genes that under certain environmental conditions are associated with some of the lowest lows of humanity, under supportive conditions are associated with the highest highs of human flourishing.

Evidence that adverse rearing environments exert negative effects particularly on children and adults presumed “vulnerable” for temperamental or genetic reasons may actually reflect something else: heightened susceptibility to the negative effects of risky environments and to the beneficial effects of supportive environments. Putatively vulnerable children and adults are especially susceptible to both positive and negative environmental effects.

Children rated highest on externalizing behavior problems by teachers across the primary school years were those who experienced the most harsh discipline prior to kindergarten entry and who were characterized by mothers at age 5 as being negatively reactive infants.

Susceptibility factors are the moderators of the relation between the environment and developmental outcome. Is it that negativity actually reflects a highly sensitive nervous system on which experience registers powerfully negatively when not regulated by the caregiver, but positively when coregulation occurs?
Referred to by some scientists as the “differential susceptibility hypothesis”, these findings shouldn’t be understated. They are revolutionary, and suggest a serious rethinking of the role of genes in the manifestation of our psychological traits and mental “illness”. Instead of all of our genes coding for particular psychological traits, it appears we have a variety of genetic mutations that are associated with sensitivity to the environment, for better and worse.

Known epigenetic modifications (cell specialization, X inactivation, genomic imprinting) all occur early in development and are stable. The discovery that epigenetic modifications continue to occur across development, and can be reversible and more dynamic, has represented a major paradigm shift in our understanding of environmental regulation of gene expression.

Glossary
Gene: Unit of heredity; a stretch of DNA that codes for a protein.
GxE: Gene-environment Interaction.
Epigenetics: Modifications to the genome that do not involve a change in nucleotide sequence.
Heritability: The proportion of total phenotypic variance that can be accounted for by genetic factors.
Logistic Regression: A statistical method for analyzing a dataset in which there are one or more independent variables that determine an outcome. The outcome is measured with a dichotomous variable (in which there are only two possible outcomes).
In logistic regression, the dependent variable is binary or dichotomous, i.e. it only contains data coded as 1 (TRUE, success, pregnant, etc.) or 0 (FALSE, failure, non-pregnant, etc.)
Transcription Factor: In molecular biology, a transcription factor (TF) (or sequence-specific DNA-binding factor) is a protein that controls the rate of transcription of genetic information from DNA to messenger RNA, by binding to a specific DNA sequence. The function of TFs is to regulate – turn on and off – genes in order to make sure that they are expressed in the right cell at the right time and in the right amount throughout the life of the cell and the organism.
Nucleotide: Organic molecules that are the building blocks of DNA and RNA. They also have functions related to cell signaling, metabolism, and enzyme reactions.
MZ: Monozygotic. Of twins derived from a single ovum (egg), and so identical.
DZ: Dizygotic. Of twins derived from two separate ova (eggs). Fraternal twin or nonidentical twin.
DNA: Deoxyribonucleic Acid.
RNA: Ribonucleic acid is a polymeric molecule essential in various biological roles in coding, decoding, regulation, and expression of genes. RNA and DNA are nucleic acids, and, along with lipids, proteins and carbohydrates, constitute the four major macromolecules essential for all known forms of life.
Polymorphism: A location in a gene that comes in multiple forms.
Allele: Natural variation in the genetic sequence; can be a change in a single nucleotide or longer stretches of DNA.
GWAS: Genome-wide Association Study.
ORs: Odds Ratios.
Phenotype: The observed outcome under study; can be the manifestation of both genetic and/or environmental factors.
Dichotomy: A division or contrast between two things that are or are represented as being opposed or entirely different.
Chromosome: A single piece of coiled DNA containing many genes, regulatory elements, and other nucleotide sequences.

Gene-Environment Interaction and Differential Susceptibility

Scott Barry Kaufman

Only a few genetic mutations have been discovered so far that demonstrate differential susceptibility effects. Most of the genes that have been discovered contribute to the production of the neurotransmitters dopamine and serotonin. Both of these biological systems contribute heavily to many aspects of engagement with the world, positive emotions, anxiety, depression, and mood fluctuations. So far, the evidence suggests (but is still tentative) that certain genetic variants under harsh and abusive conditions are associated with anxiety and depression, but that the very same genetic variants are associated with the lowest levels of anxiety, depression, and fear under supportive, nurturing conditions. There hasn’t been too much research looking at differential susceptibility effects on other systems that involve learning and exploration, however.

Enter a brand new study

Rising superstar Rachael Grazioplene and colleagues focused on the cholinergic system, a biological system crucially involved in neural plasticity and learning. Situations that activate the cholinergic system involve “expected uncertainty” such as going to a new country you’ve never been before and knowing that you’re going to face things you’ve never faced before. This stands in contrast to “unexpected uncertainty”, which occurs when your expectations are violated, such as thinking you’re going to a Las Vegas family friendly Cirque Du Soleil only to realize you’ve actually gotten a ticket to an all-male dance revue called “Thunder from Down Under” (I have no idea where that example came from). Those sorts of experiences are more strongly related to the neurotransmitter norepinephrine.

Since the cholinergic system is most active in situations when a person can predict that learning is possible, this makes the system a prime candidate for the differential susceptibility effect. As the researchers note, unpredictable and novel environments could function as either threats or incentive rewards. When the significance of the environment is uncertain, both caution and exploration are adaptive. Therefore, traits relating to anxiety or curiosity should be influenced by cholinergic genetic variants, with developmental experiences determining whether individuals find expected uncertainty either more threatening or more promising.

To test their hypothesis, they focused on a polymorphism in the CHRNA4 gene, which builds a certain kind of neural receptor that the neurotransmitter binds to. These acetylcholine receptors are distributed throughout the brain, and are especially involved in the functioning of dopamine in the striatum. Genetic differences in the CHRNA4 gene seem to change the sensitivity of the brain’s acetylcholine system because small structural changes in these receptors make acetylcholine binding more or less likely. Previous studies have shown associations between variation in the CHRNA4 gene and neuroticism as well as laboratory tests of attention and working memory.

The researchers looked at the functioning of this gene among a group of 614 children aged 8-13 enrolled in a week long day camp. Half of the children in the day camp were selected because they had been maltreated (sexual maltreatment), whereas the other half was carefully selected to come from the same socioeconomic status but not have experienced any maltreatment. This study provides the ideal experimental design and environmental conditions to test the differential susceptibility effect. Not only were the backgrounds of the children clearly defined, but also dramatically different from each other. Additionally, all children engaged in the same novel learning environment, an environment well suited for cholinergic functioning. What did they find?

Individuals with the T/T variation of the CHRNA4 gene who were maltreated showed higher levels of anxiety (Neuroticism) compared to those with the C allele of this gene. They appeared to be more likely to learn with higher levels of uncertainty. In contrast, those with the T/T allele who were not maltreated were low in anxiety (Neuroticism) and high in curiosity (Openness to Experience). What’s more, this effect was independent of age, race, and sex.

These environments, the T/T allele (which is much rarer in the general population than the C allele) may be beneficial, bringing out lower levels of anxiety and increased curiosity in response to situations containing expected uncertainty.

These results are certainly exciting, but a few important caveats are in order. For one thing, the T/T genotype is very rare in the general population, which makes it all the more important for future studies to attempt to replicate these findings. Also, we’re talking vanishingly small effects here. The CHRNA4 variant only explained at most 1% of the variation in neuroticism and openness to experience. So we shouldn’t go around trying to predict individual people’s futures based on knowledge of a single gene and a single environment.

Scientifically speaking though, this level of prediction is expected based on the fact that all of our psychological dispositions are massively polymorphic (consists of many interacting genes). Both gene-gene and gene-environment interactions must be taken into account.

Indeed, recent research found that the more sensitivity (“plasticity”) genes relating to the dopamine and serotonin systems adolescent males carried, the less selfregulation they displayed under unsupportive parenting conditions. In line with the differential susceptibility effect, the reverse was also found: higher levels of selfregulation were displayed by the adolescent males carrying more senstivity genes when they were reared under supportive parenting conditions.

The findings by Grazioplene and colleagues add to a growing literature on acetylcholine’s role in the emergence of schizophrenia and mood disorders. As the researcher’s note, these findings, while small in effect, may have maltreatment is a known risk factor for many psychiatric disorders. Children with the T/T genotype of CHRNA4 rsl 044396 may be more likely to learn fearful responses in harsh and abusive environments, but children with the very same genotype may be more likely to display curiosity and engagement in response to uncertainty under normal or supportive conditions.

While it’s profoundly difficult predicting the developmental trajectory of any single individual, this research suggests we can influence the odds that people will retreat within themselves or unleash the fundamentally human drive to explore and create.

Gene-Environment Interaction in Psychological Traits and Disorders

Danielle M. Dick

There has been an explosion of interest in studying gene-environment interactions (GxE) as they relate to the development of psychopathology. In this article, I review different methodologies to study gene-environment interaction, providing an overview of methods from animal and human studies and illustrations of gene-environment interactions detected using these various methodologies. Gene-environment interaction studies that examine genetic influences as modeled latently (e.g., from family, twin, and adoption studies) are covered, as well as studies of measured genotypes.

Importantly, the explosion of interest in gene-environment interactions has raised a number of challenges, including difficulties with differentiating various types of interactions, power, and the scaling of environmental measures, which have profound implications for detecting gene-environment interactions. Taking research on gene-environment interactions to the next level will necessitate close collaborations between psychologists and geneticists so that each field can take advantage of the knowledge base of the other.

INTRODUCTION

Gene-environment interaction (GxE) has become a hot topic of research, with an exponential increase in interest in this area in the past decade. Consider that PubMed lists only 24 citations for “gene environment interaction” prior to the year 2000, but nearly four times that many in the first half of the year 2010 alone! The projected publications on gene-environment interaction for 2008–2010 are on track to constitute more than 40% of the total number of publications on gene-environment interaction indexed in PubMed.

Where does all this interest stem from? It may, in part, reflect a merging of interests from fields that were traditionally at odds with one another. Historically, there was a perception that behavior geneticists focused on genetic influences on behavior at the expense of studying environmental influences and that developmental psychologists focused on environmental influences and largely ignored genetic factors. Although this criticism is not entirely founded on the part of either field, methodological and ideological differences between these respective fields meant that genetic and environmental influences were traditionally studied in isolation.

More recently, there has been recognition on the part of both of these fields that both genetic and environmental influences are critical components to developmental outcome and that it is far more fruitful to attempt to understand how these factors come together to impact psychological outcomes than to argue about which one is more important. As Kendler and Eaves argued in their article on the joint effect of genes and environments, published more than two decades ago:

It is our conviction that a complete understanding of the etiology of most psychiatric disorders will require an understanding of the relevant genetic risk factors, the relevant environmental risk factors, and the ways in which these two risk factors interact. Such understanding will only arise from research in which the important environmental variables are measured in a genetically informative design. Such research will require a synthesis of research traditions within psychiatry that have often been at odds with one another in the past. This interaction between the research tradition that has focused on the genetic etiology of psychiatric illness and that which has emphasized environmental causation will undoubtedly be to the benefit of both. (Kendler & Eaves 1986, p. 288)

The PubMed data showing an exponential increase in published papers on gene-environment interaction suggest that that day has arrived. This has been facilitated by the rapid advances that have taken place in the field of genetics, making the incorporation of genetic components into traditional psychological studies a relatively easy and inexpensive endeavor. But with this surge of interest in gene-environment interaction, a number of new complications have emerged, and the study of gene-environment interaction faces new challenges, including a recent backlash against studying gene-environment interaction (Risch et al. 2009). Addressing these challenges will be critical to moving research on gene-environment interaction forward in a productive way.

In this article, I first review different study designs for detecting gene-environment interaction, providing an overview of methods from animal and human studies. I cover gene-environment interaction studies that examine genetic influences as modeled latently as well as studies of measured genotypes. In the study of latent gene-environment interaction, specific genotypes are not measured, but rather genetic influence is inferred based on observed correlations between people who have different degrees of genetic and environmental sharing. Thus, latent gene-environment interaction studies examine the aggregate effects of genes rather than any one specific gene.

Molecular genetic studies, in contrast, have generally focused on one specific gene of interest at a time. Relevant examples of gene-environment interaction across these different methodologies are provided, though these are meant to be more illustrative than exhaustive, intended to introduce the reader to relevant studies and findings generated across these various designs.

Subsequently I review more conceptual issues surrounding the study of gene-environment interaction, covering the nature of gene-environment interaction effects as well as the challenges facing the study of gene-environment interaction, such as difficulties with differentiating various types of interactions, and how issues such as the scaling of environmental measures can have profound implications for studying gene-environment interaction.

I include an overview of epigenetics, a relatively new area of study that provides a potential biological mechanism by which the environment can moderate gene expression and affect behavior.

Finally, I conclude with recommendations for future directions and how we can take research on gene-environment interaction to the next level.

DEFINING GENE-ENVIRONMENT INTERACTION AND DIFFERENTIATING GENE-ENVIRONMENT CORRELATION

It is important to first address some aspects of terminology surrounding the study of gene-environment interaction. In lay terms, the phrase gene-environment interaction is often used to mean that both genes and environments are important. In statistical terms, this does not necessarily indicate an interaction but could be consistent with an additive model, in which there are main effects of the environment and main effects of genes.

But in a statistical sense an interaction is a very specific thing, referring to a situation in which the effect of one variable cannot be understood without taking into account the other variable. Their effects are not independent. When we refer to gene-environment interaction in a statistical sense, we are referring to a situation in which the effect of genes depends on the environment and/or the effect of the environment depends on genotype. We note that these two alternative conceptualizations of gene-environment interaction are indistinguishable statistically. It is this statistical definition of gene-environment interaction that is the primary focus of this review (except where otherwise noted).

It is also important to note that genetic and environmental influences are not necessarily independent factors. That is to say that although some environmental influences may be largely random, such as experiencing a natural disaster, many environmental influences are not entirely random (Kendler et al. 1993).

This phenomenon is called gene-environment correlation.

Three specific ways by which genes may exert an effect on the environment have been delineated (Plomin et al. 1977, Scarr & McCartney 1983):

(a) Passive gene-environment correlation refers to the fact that among biologically related relatives (i.e., nonadoptive families), parents provide not only their children’s genotypes but also their rearing environment. Therefore, the child’s genotype and home environment are correlated.

(b) Evocative gene-environment correlation refers to the idea that individuals’ genotypes influence the responses they receive from others. For example, a child who is predisposed to having an outgoing, cheerful disposition might be more likely to receive positive attention from others than a child who is predisposed to timidity and tears. A person with a grumpy, abrasive temperament is more likely to evoke unpleasant responses from coworkers and others with whom he/she interacts than is a cheerful, friendly person. Thus, evocative gene-environment correlation can influence the way an individual experiences the world.

(c) Active gene-environment correlation refers to the fact that an individual actively selects certain environments and takes away different things from his/her environment, and these processes are influenced by an individual’s genotype. Therefore, an individual predisposed to high sensation seeking may be more prone to attend parties and meet new people, thereby actively influencing the environments he/she experiences.

Evidence exists in the literature for each of these processes. The important point is that many sources of behavioral influence that we might consider “environmental” are actually under a degree of genetic influence (Kendler & Baker 2007), so often genetic and environmental influences do not represent independent sources of influence. This also makes it difficult to determine whether the genes or the environment is the causal agent. If, for example, individuals are genetically predisposed toward sensation seeking, and this makes them more likely to spend time in bars (a gene-environment correlation), and this increases their risk for alcohol problems, are the predisposing sensation-seeking genes or the bar environment the causal agent?

In actuality, the question is moot, they both played a role; it is much more informative to try to understand the pathways of risk than to ask whether the genes or the environment was the critical factor. Though this review focuses on gene-environment interaction, it is important for the reader to be aware that this is but one process by which genetic and environmental influences are intertwined. Additionally, gene-environment correlation must be taken into account when studying gene-environment interaction, a point that is mentioned again later in this review. Excellent reviews covering the nature and importance of gene-environment correlation also exist (Kendler 2011).

METHODS FOR STUDYING GENE-ENVIRONMENT INTERACTION

Animal Research

Perhaps the most straightforward method for detecting gene-environment interaction is found in animal experimentation: Different genetic strains of animals can be subjected to different environments to directly test for gene-environment interaction. The key advantage of animal studies is that environmental exposure can be made random to genotype, eliminating gene-environment correlation and associated problems with interpretation.

The most widely cited example of this line of research is Cooper and Zubek’s 1958 experiment, in which rats were selectively bred to perform differently in a maze-running experiment (Cooper & Zubek 1958). Under standard environmental conditions, one group of rats consistently performed with few errors (“maze bright”), while a second group committed many errors (“maze dull”). These selectively bred rats were then exposed to various environmental conditions: an enriched condition, in which rats were reared in brightly colored cages with many moveable objects, or a restricted condition, in which there were no colors or toys. The enriched condition had no effect on the maze bright rats, although it substantially improved the performance of the maze dull rats, such that there was no difference between the groups.

Conversely, the restrictive environment did not affect the performance of the maze dull rats, but it substantially diminished the performance of the maze bright rats, again yielding no difference between the groups and demonstrating a powerful gene-environment interaction.

A series of experiments conducted by Henderson on inbred strains of mice, in which environmental enrichment was manipulated, also provides evidence for gene-environment interaction on several behavioral tasks (Henderson 1970, 1972). These studies laid the foundation for many future studies, which collectively demonstrate that environmental variation can have considerable differential impact on outcome depending on the genetic make-up of the animal (Wahlsten et al. 2003).

However, animal studies are not without their limitations. Gene-environment interaction effects detected in animal studies are still subject to the problem of scale (Mather & Jinks 1982), as discussed in greater detail later in this review.

Human Research

Traditional behavior genetic designs

Demonstrating gene-environment interaction in humans has been considerably more difficult where ethical constraints require researchers to make use of natural experiments so environmental exposures are not random. Three traditional study designs have been used to demonstrate genetic influence on behavior: family studies, adoption studies, and twin studies. These designs have been used to detect gene-environment interaction also, and each is discussed in turn.

Family studies

Demonstration that a behavior aggregates in families is the first step in establishing a genetic basis for a disorder (Hewitt & Turner 1995). Decreasing similarity with decreasing degrees of relatedness lends support to genetic influence on a behavior (Gottesman 1991). This is a necessary, but not sufficient, condition for heritability. Similarity among family members is due both to shared genes and shared environment; family studies cannot tease apart these two sources of variance to determine whether familiality is due to genetic or common environmental causes (Sherman et al. 1997).

However, family studies provide a powerful method for identifying gene-environment interaction. By comparing high-risk children, identified as such by the presence of psychopathology in their parents, with a control group of low-risk individuals, it is possible to test the effects of environmental characteristics on individuals varying in genetic risk (Cannon et al. 1990).

In a high-risk study of Danish children with schizophrenic mothers and matched controls, institutional rearing was associated with an elevated risk of schizophrenia only among those children with a genetic predisposition (Cannon et al. 1990). When these subjects were further classified on genetic risk as having one or two affected parents, a significant interaction emerged between degree of genetic risk and birth complications in predicting ventricle enlargement: The relationship between obstetric complications and ventricular enlargement was greater in the group of individuals with one affected parent as compared to controls, and greater still in the group of individuals with two affected parents (Cannon et al. 1993). Another study also found that among individuals at high risk for schizophrenia, experiencing obstetric complications was related to an earlier hospitalization (Malaspina et al. 1999).

Another creative method has made use of the natural experiment of family migration to demonstrate gene-environment interaction: The high rate of schizophrenia among African-Caribbean individuals who emigrated to the United Kingdom is presumed to result from gene-environment interaction. Parents and siblings of first-generation African-Caribbean probands have risks of schizophrenia similar to those for white individuals in the area. However, the siblings of second-generation African-Caribbean probands have markedly elevated rates of schizophrenia, suggesting that the increase in schizophrenia rates is due to an interaction between genetic predispositions and stressful environmental factors encountered by this population (Malaspina et al. 1999, Moldin & Gottesman 1997).

Although family studies provide a powerful design for demonstrating gene-environment interaction, there are limitations to their utility. High-risk studies are very expensive to conduct because they require the examination of individuals over a long period of time. Additionally, a large number of high-risk individuals must be studied in order to obtain a sufficient number of individuals who eventually become affected, due to the low base rate of most mental disorders. Because of these limitations, few examples of high-risk studies exist.

Adoption studies

Adoption and twin studies are able to clarify the extent to which similarity among family members is due to shared genes versus shared environment. In their simplest form, adoption studies involve comparing the extent to which adoptees resemble their biological relatives, with whom they share genes but not family environment, with the extent to which adoptees resemble their adoptive relatives, with whom they share family environment but not genes.

Adoption studies have been pivotal in advancing our understanding of the etiology of many disorders and drawing attention to the importance of genetic factors. For example, Heston’s historic adoption study was critical in dispelling the myth of schizophrenogenic mothers in favor of a genetic transmission explaining the familiality of schizophrenia (Heston & Denney 1967).

Furthermore, adoption studies provide a powerful method of detecting gene-environment interactions and have been called the human analogue of strain-by-treatment animal studies (Plomin & Hershberger 1991). The genotype of adopted children is inferred from their biological parents, and the environment is measured in the adoptive home. Individuals thought to be at genetic risk for a disorder, but reared in adoptive homes with different environments, are compared to each other and to control adoptees.

This methodology has been employed by a number of research groups to document gene-environment interactions in a variety of clinical disorders: In a series of Iowa adoption studies, Cadoret and colleagues demonstrated that a genetic predisposition to alcohol abuse predicted major depression in females only among adoptees who also experienced a disturbed environment, as defined by psychopathology, divorce, or legal problems among the adoptive parents (Cadoret et al. 1996).

In another study, depression scores and manic symptoms were found to be higher among individuals with a genetic predisposition and a later age of adoption (suggesting a more transient and stressful childhood) than among those with only a genetic predisposition (Cadoret et al. 1990).

In an adoption study of Swedish men, mild and severe alcohol abuse were more prevalent only among men who had both a genetic predisposition and more disadvantaged adoptive environments (Cloninger et al. 1981).

The Finnish Adoptive Family Study of Schizophrenia found that high genetic risk was associated with increased risk of schizophrenic thought disorder only when combined with communication deviance in the adoptive family (Wahlberg et al. 1997).

Additionally, the adoptees had a greater risk of psychological disturbance, defined as neuroticism, personality disorders, and psychoticism, when the adoptive family environment was disturbed (Tienari et al. 1990).

These studies have demonstrated that genetic predispositions for a number of psychiatric disorders interact with environmental influences to manifest disorder.

However, adoption studies suffer from a number of methodological limitations. Adoptive parents and biological parents of adoptees are often not representative of the general population. Adoptive parents tend to be socioeconomically advantaged and have lower rates of mental problems, due to the extensive screening procedures conducted by adoption agencies (Kendler 1993). Biological parents of adoptees tend to be atypical, as well, but in the opposite way. Additionally, selective placement by adoption agencies is confounding the clear-cut separation between genetic and environmental effects by matching adoptees and adoptive parents on demographics, such as race and religion. An increasing number of adoptions are also allowing contact between the biological parents and adoptive children, further confounding the traditional genetic and environmental separation that made adoption studies useful for genetically informative research.

Finally, greater contraceptive use is making adoption increasingly rare (Martin et al. 1997). Accordingly, this research strategy has become increasingly challenging, though a number of current adoption studies continue to make important contributions to the field (Leve et al. 2010; McGue et al. 1995, 1996).

Twin studies

Twins provide a number of ways to study gene-environment interaction. One such method is to study monozygotic twins reared apart (MZA). MZAs provide a unique opportunity to study the influence of different environments on identical genotypes. In the Swedish Adoption/Twin Study of Aging, data from 99 pairs of MZAs were tested for interactions between childhood rearing and adult personality (Bergeman et al. 1988).

Several significant interactions emerged. In some cases, the environment had a stronger impact on individuals genetically predisposed to be low on a given trait (based on the cotwin’s score). For example, individuals high in extraversion expressed the trait regardless of the environment; however, individuals predisposed to low extraversion had even lower scores in the presence of a controlling family.

In other traits, the environment had a greater impact on individuals genetically predisposed to be high on the trait: Individuals predisposed to impulsivity were even more impulsive in a conflictual family environment; individuals low on impulsivity were not affected.

Finally, some environments influenced both individuals who were high and low on a given trait, but in opposite directions: Families that were more involved masked genetic differences between individuals predisposed toward high or low neuroticism, but greater genetic variation emerged in less controlling families.

The implementation of population-based twin studies, inclusion of measured environments into twin studies, and advances in biometrical modeling techniques for twin data made it possible to study gene-environment interaction within the framework of the classic twin study. Traditional twin studies involve comparisons of monozygotic (MZ) and dizy-gotic (DZ) twins reared together. MZ twins share all of their genetic variation, whereas DZ twins share on average 50% of their genetic make-up; however, both types of twins are age-matched siblings sharing their family environments. This allows heritability, or the proportion of variance attributed to additive genetic effects, to be estimated by (a) doubling the difference between the correlation found between MZ twins and the correlation found between DZ twins, for quantitative traits, or ( b ) comparing concordance rates between MZs and DZs, for qualitative disorders (McGue & Bouchard 1998).

Biometrical model-fitting made it possible for researchers to address increasingly sophisticated research questions by allowing one to statistically specify predictions made by various hypotheses and to compare models testing competing hypotheses. By modeling data from subjects who vary on exposure to a specified environment, one could test whether there is differential expression of genetic influences in different environments.

Early examples of gene-environment interaction in twin models necessitated “grouping” environments to fit multiple group models. The basic idea was simple: Fit models to data for people in environment 1 and environment 2 separately and then test whether there were significant differences in the importance of genetic and environmental factors across the groups using basic structural equation modeling techniques. In an early example of gene-environment interaction, data from the Australian twin register were used to test whether the relative importance of genetic effects on alcohol consumption varied as a function of marital status, and in fact they did (Heath et al. 1989).

Having a marriage-like relationship reduced the impact of genetic influences on drinking: Among the younger sample of twins, genetic liability accounted for but half as much variance in drinking among married women (31%) as among unmarried women (60%). A parallel effect was found among the adult twins: Genetic effects accounted for less than 60% of the variance in married respondents but more than 76% in unmarried respondents (Heath et al. 1989).

In an independent sample of Dutch twins, religiosity was also shown to moderate genetic and environmental influences on alcohol use initiation in females (with nonsignificant trends in the same direction for males): In females without a religious upbringing, genetic influences accounted for 40% of the variance in alcohol use initiation compared to 0% in religiously raised females. Shared environmental influences were far more important in the religious females (Koopmans et al. 1999).

In data from our population-based Finnish twin sample, we also found that regional residency moderates the impact of genetic and environmental influences on alcohol use. Genetic effects played a larger role in longitudinal drinking patterns from late adolescence to early adulthood among individuals residing in urban settings, whereas common environmental effects exerted a greater in-fluence across this age range among individuals in rural settings (Rose et al. 2001).

When one has pairs discordant for exposure, it is also possible to ask about genetic correlation between traits displayed in different environments.

One obvious limitation of modeling gene-environment interaction in this way was that it constrained investigation to environments that fell into natural groupings (e.g., married/unmarried; urban/rural) or it forced investigators to create groups based on environments that may actually be more continuous in nature (e.g., religiosity). In the first extension of this work to quasi-continuous environmental moderation, we developed a model that allowed genetic and environmental influences to vary as a function of a continuous environmental moderator and used this model to follow-up on the urban/rural interaction reported previously (Dick et al. 2001).

We believed it likely that the urban/rural moderation effect reflected a composite of different processes at work. Accordingly, we expanded the analyses to incorporate more specific information about neighborhood environments, using government-collected information about the specific municipalities in which the twins resided (Dick et al. 2001). We found that genetic influences were stronger in environments characterized by higher rates of migration in and out of the municipality; conversely, shared environmental influences predominated in local communities characterized by little migration.

We also found that genetic predispositions were stronger in communities composed of a higher percentage of young adults slightly older than our age-18 Finnish twins and in regions where there were higher alcohol sales.

Further, the magnitude of genetic moderation observed in these models that allowed for variation as a function of a quasi-continuous environmental moderator was striking, with nearly a fivefold difference in the magnitude of genetic effects between environmental extremes in some cases.

The publication of a paper the following year (Purcell 2002) that provided straightforward scripts for continuous gene-environment interaction models using the most widely used program for twin analyses, Mx (Neale 2000), led to a surge of papers studying gene-environment interaction in the twin literature. These scripts also offered the advantage of being able to take into account gene-environment correlation in the context of gene-environment interaction. This was an important advance because previous examples of gene-environment interaction in twin models had been limited to environments that showed no evidence of genetic effects so as to avoid the confounding of gene-environment interaction with gene-environment correlation.

Using these models, we have demonstrated that genetic influences on adolescent substance use are enhanced in environments with lower parental monitoring (Dick et al. 2007c) and in the presence of substance-using friends (Dick et al. 2007b). Similar effects have been demonstrated for more general externalizing behavior: Genetic influences on antisocial behavior were higher in the presence of delinquent peers (Button et al. 2007) and in environments characterized by high parental negativity (Feinberg et al. 2007), low parental warmth (Feinberg et al. 2007), and high paternal punitive discipline (Button et al. 2008).

Further, in an extension of the socioregional-moderating effects observed on age-18 alcohol use, we found a parallel moderating role of these socioregional variables on age-14 behavior problems in girls in a younger Finnish twin sample. Genetic influences assumed greater importance in urban settings, communities with greater migration, and communities with a higher percentage of slightly older adolescents.

Other psychological outcomes have also yielded significant evidence of gene-environment interaction effects in the twin literature. For example, a moderating effect, parallel to that reported for alcohol consumption above, has been reported for depression symptoms (Heath et al. 1998) in females. A marriage-like relationship reduced the influence of genetic liability to depression symptoms, paralleling the effect found for alcohol consumption: Genetic factors accounted for 29% of the variance in depression scores among married women, but for 42% of the variance in young unmarried females and 51% of the variance in older unmarried females (Heath et al. 1998).

Life events were also found to moderate the impact of factors influencing depression in females (Kendler et al. 1991). Genetic and/or shared environmental influences were significantly more important in influencing depression in high-stress than in low-stress environments, as defined by a median split on a life-event inventory, although there was insufficient power to determine whether the moderating influence was on genetic or environmental effects.

More than simply accumulating examples of moderation of genetic influence by environmental factors, efforts have been made to integrate this work into theoretical frameworks surrounding the etiology of different clinical conditions. This is critical if science is to advance beyond individual observations to testable broad theories.

A 2005 review paper by Shanahan and Hofer suggested four processes by which social context may moderate the relative importance of genetic effects (Shanahan & Hofer 2005).

The environment may (a) trigger or (b) compensate for a genetic predisposition, (c) control the expression of a genetic predisposition, or (d ) enhance a genetic predisposition (referring to the accentuation of “positive” genetic predispositions).

These processes are not mutually exclusive and can represent different ends of a continuum. For example, the interaction between genetic susceptibility and life events may represent a situation whereby the experience of life events triggers a genetic susceptibility to depression. Conversely, “protective” environments, such as marriage-like relationships and low stress levels, can buffer against or reduce the impact of genetic predispositions to depressive problems.

Many different processes are likely involved in the gene-environment interactions observed for substance use and antisocial behavior. For example, family environment and peer substance use/delinquency likely constitute a spectrum of risk or protection, and family/friend environments that are at the “poor” extreme may trigger genetic predispositions toward substance use and antisocial behavior, whereas positive family and friend relationships may compensate for genetic predispositions toward substance use and antisocial behavior.

Social control also appears to be a particularly relevant process in substance use, as it is likely that being in a marriage-like relationship and/or being raised with a religious upbringing exert social norms that constrain behavior and thereby reduce genetic predispositions toward substance use.

Further, the availability of the substance also serves as a level of control over the ability to express genetic predispositions, and accordingly, the degree to which genetic influences will be apparent on an outcome at the population level. In a compelling illustration of this effect, Boardman and colleagues used twin data from the National Survey of Midlife Development in the United States and found a significant reduction in the importance of genetic influences on people who smoke regularly following legislation prohibiting smoking in public places (Boardman et al. 2010).

Molecular analyses

All of the analyses discussed thus far use latent, unmeasured indices of genetic influence to detect the possible presence of gene-environment interaction. This is largely because it was possible to test for the presence of latent genetic influence in humans (via comparisons of correlations between relatives with different degrees of genetic sharing) long before molecular genetics yielded the techniques necessary to identify specific genes influencing complex psychological disorders.

However, recent advances have made the collection of deoxyribonucleic acid (DNA) and resultant genotyping relatively cheap and straightforward. Additionally, the publication of hig profile papers brought gene-environment interaction to the forefront of mainstream psychology. In a pair of papers published in Science in 2002 and 2003, respectively, Caspi and colleagues analyzed data from a prospective, longitudinal sample from a birth cohort from New Zealand, followed from birth through adulthood.

In the 2002 paper, they reported that a functional polymorphism in the gene encoding the neurotransmitter-metabolizing enzyme monoamine oxidase A (MAOA) moderated the effect of maltreatment: Males who carried the genotype conferring high levels of MAOA expression were less likely to develop antisocial problems when exposed to maltreatment (Caspi et al. 2002). In the 2003 paper, they reported that a functional polymorphism in the promoter region of the serotonin transporter gene (5-HTT) was found to moderate the influence of stressful life events on depression. Individuals carrying the short allele of the 5-HTT promoter polymorphism exhibited more depressive symptoms, diagnosable depression, and suicidality in relation to stressful life events than did individuals homozygous for the long allele (Caspi et al. 2003).

Both studies were significant in demonstrating that genetic variation can moderate individuals’ sensitivity to environmental events.

These studies sparked a multitude of reports that aimed to replicate, or to further extend and explore, the findings of the original papers, resulting in huge literatures surrounding each reported gene-environment interaction in the years since the original publications (e.g., Edwards et al. 2009, Enoch et al. 2010, Frazzetto et al. 2007, Kim-Cohen et al. 2006, McDermott et al. 2009,Prom-Wormley et al. 2009, Vanyukov et al. 2007, Weder et al. 2009). It is beyond the scope of this review to detail these studies; however, of note was the publication in 2009 of a highly publicized meta-analysis of the interaction between 5-HTT, stressful life events, and risk of depression that concluded there was “no evidence that the serotonin transporter genotype alone or in interaction with stressful life events is associated with an elevated risk of depression in men alone, women alone, or in both sexes combined” (Risch et al. 2009). Further, the authors were critical of the rapid embracing of gene-environment interaction and the substantial resources that have been devoted to this research.

The paper stimulated considerable backlash against the study of gene-environment interactions, and the pendulum appeared to be swinging back the other direction. However, a recent review by Caspi and colleagues entitled “Genetic Sensitivity to the Environment: The Case of the Serotonin Transporter Gene and Its Implications for Studying Complex Diseases and Traits” highlighted the fact that evidence for involvement of 5-HTT in stress sensitivity comes from at least four different types of studies, including observational studies in humans, experimental neuroscience studies, studies in nonhuman primates, and studies of 5HTT mutations in rodents (Caspi et al. 2010).

Further, the authors made the distinction between different cultures of evaluating gene-environment interactions: a purely statistical (theory-free) approach that relies wholly on meta-analysis (e.g., such as that taken by Risch et al. 2009) versus a construct-validity (theory-guided) approach that looks for a nomological network of convergent evidence, such as the approach that they took.

It is likely that this distinction also reflects differences in training and emphasis across different fields. The most cutting-edge genetic strategies at any given point, though they have changed drastically and rapidly over the past several decades, have generally involved atheoretical methods for gene identification (Neale et al. 2008). This was true of early linkage analyses, where ~400 to 1,000 markers were scanned across the genome to search for chromosomal regions that were shared by affected family members, suggesting there may be a gene in that region that harbored risk for the particular outcome under study. This allowed geneticists to search for genes without having to know anything about the underlying biology, with the ideas that the identification of risk genes would be informative as to etiological processes and that our understanding of the biology of most psychiatric conditions is limited.

Although it is now recognized that linkage studies were underpowered to detect genes of small effect, such as those now thought to be operating in psychiatric conditions, this atheoretical approach was retained in the next generation of gene-finding methods that replaced linkage, the implementation of genome-wide association studies (GWAS) (Cardon 2006). GWAS also have the general framework of scanning markers located across the entire genome in an effort to detect association between genetic markers and disease status; however, in GWAS over a million markers (or more, on the newest genetic platforms) are analyzed.

The next technique on the horizon is sequencing, in which entire stretches of DNA are sequenced to know the exact base pair sequence for a given region (McKenna et al. 2010).

From linkage to sequencing, common across all these techniques is an atheoretical framework for finding genes that necessarily involves conducting very large numbers of tests. Accordingly, there has been great emphasis in the field of genetics on correction for multiple testing (van den Oord 2007). In addition, the estimated magnitude of effect size of genetic variants thought to influence complex behavioral outcomes has been continually shifted downward as studies that were sufficiently powered to detect effect sizes previously thought to be reasonable have failed to generate positive findings (Manolio et al. 2009). GWAS have led the field to believe that genes influencing complex behavioral outcomes likely have odds ratios (ORs) on the order of magnitude of 1.1. This has led to a need for incredibly large sample sizes, requiring meta-analytic GWAS efforts with several tens of thousands of subjects (Landi et al. 2009, Lindgren et al. 2009).

It is important to note there has been increasing attention to the topic of gene-environment interaction from geneticists (Engelman et al. 2009). This likely reflects, in part, frustration and difficulty with identifying genes that impact complex psychiatric outcomes. Several hypotheses have been put forth as possible explanations for the failure to robustly detect genes involved in psychiatric outcomes, including a genetic model involving far more genes, each of very small effect, than was previously recognized, and failure to pay adequate attention to rare variants, copy number variants, and gene-environment interaction (Manolio et al. 2009).

Accordingly, gene-environment interaction is being discussed far more in the area of gene finding than in years past; however, these discussions often involve atheoretical approaches and center on methods to adequately detect gene-environment interaction in the presence of extensive multiple testing (Gauderman 2002, Gauderman et al. 2010). The papers by Risch et al. (2009) and Caspi et al. (2010) on the interaction between 5-HTT, life stress, and depression highlight the conceptual, theoretical, and practical differences that continue to exist between the fields of genetics and psychology surrounding the identification of gene-environment interaction effects.

THE NATURE OF GENE-ENVIRONMENT INTERACTION

An important consideration in the study of gene-environment interaction is the nature, or shape, of the interaction that one hypothesizes. There are two primary types of interactions.

One type of interaction is the fan-shaped interaction. In this type of interaction, the influence of genotype is greater in one environmental context than in another. This is the kind of interaction that is hypothesized by a diathesis-stress framework, whereby genetic influences become more apparent, i.e., are more strongly related to outcome, in the presence of negative environmental conditions. There is a reduced (or no) association of genotype with outcome in the absence of exposure to particular environmental conditions.

The literature surrounding depression and life events would be an example of a hypothesized fan-shaped interaction: When life stressors are encountered, genetically vulnerable individuals are more prone to developing depression, whereas in the absence of life stressors, these individuals may be no more likely to develop depression. In essence, it is only when adverse environmental conditions are experienced that the genes “come on-line.”

Gene-environment interactions in the area of adolescent substance use are also hypothesized to be fan-shaped, where some environmental conditions will allow greater opportunity to express genetic predispositions, allowing for more variation by genotype, and other environments will exert social control in such a way as to curb genetic expression (Shanahan & Hofer 2005), leading to reduced genetic variance.

Twin analyses yielding evidence of genetic influences being more or less important in different environmental contexts are generally suggestive of fan-shaped interactions. Changes in the overall heritability do not necessarily dictate that any one specific susceptibility gene will operate in a parallel manner; however, a change in heritability suggests that at least a good portion of the involved genes (assuming many genes of approximately equal and small effect) must be operating in that manner for a difference in heritability by environment to be detectable.

The diathesis-stress model has largely been the dominant model in psychiatry. Gene-finding efforts have focused on the search for vulnerability genes, and gene-environment interaction has been discussed in the context of these genetic effects becoming more or less important under particular environmental conditions.

Different types of gene-environment interactions.

More recently, an alternative framework has been proposed by Belsky and colleagues, the differential susceptibility hypothesis, in which the same individuals who are most adversely affected by negative environments may also be those who are most likely to benefit from positive environments. Rather than searching for “vulnerability genes” influencing psychiatric and behavioral outcomes, they propose the idea of “plasticity genes,” or genes involved in responsivity to environmental conditions (Belsky et al. 2009).

Belsky and colleagues reviewed the literatures surrounding gene-environment interactions associated with three widely studied candidate genes, MAOA, 5-HTT, and DRD4, and suggested that the results provide evidence for differential susceptibility associated with these genes (Belsky et al. 2009).

Their hypothesis is closely related to the concept of biological sensitivity to context (Ellis & Boyce 2008). The idea of biological sensitivity to context has its roots in evolutionary developmental biology, whereby selection pressures should favor genotypes that support a range of phenotypes in response to environmental conditions because this flexibility would be beneficial from the perspective of survival of the species. However, biological sensitivity to context has the potential for both positive effects under more highly supportive environmental conditions and negative effects in the presence of more negative environmental conditions. This theory has been most fully developed and discussed in the context of stress reactivity (Boyce & Ellis 2005), where it has been demonstrated that highly reactive children show disproportionate rates of morbidity when raised in adverse environments, but particularly low rates when raised in low-stress, highly supportive environments (Ellis et al. 2005). In these studies, high reactivity was defined by response to different laboratory challenges, and the authors noted that the underlying cellular mechanisms that would produce such responses are currently unknown, though genetic factors are likely to play a role (Ellis & Boyce 2008).

Although fan-shaped and crossover interactions are theoretically different, in practice, they can be quite difficult to differentiate. One can imagine several “variations on the theme” for both fan-shaped and crossover interactions. In general for a fan-shaped interaction, a main effect of genotype will be present as well as a main effect of the environment. There is a main effect of genotype at both environmental extremes; it is simply far stronger in environment 5 (far right side of the graph) as compared to environment 1 (far left side). But one could imagine a fan-shaped interaction where there was no genotypic effect at one extreme (e.g., the lines converge to the same phenotypic mean at environment).

Further, fan-shaped interactions can differ in the slope of the lines for each genotype, which indicate how much the environment is modifying genetic effects. In the crossover interaction shown above, the lines cross at environment 3 (i.e., in the middle). But crossover interactions can vary in the location of the crossover. It is possible that crossing over only occurs at the environmental extreme.

As previously noted, the crossing over of the genotypic groups in the Caspi et al. publications of the interactions between the 5-HTT gene, life events, and depression (Caspi et al. 2003) and between MAOA, maltreatment, and antisocial behavior (Caspi et al. 2002) occurred at the extreme low ends of the environmental measures, and the degree of crossing over was quite modest. Rather, the shape of the interactions (and the way the interactions were conceptualized in the papers) was largely fan-shaped, whereby certain genotypic groups showed stronger associations with outcome as a function of the environmental stressor.

Also, in both cases, the genetic variance was far greater under one environmental extreme than the other, rather than being approximately equivalent at both ends of the distribution, but with genotypic effects in opposite directions. In general, it is assumed that main effects of genotype will not be detected in crossover interactions, but this will actually depend on the frequency of the different levels of the environment. This is also true of fan-shaped interactions, but to a lesser degree.

Evaluating the relative importance, or frequency of existence, of each type of interaction is complicated by the fact that there is far more power to detect crossover interactions than fan-shaped interactions. Knowing that most of our genetic studies are likely underpowered, we would expect a preponderance of crossover effects to be detected as compared to fan-shaped effects purely as a statistical artifact. Further, even when a crossover effect is observed, power considerations can make it difficult to determine if it is “real.” For example, an interaction observed in our data between the gene CHRM2, parental monitoring, and adolescent externalizing behavior yielded consistent evidence for a gene-environment interaction, with a crossing of the observed regression lines. However, the mean differences by genotype were not significant at either end of the environmental continuum, so it is unclear whether the crossover reflected true differential susceptibility or simply overfitting of the data across the environmental levels containing the majority of the observations, which contributed to a crossing over of the regression lines at one environmental extreme (Dick et al. 2011).

Larger studies would have greater power to make these differentiations; however, there is the unfortunate paradox that the samples with the greatest depth of phenotypic information, allowing for more complex tests about risk associated with particular genes, usually have much smaller sample sizes due to the trade-off necessary to collect the rich phenotypic information. This is an important issue for gene-environment interaction studies in general: Most have been underpowered, and this raises concerns about the likelihood that detected effects are true positives. There are several freely available programs to estimate power (Gauderman 2002, Purcell et al. 2003), and it is critical that papers reporting gene-environment interaction effects (or a lack thereof) include information about the power of their sample in order to interpret the results.

Another widely contested issue is whether gene-environment interactions should be examined only when main effects of genotype are detected. Perhaps not surprisingly, this is the approach most commonly advocated by statistical geneticists (Risch et al. 2009) and that was recommended by the Psychiatric GWAS Consortium (Psychiatr. GWAS Consort. Steer. Comm. 2008). However, this strategy could preclude the detection of crossover interaction effects as well as gene-environment interactions that occur in the presence of relatively low-frequency environments. In addition, if genetic effects are conditional on environmental exposure, main effects of genotype could vary across samples, that is to say, a genetic effect could be detected in one sample and fail to replicate in another if the samples differ on environmental exposure.

Another issue with the detection and interpretation of gene-environment interaction effects involves the range of environments being studied. For example, if we assume that the five levels of the environment shown above represent the true full range of environments that exist, if a particular study only included individuals from environments 3–5, it would conclude that there is a fan-shaped gene-environment interaction. Belsky and colleagues (2009) have suggested this may be particularly problematic in the psychiatric literature because only in rare exceptions (Bakermans-Kranenburg & van Ijzendoorn 2006, Taylor et al. 2006) has the environment included both positive and negative ends of the spectrum. Rather, the absence of environmental stressors has usually constituted the “low” end of the environment, e.g., the absence of life stressors (Caspi et al. 2003) or the absence of maltreatment (Caspi et al. 2002). This could lead individuals to conclude there is a fan-shaped interaction because they are essentially failing to measure, with reference to figure above, environments 0-3, which represent the positive end of the environmental continuum. One can imagine a number of other incorrect conclusions that could be drawn about the nature of gene-environment interaction effects as a result of restricted range of environmental measures. For example, in B, measurement of individuals from environments 0-3 would lead one to conclude that genetic effects play a stronger role at lower levels of environmental exposure. Measurement of individuals from environments 3-5 would lead one to conclude that genetic effects play a stronger role at higher levels of exposure to the same environmental variable. In Figure A, if measurement of individuals was limited to environments 0-3, depending on sample size, there may be inadequate power to detect deviation from a purely additive genetic model, e.g., the slope of the genotypic lines may not be significantly different.

It is also important to note that not only are there several scenarios that would lead one to make incorrect conclusions about the nature of a gene-environment interaction effect, there are also scenarios that would lead one to conclude that a gene-environment interaction exists when it actually does not. Several of these are detailed in a sobering paper by my colleague Lindon Eaves, in which significant evidence for gene-environment interaction was detected quite frequently using standard regression methods, when the simulated data reflected strictly additive models (Eaves 2006). This was particularly problematic when using logistic regression where a dichotomous diagnosis was the outcome. The problem was further exaggerated when selected samples were analyzed.

An additional complication with evaluating gene-environment interactions in psychology is that often our environmental measures don’t have absolute scales of measurement. For example, what is the “real” metric for measuring a construct like parent-child bonding, or maltreatment, or stress? This becomes critical because fan-shaped interactions are very sensitive to scaling. Often a transformation of the scale scores will make the interaction disappear. What does it mean if the raw variable shows an interaction but the log transformation of the scale scores does not? Is the interaction real? Is one metric for measuring the environment a better reflection of the “real” nature of the environment than another?

Many of the environments of interest to psychologists do not have true metrics, such as those that exist for measures such as height, weight, or other physiological variables. This is an issue for the study of gene-environment interaction. It becomes even more problematic when you consider that logistic regression is the method commonly used to test for gene-environment interactions with dichotomous disease status outcomes. Logistic regression involves a logarithmic transformation of the probability of being affected. By definition, this changes the nature of the relationship between the variables being modeled. This compounds problems associated with gene-environment interactions being scale dependent.

EPIGENETICS: A POTENTIAL BIOLOGICAL MECHANISM FOR GENE-ENVIRONMENT INTERACTION

An enduring question remains in the study of gene-environment interaction: how does the environment “get under the skin”? Stated in another way:

What are the biological processes by which exposure to environmental events could affect outcome?

Epigenetics is one candidate mechanism. Excellent recent reviews on this topic exist (Meaney 2010, Zhang & Meaney 2010), and I provide a brief overview here.

It is important to note, however, that although epigenetics is increasingly discussed in the context of gene-environment interaction, it does not relate directly to gene-environment interaction in the statistical sense, as differentiated previously in this review. That is to say that epigenetic processes likely tell us something about the biological mechanisms by which the environment can affect gene expression and impact behavior, but they are not informative in terms of distinguishing between additive versus interactive environmental effects.

Although variability exists in defining the term, epigenetics generally refers to modifications to the genome that do not involve a change in nucleotide sequence. To understand this concept, let us review a bit about basic genetics.

The expression of a gene is influenced by transcription factors (proteins), which bind to specific sequences of DNA. It is through the binding of transcription factors that genes can be turned on or off. Epigenetic mechanisms involve changes to how readily transcription factors can access the DNA. Several different types of epigenetic changes are known to exist that involve different types of chemical changes that can regulate DNA transcription.

One epigenetic process that affects transcription binding is DNA methylation. DNA methylation involves the addition of a methyl group (CH3) onto a cytosine (one of the four base pairs that make up DNA). This leads to gene silencing because methylated DNA hinders the binding of transcription factors.

A second major regulatory mechanism is related to the configuration of DNA. DNA is wrapped around clusters of histone proteins to form nucleosomes. Together the nucleosomes of DNA and histone are organized into chromatin. When the chromatin is tightly condensed, it is difficult for transcription factors to reach the DNA, and the gene is silenced. In contrast, when the chromatin is opened, the gene can be activated and expressed. Accordingly, modifications to the histone proteins that form the core of the nucleosome can affect the initiation of transcription by affecting how readily transcription factors can access the DNA and bind to their appropriate sequence.

Epigenetic modifications of the genome have long been known to exist. For example, all cells in the body share the same DNA; accordingly, there must be a mechanism whereby different genes are active in liver cells than, for example, brain cells. The process of cell specialization involves silencing certain portions of the genome in a manner specific to each cell. DNA methylation is a mechanism known to be involved in cell specialization.

Another well known example of DNA methylation involves X-inactivation in females. Because females carry two copies of the X chromosome, one must be inactivated. The silencing of one copy of the X chromosome involves DNA methylation.

Genomic imprinting is another long established principle known to involve DNA methylation. In genomic imprinting the expression of specific genes is determined by the parent of origin. For example, the copy of the gene inherited from the mother is silenced, while the copy inherited from the father is active (or vice versa). The silent copy is inactive through processes involving DNA methylation. These changes all involve epigenetic processes parallel to those currently attracting so much attention.

However, the difference is that these known epigenetic modifications (cell specialization, X inactivation, genomic imprinting) all occur early in development and are stable.

The discovery that epigenetic modifications continue to occur across development, and can be reversible and more dynamic, has represented a major paradigm shift in our understanding of environmental regulation of gene expression.

Animal studies have yielded compelling evidence that early environmental manipulations can be associated with long-term effects that persist into adulthood. For example, maternal licking and grooming in rats is known to have long-term influences on stress response and cognitive performance in their offspring (Champagne et al. 2008, Meaney 2010). Further, a series of studies conducted in macaque monkeys demonstrates that early rearing conditions can result in long-term increased aggression, more reactive stress response, altered neurotransmitter functioning, and structural brain changes (Stevens et al. 2009). These findings parallel research in humans that suggests that early life experiences can have long-term effects on child development (Loman & Gunnar 2010). Elegant work in animal models suggests that epigenetic changes may be involved in these associations (Meaney 2010, Zhang & Meaney 2010).

Evaluating epigenetic changes in humans is more difficult because epigenetic marks can be tissue specific. Access to human brain tissue is limited to postmortem studies of donated brains, which are generally unique and unrepresentative samples and must be interpreted in the context of those limitations. Nonetheless, a recent study of human brain samples from the Quebec Suicide Brain Bank found evidence of increased DNA methylation of the exon 1F promoter in hippocampal samples from suicide victims compared with controls, but only if suicide was accompanied with a history of childhood maltreatment (McGowan et al. 2009). Importantly, this paralleled epigenetic changes originally observed in rat brain in the ortholog of this locus.

Another line of evidence suggesting epigenetic changes that may be relevant in humans is the observation of increasing discordance in epigenetic marks in MZ twins across time. This is significant because MZ twins have identical genotypes, and therefore, differences between them are attributed to environmental influences. In a study by Fraga and colleagues (2005), MZ twins were found to be epigenetically indistinguishable during the early years of life, but older MZ twins exhibited remarkable differences in their epigenetic profiles. These findings suggest that epigenetic changes may be a mechanism by which environmental influences contribute to the differences in outcome observed for a variety of psychological traits of interest between genetically identical individuals.

The above studies complement a growing literature demonstrating differences in gene expression in humans as a function of environmental experience. One of the first studies to analyze the relationship between social factors and human gene expression compared healthy older adults who differed in the extent to which they felt socially connected to others (Cole et al. 2007). Using expression profiles obtained from blood cells, a number of genes were identified that showed systematically different levels of expression in people who reported feeling lonely and distant from others.

Interestingly, these effects were concentrated among genes that are involved in immune response.

The results provide a biological mechanism that could explain why socially isolated individuals show heightened vulnerability to diseases and illnesses related to immune function.

Importantly, they demonstrate that our social worlds can exert biologically significant effects on gene expression in humans (for a more extensive review, see Cole 2009).

CONCLUSIONS

This review has attempted to provide an overview of the study of gene-environment interaction, starting with early animal studies documenting gene-environment interaction, to demonstrations of similar effects in family, adoption, and twin studies.

Advances in twin modeling and the relative ease with which gene-environment interaction can now be modeled has led to a significant increase in the number of twin studies documenting changing importance of genetic influence across environmental contexts. There is now widespread documentation of gene-environment interaction effects across many clinical disorders (Thapar et al. 2007).

These findings have led to more integrated etiological models of the development of clinical outcomes. Further, since it is now relatively straightforward and inexpensive to collect DNA and conduct genotyping, there has been a surge of studies testing for gene-environment interaction with specific candidate genes.

Psychologists have embraced the incorporation of genetic components into their studies, and geneticists who focus on gene finding are now paying attention to the environment in an unprecedented way. However, now that the initial excitement surrounding gene-environment interaction has begun to wear off, a number of challenges involved in the study of gene-environment interaction are being recognized.

These include difficulties with interpreting interaction effects (or the lack thereof), due to issues surrounding the measurement and scaling of the environment, and statistical concerns surrounding modeling gene-environment interactions and the nature of their effects.

So where do we go from here? Individuals who jumped on the gene-environment interaction bandwagon are now discovering that studying this process is harder than it first appeared. But there is good reason to believe that gene-environment interaction is a very important process in the development of clinical disorders. So rather than abandon ship, I would suggest that as a field, we just need to proceed with more caution.

SUMMARY POINTS

– Gene-environment interaction refers to the phenomenon whereby the effect of genes depends on the environment, or the effect of the environment depends on genotype. There is now widespread documentation of gene-environment interaction effects across many clinical disorders, leading to more integrated etiological models of the development of clinical outcomes.

– Twin, family, and adoption studies provide methods to study gene-environment interaction with genetic effects modeled latently, meaning that genes are not directly measured, but rather genetic influence is inferred based on correlations across relatives. Advances in genotyping technology have contributed to a proliferation of studies testing for gene-environment interaction with specific measured genes. Each of these designs has its own strengths and limitations.

– Two types of gene-environment interaction have been discussed in greatest detail in the literature: fan-shaped interactions, in which the influence of genotype is greater in one environmental context than in another; and crossover interactions, in which the same individuals who are most adversely affected by negative environments may also be those who are most likely to benefit from positive environments. Distinguishing between these types of interactions poses a number of challenges.

– The range of environments studied and the lack of a true metric for many environmental measures of interest create difficulties for studying gene-environment interactions. Issues surrounding power, and the use of logistic regression and selected samples, further compound the difficulty of studying gene-environment interactions. These issues have not received adequate attention by many researchers in this field.

– Epigenetic processes may tell us something about the biological mechanisms by which the environment can affect gene expression and impact behavior. The growing literature demonstrating differences in gene expression in humans as a function of environmental experience demonstrates that our social worlds can exert biologically significant effects on gene expression in humans.

– Much of the current work on gene-environment interactions does not take advantage of the state of the science in genetics or psychology; advancing this area of study will require close collaborations between psychologists and geneticists.

Differential Susceptibility to Environmental Influences

Jay Belsky

Evidence that adverse rearing environments exert negative effects particularly on children and adults presumed “vulnerable” for temperamental or genetic reasons may actually reflect something else: heightened susceptibility to the negative effects of risky environments and to the beneficial effects of supportive environments.

Building on Belsky’s (Belsky & Pluess) evolutionary inspired differential susceptibility hypothesis, stipulating that some individuals, including children, are more affected, both for better and for worse, by their environmental exposures and developmental experiences, recent research consistent with this claim is reviewed. It reveals that in many cases, including both observational field studies and experimental intervention ones, putatively vulnerable children and adults are especially susceptible to both positive and negative environmental effects. In addition to reviewing relevant evidence, unknowns in the differential susceptibility equation are highlighted.

Introduction

Most students of child development probably do not presume that all children are equally susceptible to rearing (or other environmental) effects; a long history of research on interactions between parenting and temperament, or parenting by temperament interactions, clearly suggests otherwise. Nevertheless, it remains the case that most work still focuses on effects of environmental exposures and developmental experiences that apply equally to all children so-called main effects of parenting or poverty or being reared by a depressed mother, thus failing to consider interaction effects, which reflect the fact that whether, how, and how much these contextual conditions influence the child may depend on the child’s temperament or some other characteristic of individuality.

Research on parenting-by-temperament interactions is based on the premise that what proves effective for some individuals in fostering the development of some valued outcome, or preventing some problematic one may simply not do so for others. Commonly tested are diathesis-stress hypotheses derived from multiplerisk/transactional frameworks in which individual characteristics that make children “vulnerable” to adverse experiences placing them “at risk” of developing poorly are mainly influential when there is at the same time some contributing risk from the environmental context (Zuckerman, 1999).

Diathesis refers to the latent weakness or vulnerability that a child or adult may carry (e.g., difficult temperament, particular gene), but which does not manifest itself, thereby undermining well-being, unless the individual is exposed to conditions of risk or stress.

After highlighting some research consistent with a diathesis-stress or dual-risk perspective, I raise questions on the basis of other findings about how the first set of data has been interpreted, advancing the evolutionary inspired proposition that some children, for temperamental or genetic reasons, are actually more susceptible to both (a) the adverse effects of unsupportive parenting and (b) the beneficial effects of supportive rearing.

Finally, I draw conclusions and highlight some “unknowns in the differential-susceptibility equation.”

Diathesis-Stress, Dual-Risk and Vulnerability

The view that infants and toddlers manifesting high levels of negative emotion are at special risk of problematic development when they experience poor quality rearing is widespread.

Evidence consistent with this view can be found in the work of Morrell and Murray, who showed that it was only highly distressed and irritable 4-month-old boys who experienced coercive and rejecting mothering at this age who continued to show evidence, 5 months later, of emotional and behavioural dysregulation. Relatedly, Belsky, Hsieh, and Cernic observed that infants who scored high in negative emotionality at 12 months of age and who experienced the least supportive mothering and fathering across their second and third years of life scored highest on externalizing problems at 36 months of age. And Deater, Deckard and Dodge reported that:

Children rated highest on externalizing behavior problems by teachers across the primary school years were those who experienced the most harsh discipline prior to kindergarten entry and who were characterized by mothers at age 5 as being negatively reactive infants.

The adverse consequences of the co-occurrence of a child risk factor (ie, a diathesis; e.g., negative emotionality) and problematic parenting also is evident in Caspi and Moflitt’s ground breaking research on gene-by-environment (GXE) interaction. Young men followed from early childhood were most likely to manifest high levels of antisocial behavior when they had both (a) a history of child maltreatment and (b) a particular variant of the MAO-A gene, a gene previously linked to aggressive behaviour. Such results led Rutter, like others, to speak of “vulnerable individuals,” a concept that also applies to children putatively at risk for compromised development due to their behavioral attributes. But is “vulnerability” the best way to conceptualize the kind of person-environment interactions under consideration?

Beyond Diathesis, Stress, DualRisk and Vulnerability

Working from an evolutionary perspective, Belsky (Belsky & Pluess) theorized that children, especially within a family, should vary in their susceptibility to both adverse and beneficial effects of rearing influence. Because the future is uncertain, in ancestral times, just like today, parents could not know for certain (consciously or unconsciously) what rearing strategies would maximise reproductive fitness, that is, the dispersion of genes in future generations, the ultimate goal of Darwinian evolution.

To protect against all children being steered, inadvertently, in a parental direction that proved disastrous at some later point in time, developmental processes were selected to vary children’s susceptibility to rearing (and other environmental influences).

In what follows, I review evidence consistent with this claim which highlights early negative emotionality and particular candidate genes as “plasticity factors” making individuals more susceptible to both supportive and unsupportive environments, that is, “for better and for worse”.

Negative Emotionality as Plasticity Factor

The first evidence which Belsky could point to consistent with his differential susceptibility hypothesis concerned early negative emotionality. Children scoring high on this supposed “risk factor”, particularly in the early years, appeared to benefit disproportionately from supportive rearing environments.

Feldman, Greenbaum, and Yirmiya found, for example, that 9-month-olds scoring high on negativity who experienced low levels of synchrony in mother-infant interaction manifested more noncompliance during clean-up at age two than other children did. When such infants experienced mutually synchronous mother-infant interaction, however, they displayed greater self-control than did children manifesting much less negativity as infants. Subsequently, Kochanska, Aksan, and Joy observed that highly fearful 15-month-olds experiencing high levels of power-assertive paternal discipline were most likely to cheat in a game at 38 months, yet when cared for in a supportive manner such negatively emotional, fearful toddlers manifested the most rule-compatible conduct.

In the time since Belsky and Pluess reviewed evidence like that just cited, highlighting the role of negative emotionality as a “plasticity factor”, even more evidence to this effect has emerged in the case of children. Consider in this regard work linking (1) maternal empathy and anger with externalizing problems; (2) mutual responsiveness observed in the mother-child dyad with effortful control; (3) intrusive maternal behavior and poverty with executive functioning; and (4) sensitive parenting with social, emotional and cognitive-academic development.

Experimental studies designed to test Belsky’s differential susceptibility hypothesis are even more suggestive than the longitudinal correlational evidence just cited. Blair discovered that it was highly negative infants who benefited most in terms of both reduced levels of externalizing behavior problems and enhanced cognitive functioning from a multi-faceted infant-toddler intervention program whose data he reanalyzed. Thereafter, Klein Velderman, Bakermans-Kranenburg, Juffer, and van Ijzendoorn found that experimentally induced changes in maternal sensitivity exerted greater impact on the attachment security of highly negatively reactive infants than it did on other infants. In both experiments, environmental influences on “vulnerable” children were for better instead of for worse.

As it turns out, there is ever growing experimental evidence that early negative emotionality is a plasticity factor. Consider findings showing that it is infants who score relatively low on irritability as newborns who fail to benefit from an otherwise security promoting intervention and infants who show few, if any, mild perinatal adversities known to be related to limited negative emotionality who fail to benefit from computer based instruction otherwise found to promote preschoolers’ phonemic awareness and early literacy.

In other words, only the putatively “vulnerable”, those manifesting or likely to manifest high levels of negativity experienced developmental enhancement as a function of the interventions cited. Similar results emerge among older children, as Scott and O’Connor’s parenting intervention resulted in the most positive change in conduct among emotionally dysregulated children (i.e., loses temper, angry, touchy).

Genes as Plasticity Factors

Perhaps nowhere has the diathesis-stress framework informed person-X-environment interaction research more than in the study of GXE interaction. Recent studies involving measured genes and measured environments also document both for better and for worse environmental effects, in the case of susceptible individuals as it turns out. Here I consider evidence pertaining to two specific candidate genes before turning attention to research examining multiple genes at the same time.

DRD4

One of the most widely studied genetic polymorphisms in research involving measured genes and measured environments pertains to a particular allele (or variant) of the dopamine receptor gene, DRD4. Because the dopaminergic system is engaged in attentional, motivational, and reward mechanisms and one variant of this polymorphism, the 7-repeat allele, has been linked to lower dopamine reception efficiency. Van Ijzendoorn and Bakerman Kranenburg predicted this allele would moderate the association between maternal unresolved loss or trauma and infant attachment disorganization. Having the 7-repeat DRD4 allele substantially increased risk for disorganization in children exposed to maternal unresolved loss/trauma, as expected, consistent with the diathesis-stress framework; yet when children with this supposed “vulnerability gene” were raised by mothers who had no unresolved loss, they displayed significantly less disorganization than agemates without the allele, regardless of mothers’ unresolved loss status.

Similar results emerged when the interplay between DRD4 and observed parental insensitivity in predicting externalizing problems was studied in a group of 47 twins. Children carrying the 7-repeat DRD4 allele raised by insensitive mothers displayed more externalizing behaviors than children without the DRD4 7-repeat (irrespective of maternal sensitivity), whereas children with the 7-repeat allele raised by sensitive mothers showed the lowest levels of externalizing problem behavior.

Such results suggest that conceptualizing the 7-repeat DRD4 allele exclusively in risk-factor terms is misguided, as this variant of the gene seems to heighten susceptibility to a wide variety of environments, with supportive and risky contexts promoting, respectively, positive and negative functioning.

In the time since I last reviewed such differential susceptibility related evidence, ever more GXE findings pertaining to DRD4 (and other polymorphisms) have appeared consistent with the notion that there are individual differences in developmental plasticity. Consider in this regard recent differential susceptibility related evidence showing heightened or exclusive susceptibility of individuals carrying the 7repeat allele when the environmental predictor and developmental outcome were, respectively, (a) maternal positivity and prosocial behavior; (b) early nonfamilial childcare and social competence; (c) contextual stress and support and adolescent negative arousal; (d) childhood adversity and young adult persistent alcohol dependence; and (e) newborn risk status (i.e., gestational age, birth weight for gestational age, length of stay in NICU) and observed maternal sensitivity.

Especially noteworthy, perhaps are the results of a meta-analysis of GXE research involving dopamine related genes showing that children eight and younger respond to positive and negative developmental experiences and environmental exposures in a manner consistent with differential susceptibility.

As in the case of negative emotionality, intervention research also underscores the susceptibility to 7-repeat carriers of the DRD4 gene to benefit disproportionately from supportive environments. Kegel, Bus and van I]zendoorn tested and found support for the hypothesis that it would be DRD4-7R carriers who would benefit from specially designed computer games promoting phonemic awareness and, thereby, early literacy in their randomized control trial (RCT). Other such RCT results point in the same direction with regard to DRD4-7R, including research on African American teenagers in which substance use was the outcome examined.

5-HTTLPR

Perhaps the most studied polymorphism in research on GXE interactions is the serotonin transporter gene, 5-HTTLPR. Most research distinguishes those who carry one or two short alleles (8/3, 3/1) and those homozygous for the long allele (1/1). The short allele has generally been associated with reduced expression of the serotonin transporter molecule, which is involved in the reuptake of serotonin from the synaptic cleft and thus considered to be related to depression, either directly or in the face of adversity. Indeed, the short allele has often been conceptualized as a “depression gene”.

Caspi and associates were the first to show that the 5-HTTLPR moderates effects of stressful life events during early adulthood on depressive symptoms, as well as on probability of suicide ideation/attempts and of major depression episode at age 26 years. Individuals with two 3 alleles proved most adversely affected whereas effects on 1/1 genotypes were weaker or entirely absent. Of special significance, however, is that carriers of the 3/3 allele scored best on the outcomes just mentioned when stressful life events were absent, though not by very much.

Multiple research groups have attempted to replicate Caspi et al.’’s findings of increased vulnerability to depression in response to stressful life events for individuals with one or more copies of the 5 allele, with many succeeding, but certainly not all. The data presented in quite a number of studies indicates, however, that individuals carrying short alleles (s/s, s/l) did not just function most poorly when exposed to many stressors, but best, showing least problems when encountering few or none. Calling explicit attention to such a pattern of results, Taylor and associates reported that young adults homozygous for short alleles (s/s) manifested greater depressive symptomatology than individuals with other allelic variants when exposed to early adversity (i.e., problematic child rearing history), as well as many recent negative life events, yet the fewest symptoms when they experienced a supportive early environment or recent positive experiences. The same for-better-and-for-worse pattern of results concerning depression are evident in Eley et al.’s research on adolescent girls who were and were not exposed to risky family environments.

The effect of 5-HTTLPR in moderating environmental influences in a manner consistent with differential susceptibility is not restricted to depression and its symptoms. It also emerges in studies of anxiety and ADHD, particularly ADHD which persists into adulthood. In all these cases, emotional abuse in childhood or a generally adverse childrearing environment, it proved to be those individuals carrying short alleles who responded to developmental or concurrent experiences in a for-better-and-for-worse manner, depending on the nature of the experience in question.

Since last reviewing such 5-HTTLPR-related GXE research consistent with differential susceptibility, ever more evidence in line with the just cited work has emerged. Consider in this regard evidence showing for-better-and-for-worse results in the case of those carrying one or more short alleles of 5-HTTLPR when the rearing predictor and child outcome were, respectively, (a) maternal responsiveness and child moral internalization, (b) child maltreatment and children’s antisocial behavior, and (c) supportive parenting and children’s positive affect.

Differential susceptibility related findings also emerged (among male African-American adolescents) when (d) perceived racial discrimination was used to predict conduct problems; (e) when life events were used to predict neuroticism, and (f) life satisfaction of young adults; and (g) when retrospectively reported childhood adversity was used to explain aspects of impulsivity among college students (e.g., pervasive influence of feelings, feelings trigger action). Especially noteworthy are the results of a recent meta-analysis of GXE findings pertaining to children under 18 years of age, showing that short allele carriers are more susceptible to the effects of both positive and negative developmental experiences and environmental exposures, at least in the case of Caucasians.

As was the case with DRD4, there is also evidence from intervention studies documenting differential susceptibility. Consider in this regard Drury and associates data showing that it was only children growing up in Romanian orphanages who carried 5-HTTLPR short alleles who benefited from being randomly assigned to high quality foster care in terms of reductions in the display of indiscriminant friendliness. Eley and associates also documented intervention benefits restricted to short allele carriers in their study of cognitive behavior therapy for children suffering from severe anxiety, but their design included only treated children (i.e., did not involve a randomly assigned control group).

Polygenetic Plasticity

Most GxE research, like that just considered, has focused on one or another polymorphism, like DRD4 or 5-HTTLPR. In recent years, however, work has emerged focusing on multiple polymorphisms and thus reflecting the operation of epistatic (i.e., GXG) interactions, as well as GxGxE ones.

One can distinguish polygenetic GxE research in terms of the basis used for creating multigene composites. One strategy involves identifying genes which show main effects and then compositing only these to then test an interaction with some environmental parameter. Another approach is to composite genes for a secondary, follow-up analysis that have been found in a first round of inquiry to generate significant GxE interactions.

When Cicchetti and Rogosch applied this approach using four different polymorphisms, they found that as the number of sensitivity-to-the-environment alleles increased, so did the degree to which maltreated and non-maltreated low-income children differed on a composite measure of resilient functioning in a for-better-and-for-worse manner.

A third approach which has now been used successfully a number of times to chronicle differential susceptibility involves compositing a set of genes selected on an apriori basis before evaluating GxE. Consider in this regard evidence indicating that 2-gene composites moderate links (a) between sexual abuse and adolescent depression/anxiety and somatic symptoms (b) between perceived racial discrimination and risk related cognitions reflecting a fast vs. slow life-history strategy (c) between contextual stress/support and aggression in young adulthood and (d) between social class and post-partum depression.

Of note, too is evidence that a 3-gene composite moderates the relation between a hostile, demoralizing community and family environment and aggression in early adulthood and that a 5-gene composite moderates the relation between parenting and adolescent self-control.

Given research already reviewed, it is probably not surprising that there is also work examining genetically moderated intervention effects focusing on multi-gene composites rather than singular candidate genes. Consider in this regard the Drury et al.’s findings showing that even though the genetic polymorphism brain derived neurotrophic factor, BDNF, did not all by itself operate as a plasticity factor when it came to distinguishing those who did and did not benefit from the aforementioned foster-care intervention implemented with institutionalized children in Romania, the already-noted moderating effect of 5-HTTLPR was amplified if a child carried Met rather than Val alleles of BDNF along with short 5-HTTLPR alleles. In other words, the more plasticity alleles children carried, the more their indiscriminate friendliness declined over time when assigned to foster care and the more it increased if they remained institutionalized.

Consider next Brody, Chen and Beach’s confirmed prediction that the more GABAergic and Dopaminergic genes African American teens carried, the more protected they were from increasing their alcohol use over time when enrolled in a whole-family prevention program. Such results once again call attention to the benefits of moving beyond single polymorphisms when it comes to operationalizing the plasticity phenotype. They also indicate that even if a single gene may not by itself moderate an intervention (or other environmental) effect, it could still play a role in determining the degree to which an individual benefits. These are insights future investigators and interventionists should keep in mind when seeking to illuminate “what works for whom?”

Unknowns in the Differential Susceptibility Equation

The notion of differential susceptibility, derived as it is from evolutionary theorizing, has gained great attention in recent years, including a special section in the journal Development and Psychopathology.

Although research summarized here suggests that the concept has utility, there are many “unknowns,” several of which are highlighted in this concluding section.

Domain General or Domain Specilic?

Is it the case that some children, perhaps those who begin life as highly negatively emotional, are more susceptible both to a wide variety of rearing influences and with respect to a wide variety of developmental outcomes as is presumed in the use of concepts like “fixed” and “plastic” strategists, with the latter being highly malleable and the former hardly at all? Boyce and Ellis contend that a general psychobiological reactivity makes some children especially vulnerable to stress and thus to general health problems. Or is it the case, as Belsky wonders and Kochanska, Aksan, and Joy argue, that different children are susceptible to different environmental influences (e.g., nurturance, hostility) and with respect to different outcomes? Pertinent to this idea are findings of Caspi and Mofiitt indicating that different genes differentially moderated the effect of child maltreatment on antisocial behavior (MAO-A) and on depression (5HTT).

Continuous Versus Discrete Plasticity?

The central argument that children vary in their susceptibility to rearing influences raises the question of how to conceptualize differential susceptibility: categorically (some children highly plastic and others not so at all) or continuously (some children simply more malleable than others)? It may even be that plasticity is discrete for some environment-outcome relations, with some individuals affected and others not at all (e.g., gender specific effects), but that plasticity is more continuous for other susceptibility factors (e.g., in the case of the increasing vulnerability to stress of parents with decreasing dopaminergic efficiency. Certainly the work which composites multiple genotypes implies that there is a “plasticity gradient”, with some children higher and some lower in plasticity.

Mechanisms

Susceptibility factors are the moderators of the relation between the environment and developmental outcome, but they do not elucidate the mechanism of differential influence.

Several (non-mutually exclusive) explanations have been advanced for the heightened susceptibility of negatively emotional infants. Suomi posits that the timidity of “uptight” infants affords them extensive opportunity to learn by watching, a view perhaps consistent with Bakermans-Kranenburg and van Ijzendoorn’s aforementioned findings pertaining to DRD4, given the link between the dopamine system and attention. Kochanska et al., contend that the ease with which anxiety is induced in fearful children makes them highly responsive to parental demands.

And Belsky speculates that negativity actually reflects a highly sensitive nervous system on which experience registers powerfully negatively when not regulated by the caregiver but positively when coregulation occurs, a point of view somewhat related to Boyce and Ellis’ proposal that susceptibility may reflect prenatally programmed hyper-reactivity to stress.

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Chronic Childhood Stress and a Dysfunctional Family – Kylie Matthews * Different Adversities Lead to Similar Health Problems – Donna Jackson Nakazawa.

Children from unhappy, dysfunctional families who experience chronic adversity undergo changes in brain architecture that create lasting physical scars, that look pretty similar no matter who you are, where you lived, or what happened to make you unhappy when you were growing up.

Happy families may succeed not because of what they do right, but because of everything they don’t do wrong.

The stress of Adverse Childhood Experiences causes toxicity to the neurons and neural pathways that integrate different areas of the brain. These brain changes have a profound effect on our decision making abilities, self regulatory processes, attention, emotional regulation, thoughts, and behavior.

Cutting her mother out of her life was the only conceivable way she could survive.
Janet Camilleri reveals why she cut ties with her mother.

Kylie Matthews

What do you do when a close family relationship, such as a parent or sibling, becomes so dysfunctional it’s toxic?

For some, completely cutting off from that person can be the only solution for them to heal and move forward but it‘s by no means ever an easy one.

Blogger and mother of two Janet Camilleri, 51, is a survivor of a childhood overshadowed by violence and psychological abuse so profound that cutting her mother out of her life was the only conceivable way she could survive.

“My mother was violent, irrational her mood could change at the drop of a hat,” she recalls. “I call it the Dr Jekyll and Mr Hyde personality because she was a very outgoing, extroverted, life of the party type person in the company of others but at home she was like the devil and you just never knew what would trigger her.

I would have ended up a basket case if I’d kept her in my life as just a phone call with her would reduce me to a quivering lump of jelly, that was the effect she had on me. For the sake of my own marriage and children, I had to cut her off to look after my own mental health.”

My Mum, the narcissist

Janet describes her mother regularly sabotaging her school work, throwing things around the room in a rage, embarrassing her at school and in front of friends, playing favourites with her siblings, using her as a gobetween to pitch venom at her father and regularly inflicting physical violence in the home.

In hindsight, Janet says she recognises that her mother had many severe narcissistic traits exacerbated by other personality disorders, and underlined by a clinical diagnosis of bipolar disorder.

Helen Gibbons, Director and Principal Psychologist of Australia’s Autogenic Therapy and Training Institute, says that toxic behaviour in families can be identified by dysfunctional dynamics.

“Most commonly you see in any dysfunctional set up narcissistic traits in one or more family members that, in its most severe form, can result in premeditated abusive, manipulative and controlling behaviours,” she says.

Narcissism is a condition that presents a set of personality traits such as arrogance, selfcentredness, manipulation, a lack of empathy and remorse, dishonesty, dominance, a strong sense of entitlement, an inability to handle criticism and a grandiose sense of self.

When children grow up in the shadow of a severe narcissist, Ms Gibbons says their emotional needs are seldom met.

“These children are having their brains shaped based on a lack of positive stimulation, love and validation, which does seem to impact heavily on the formation of their limbic system and, in particular, the amygdala, the centre of emotional control in the brain,” she says.

Janet describes her mother’s behaviour becoming increasingly worse after her parents separated and, as her mother’s mental health continued to deteriorate, at the age of just 10 years old, Janet was thrust into the role of ‘carer’ for her younger siblings.

“For a lot of it I protected the younger ones; I was like a mother figure to them because Mum just wasn’t capable of it,” she explains. “It was a lot of responsibility Mum dumped a lot of stuff on me that a kid that age should never be exposed to.”

Leaving home

One Christmas, things came to a head and Janet says she stood up to her mother for the first time and told her she was leaving, to which her mother replied, ‘If you leave, you will never be able to come back’.

“I was nearly 20 years old and I was like, ‘I just can’t do this anymore’. I cut off from her then and we didn’t talk after that for about eight months,” she says. “I had no money, no job and very little support; I just had to survive.”

Janet tried to reinstate contact with her mum at least three times after that. “I tried really hard but it was always awkward and strained,” she says. ”She always upset me whenever we spoke on the phone.”

Janet continued to walk on eggshells, as she had always done, and accommodated poor behaviour to keep the peace, even forgiving her mother for not attending her wedding. But just prior to the birth of her first child, after yet another argument, Janet decided enough was enough and cut off from her mother for the last time.

Cutting off communication

Ms Gibbons says that for people like Janet, any attempt to communicate and rectify problems in a rational way with the narcissistic family member would most likely result in even more abusive behaviour.

“Malignant narcissists are experts at blaming others and the family scapegoat is always the easiest target so cutting off contact may be the only option available to them for a peaceful life,” she says. “No contact literally means no contact ..You don’t explain yourself, you disappear, block them on Facebook and don’t return phone calls.”

Once you’ve gone ‘no contact’, however, you can go into shock and potentially suffer from acute stress symptoms.

“It can be a very lonely and confusing time going no contact because you may find that you are not getting the understanding, support and validation you so desperately need from those around you,” Ms Gibbons says. “When you tell your friends, a lot of people, even though they’re well meaning, believe that all mothers love their children.

“A very common experience is that the friends that you want to believe and validate you will immediately try and support the mother in some way, by saying, ‘Oh yes, but she loves you’ or, ‘Being a parent is difficult’, so it can be very lonely and confusing.”

Janet says the pressure she felt from her family, friends and colleagues to reconcile with her mother was significant. “I was part of a church and the pressure I felt was huge,” she says. “In church, nobody could understand because it’s like, ‘Honour thy father and thy mother’ and all that and I felt like the lowest of the low for not being able to do that.

“I remember talking to somebody at work once, an older fellow, I was pretty bitter and upset at the time, and I mentioned something about my mum that was probably not very nice and he turned to me and said, ‘I think it’s disgusting the way you talk about your mother’. I was just gobsmacked.”

The toxic devastation

Janet went on to survive her childhood but says by the time she managed to escape it, the damage had already been done. “I just tried to be a good kid and to stay out of trouble … I didn’t want to attract her attention because she’d thump me if I did,” she says. “Growing up in a household like mine leads to a few issues so I’ve been and seen a psychologist to help me out at different times.”

Ms Gibbons can’t stress enough the importance of therapy for people who have experienced this kind of trauma.

“Therapy is really important for someone who has suffered abuse from narcissistic family members,” she says. ”it’s so important to speak with a psychologist who is experienced in psychological abuse and to work through the impact that those relationships have had on you so that you can start to make better, healthier choices.”

Janet suffered from Post Traumatic Stress Disorder (PTSD) after leaving home, which later developed into postnatal depression after the birth of both her children.

“I remember going shopping with my kids and seeing other young women with their babies and their mums by their side and just bursting into tears,” she says. “I was like, ‘Why don’t I have a mum like that?‘ I have a wonderful, supportive husband but it very much felt like I was on my own at that time.”

The final blow

It was five years after her mother’s death that Janet first learnt of her passing by accident. And despite having been estranged from her mother for almost 20 years, her grief sent her into a spiral of total despair.

“I was just devastated, I always thought I’d done my mourning when the kids were little because that was a really tough time and I’d grieved the loss of the relationship then, but I think deep down I always hoped that one day a miracle would happen and we’d work it out,” she says. “Even though we were estranged, I never wished ill for her and I sincerely wanted Mum to be happy, despite everything.”

To add insult to injury, Janet learned that she hadn’t been told of her mother’s death at the time because her mum had specifically requested she and her siblings not be. “To learn that she had been so bitter, so twisted and angry, right up until the moment of her death makes me very sad,” she says.

Hope and healing

Despite the devastation she felt over her mother’s passing, Janet says she has no regrets about cutting off communication.

“I didn’t feel guilty when I found out because I knew I’d done everything I humanly could to try and have a relationship with my mother and that no matter what I did, I would never, ever have pleased her so it was never going to work,” she says.

“It helped that I had my wonderful husband beside me saying, ‘You need to get rid of this influence in your life’ and he helped me to be strong and to realise that other people might not approve but that it was something I had to do.”

Some years ago, while driving her young children to school, Janet recalls pulling up beside a bus that had an advertisement about child abuse. “A little voice from the back seat asked, ‘That’s what happened to you, didn’t it, Mummy?‘ and I said, ‘Yes, it was, she says.

“And they’d replied, ‘It’s OK, Mummy, we love you now’.”

Different Adversities Lead to Similar Health Problems

Donna Jackson Nakazawa

The opening line of Tolstoy’s Anna Karenina, “Happy families are all alike; every unhappy family is unhappy in its own way.”, has inspired a philosophical dictum called “The Anna Karenina Principle.” The idea is this: it’s possible to fail at something in many ways; it’s far harder to succeed at something, because success requires not failing in any of those ways.

Happy families may succeed not because of what they do right, but because of everything they don’t do wrong.

And according to ACE research, 64 percent of us grew up in families in which at least one thing went wrong: we’ve had at least one Adverse Childhood Experience. Every one of these unhappy families may be unhappy in its own, unique way. But there is one way in which unhappy families are alike, according to neurobiologists who study childhood adversity:

Children from unhappy, dysfunctional families who experience chronic adversity undergo changes in brain architecture that create lasting physical scars that look pretty similar no matter who you are, where you lived, or what happened to make you unhappy when you were growing up.

How Your Biography Becomes Your Biology

To better understand how toxic childhood stress changes our brain, let’s first review how our stress response is supposed to work when it’s functioning optimally.

Let’s say you’re lying in bed and everyone else in the house is asleep. It’s one am. You hear a creak on the steps. Then another creak. Now it sounds as if someone is in the hallway. You feel a sudden rush of alertness, even before your conscious mind weighs the possibilities of what might be going on. A small region in your brain known as the hypothalamus releases hormones that stimulate two little glands, the pituitary and adrenal glands, to pump chemicals throughout your body. Adrenaline and cortisol trigger immune cells to secrete powerful messenger molecules that whip up your body’s immune response.

Your pulse drums under your skin as you lie there, listening. The hair on the surface of your arms stands up. Muscles tighten. Your body gets charged up to do battle in order to protect life and limb.

Then you recognize those footsteps as those of your teenager coming up the steps after finishing his midnight bowl of cereal. Your body relaxes. Your muscles loosen. The hair on your arms flattens back down. Your hypothalamus, as well as your pituitary and adrenal glands, the “HPA stress axis”, calm down. And, whew, so do you.

When you have a healthy stress response, you respond quickly and appropriately to stress. After the stressful event, your body dampens down the fight-or-flight response. Your system recovers and returns to a baseline state of rest and recovery. In other words, you pass through both the first and the second half of the human stress cycle, coming full circle.

Even so, emotions affect our body in real and significant ways. Emotions are physical. We feel a “knot in our stomach,” or get “all choked up,” or see a relative or coworker as a “big pain in the neck.”

There is a powerful relationship between mental stress and physical inflammation. When we experience stressful emotions, anger, fear, worry, anxiety, rumination, grief, loss, the HPA axis releases stress hormones, including cortisol and inflammatory cytokines, that promote inflammation.

Let’s say your immune system has to fight a viral or bacterial infection. Lots of white blood cells charge to the site of the infection. Those white blood cells secrete inflammatory cytokines to help destroy the infiltrating pathogens and repair damaged tissues. However, when those cytokines aren’t well regulated, or become too great in number, rather than repair tissue, they cause tissue damage. Toxic shock syndrome is an extreme example of how this can happen in the body very quickly.

More subtle types of tissue damage can happen slowly, over time, in response to chronic stress. When your system is repeatedly overstimulated, it begins to downshift its response to stress. On the face of it, that might sound like it’s a good thing, as if a downshifted stress response should translate into less inflammation, right?

But remember, this stress response is supposed to react to a big stressor, pump into defensive action, then quickly recover and return to a state of quiet homeostasis, relaxing into rest and recovery.

The problem is, when you are facing a lot of chronic stress, the stress response never shuts off. You’re caught, perpetually, in the first half of the stress cycle. There is no state of recovery. Instead, the stress response is always mildly on, pumping out a chronic low dose of inflammatory chemicals.

The stress glands, the hypothalamus, the HPA axis, secrete low levels of stress hormones all the time, leading to chronic cytokine activity and inflammation.

In simplest terms: chronic stress leads to a dysregulation of our stress hormones, which leads to unregulated inflammation. And inflammation translates into symptoms and disease.

This is the basic science on how stress hormones play a part in orchestrating our immune function and the inflammatory process. And it explains why we see such a significant link between individuals who experience chronic stress and significantly higher levels of inflammation and disease.

As Stanford professor Robert Sapolsky, PhD, a MacArthur Fellowship recipient for his research on the neurobiological impact of emotional stress on the immune system, has said:

“The stress response does more damage than the stressor itself as we wallow in stress hormones.”

Research bears out the relationship between stress and physical inflammation. For example, adults under the stress of taking care of spouses with dementia display increased levels of a cytokine that increases inflammation. Likewise, if an adult sibling dies, your risk of having a heart attack rises greatly. If you’re pregnant and face a big, stressful event, your chance of miscarrying doubles. Encountering serious financial problems raises a man’s risk of falling down and being injured in the months that follow. A child’s death triples a parent’s chance of developing multiple sclerosis. States of intense emotional fear or loss can precipitate a type of cardiomyopathy known as “broken heart syndrome,” a severe physical weakening of the heart muscle that presents almost exactly like, and is often misdiagnosed as, a full-blown heart attack.

Why Stress Is More Damaging to a Child

Emotional stress in adult life affects us on a physical level in quantifiable, life-altering ways.

But when children or teens meet up with emotional stressors and adversity, they leave even deeper scars.

These potential stressors include chronic put-downs, emotional neglect, parental divorce, a parent’s death, the mood shifts of a depressed or addicted parent, sexual abuse, medical trauma, the loss of a sibling, and physical or community violence. In each case, the HPA (hypothalamus-pituitary-adrenal) stress response can become reprogrammed so that it revs up one’s inflammatory stress hormone response for the rest of one’s life.

In young and growing children, the HPA stress axis is developing, and healthy maturation is heavily influenced by the safety or lack of safety we encounter in the day-to-day environment. When a young brain is repeatedly thrust into a state of hyperarousal or anxiety because of what’s happening at a child’s home, community, or school, the stress axis gets tipped into reaction over and over again, and the body becomes routinely flooded with inflammatory stress neurochemicals. This can lead to deep physiological changes that lead to long lasting inflammation and disease.

More than half of women suffering from irritable bowel syndrome report childhood trauma. Children whose parents divorce are far more likely to have strokes as adults. ACE Scores are linked to a far greater likelihood of diseases including cancer, lung disease, diabetes, asthma, headaches, ulcers, multiple sclerosis, lupus, irritable bowel syndrome, and chronic fatigue.

The more categories of Adverse Childhood Experiences a child has faced, the greater the chances of developing heart disease as an adult. Again, a child who has 7 or more ACEs grows up with a 360 percent higher chance of developing heart disease.

Medical Adverse Experience

Not all Adverse Childhood Experiences are about poor parenting.

Michele had the kind of lovely parents who created a home life that fits the happy family mold; they gave their son and daughter all the parental love and support that every child deserves. “Life was good,” Michele says. Then, when she was thirteen years old, she had a bladder infection and was placed on a routine course of antibiotics. “Within twenty-four hours I had a headache and rash.”

Michele’s doctor told Michele’s mom, “it’s a virus.”

But the rash didn’t go away. Michele started wincing at bright lights. The eye doctor couldn’t figure out what was wrong. Blisters began developing along her upper lip. The pediatrician didn’t know what to do, so Michele’s parents took her to the hospital. They saw a dermatologist who had read about Michele’s symptoms in an article. He thought she might have Stevens-Johnson syndrome, or SJS, a rare illness caused by a severe allergic reaction to a medication.

Michele was admitted to Columbia Presbyterian hospital in New York City. Within twenty four hours blisters the size of large hands broke out across her body. At first, they covered “30 percent of my body, then 100 percent,” Michele says. She was diagnosed with an advanced form of SJS, known as toxic epidermal necrolysis syndrome, or TENS. The bowl sized blisters began to “connect and combine until my entire torso was one enormous blister. Even my corneas were blistered.”

Today, when patients develop TENS, they’re put in an induced coma, because the physical pain is simply too unbearable. But in 1981, when Michele was diagnosed with the illness, doctors “just watched the progression.” Her physicians converted Michele’s hospital room into a burn unit, she looked like a burn victim, so she was treated as if she’d been rescued from a fire. “I felt as if I were being scalped over every inch of my skin.” Michele says she started dissociating from her body. “My body and l parted ways in that hospital, we stopped talking to each other. I couldn’t bear to feel that pain.”

Miraculously, Michele survived. She missed two months of school, while her mom helped to nurse her back to health. Little by little, life began to regain a rhythm of normality, except for the fear Michele still carried within. Every year on the anniversary of the day she was first admitted to the hospital, “my hair would fall out,” she says. “Then it would grow slowly back in.” Michele attended the University of Pennsylvania and held it together, but the whole time, she says, “I was having insomnia and recurring nightmares.” In her late twenties she was diagnosed with chronic fatigue, Epstein-Barr virus, and irritable bowel syndrome. “I had terrible muscle pains all over my body and chronic sinus infections. I had trouble sitting still for even five minutes because of the pain.” Her liver enzymes went “sky high.” It was, she says, “one mysterious illness after another.”

And then, at the age of thirty five, Michele’s doctor sat her down and told her that she had “severe, advanced osteoporosis.” Her bones were going to start disintegrating, he said. “If we don’t get this under control, sometime in the next ten years your bones are going to spontaneously crumble.”

Michele’s early adversity had nothing to do with bad parenting. But her early life stress was extreme, and the damage that stress did to her developing immune system and cells was just as corrosive.

Life is complex and messy, and suffering comes in many forms. Bad things happen. Parents get sick or pass away. Accidents come out of nowhere, as do medical crises.

How do the biophysical changes and inflammation triggered by very different types of early childhood adversity translate years later into autoimmune diseases, heart disease, and cancer?

Flipping Crucial Genetic Switches

On an unusually brisk December morning, Margaret McCarthy, PhD, professor of neuroscience at the University of Maryland School of Medicine, meets me at a downtown Baltimore coffee shop. Her schedule is tight, so we pick up two cups of soup to go and head to her office. As we enter the hall that serves as the main artery for McCarthy’s four room lab, we pass a sign that says, “Research saves lives,” on a large photo of a young, smiling girl holding a stuffed bunny. McCarthy has taught science for years to med students, grad students, and even high schoolers, whom she takes on as lab assistants to help “turn them on to science.”

She offers a primer on what research has unveiled about childhood adversity and altered brain development.

“Early stress causes changes in the brain that reset the immune system so that either you no longer respond to stress or you respond in an exacerbated way and can’t shut off that stress response,” she says.

This change to our lifelong stress response happens through a process known as epigenetics. Epigenetic changes occur when early environmental influences both good (nurturing caregivers, a healthy diet, clean air and water) and bad (stressful conditions, poor diet, infections, or harmful chemicals) permanently alter which genes become active in the body.

These epigenetic shifts take place due to a process called gene methylation. McCarthy explains, “Our DNA is not just sitting there. It’s wrapped up very tightly and coated in protected proteins, which together make up the chromosome. It doesn’t matter what your genome is; what matters is how your genome is expressed. And for genes to be expressed properly, the chromosome has to be unwound and opened up, like a flower, right at that particular gene.”

McCarthy unfurls the fingers of both hands. “Imagine this,” she says. “You’re watching a flower bloom, and as it opens up, it’s covered with blemishes.” She folds several of her fingers back in, as if they’re suddenly unable to budge. “Those blemishes keep it from flourishing as it otherwise would. If, when our DNA opens up, it’s covered with these methylation marks, that gene can’t express itself properly in the way that it should.”

When such “epigenetic silencing” occurs, McCarthy continues, these small chemical markers, also known as methyl groups, adhere to specific genes that are supposed to govern the activity of stress hormone receptors in our brain. These chemical markers silence important genes in the segment of our genome that oversees our hippocampus’s regulation of stress hormones in adulthood. When the brain can’t moderate our biological stress response, it goes into a state of constant hyperarousal and reactivity. Inflammatory hormones and chemicals keep coursing through the body at the slightest provocation.

In other words, when a child is young and his brain is still developing, if he is repeatedly thrust into a state of fight or flight, this chronic stress state causes these small, chemical markers to disable the genes that regulate the stress response, preventing the brain from properly regulating its response for the rest of his life.

Researcher Joan Kaufman, PhD, director of the Child and Adolescent Research and Education (CARE) program at Yale School of Medicine, analyzed the DNA in the saliva of ninety six children who’d been taken away from their parents due to abuse or neglect as well as that of ninety six other children who were living in what we might think of as seemingly happy family settings. Kaufman found significant differences in epigenetic markers in the DNA of the children who’d faced hardship, in almost three thousand sites on their DNA, and on all twenty three chromosomes.

The children who’d been maltreated and separated from their parents showed epigenetic changes in specific sites on the human genome that determine how appropriately and effectively they will later respond to life’s stressors.

Seth Pollak, PhD, professor of psychology and director of the Child Emotion Laboratory at the University of Wisconsin, found that fifty children with a history of adversity and trauma showed changes in a gene that helps to manage stress by signaling the cortisol response to quiet down so that the body can return to a calm state after a stressor. But because this gene was damaged, the body couldn’t rein in its heightened stress response. Says Pollak:

“A crucial set of brakes are off.”

This is only one of hundreds of genes that are altered when a child faces adversity.

When the HPA stress axis is overloaded in childhood or the teenage years, it leads to long lasting side effects, not just because of the impact stress has on us at that time in our lives, but also because early chronic stress biologically reprograms how we will react to stressful events for our entire lives. That long term change creates a new physiological set point for how actively our endocrine and immune function will churn out a damaging cocktail of stress neurochemicals that barrage our bodies and cells when we’re thirty, forty, fifty, and beyond. Once the stress system is damaged, we overrespond to stress and our ability to recover naturally from that reactive response mode is impaired. We’re always responding.

Imagine for a moment that your body receives its stress hormones and chemicals through an IV drip that’s turned on high when needed, and when the crisis passes, it’s switched off again. Now think of it this way: kids whose brains have undergone epigenetic changes because of early adversity have an inflammation promoting drip of fight-or-flight hormones turned on high every day, and there is no off switch.

When the HPA stress system is turned on and revved to go all the time, we are always caught in that first half of the stress cycle. We unwittingly marinate in those inflammatory chemicals for decades, which sets the stage for symptoms to be at full throttle years down the road, in the form of irritable bowel syndrome, autoimmune disease, fibromyalgia, chronic fatigue, fibroid tumors, ulcers, heart disease, migraines, asthma, and cancer.

These changes that make us vulnerable to specific diseases are already evident in childhood. Joan Kaufman and her colleagues discovered, in the first study to find such direct correlations, that:

Children who had been neglected showed significant epigenetic differences “across the entire genome” including in genes implicated in cardiovascular disease, diabetes, obesity, and cancer.

Yet by the time signs of an autoimmune condition creep up at forty or a heart condition rears its head at fifty, we often can’t link what happened when we were children to our adult illness. We become used to that old sense of emotional stress, of not being okay. It just seems normal. We have a long daily commute, a thirty year mortgage, and our particular mix of family dynamics. We generally deal with it and we’re usually okay. Then something minuscule happens: we have an argument with our sister over something said at a family dinner; we get a notice in the mail that our insurance isn’t going to cover a whopping medical bill; the refrigerator tanks the day before a big dinner party; our boss approves a colleague’s ideas in a meeting and ignores ours; a car honks long and hard as it swerves from behind to cut in front of us on the freeway. We react to these events as if they are a matter of life or death. We trigger easily. We begin to realize that we’re not so fine.

An adult who came of age without experiencing traumatic childhood stress might meet the same stressor and experience that same spike in cortisol, but once that stressor has passed, he or she quickly returns to a state of rest and relaxation. But if we had early trauma, our adult HPA stress axis can’t distinguish between real danger and perceived stress. Each time we get sidetracked by a stressful event, it sends split-second signals that cause our immune system to rev into high gear. We get that adrenaline rush but the genes that should tell our stress system to return to a state of rest and relaxation don’t do their job.

Over days and years, the disparity between a long “cortisol recovery” period and a short one makes a significant, life changing difference in the number of hours we spend marinating in our own inflammatory stress hormones. And over time, that can deeply distort your life.

The Ever Alert Child

Adults with Adverse Childhood Experiences are on alert. It’s a habit they learned in childhood, when they couldn’t be sure when they’d face the next high tension situation.

After her terrifying childhood illness, Michele never felt at peace, or whole, as an adult: “I was afraid I could be blindsided by any small medical crisis that could morph and change my entire life.”

Laura, as an adult, holds a high profile DC job that requires lightning decisions and heightened awareness. She’s good at it since, as a child, Laura and her brain learned to always be on high alert for the next snipe from her mother, as if being prepared could make it hurt less. “I became an expert at gauging my mom’s moods,” she says. “Whenever I was in the same room with her, I was thinking about how to slink away.”

By the time she was nine, Laura had learned to be “unconsciously on the lookout for a very subtle narrowing of my mom’s eyes,” which would tell her that she was about to be blamed for “something I didn’t even know that I’d done, like eating half of a sandwich in the fridge or taking too long to tie my shoe.” Laura grew up “learning to toe my way forward, as if blindfolded, to figure out what was coming next, where the next emotional ledge might be, so I wouldn’t get too near to my mother’s sharp edges?

From Laura’s perspective, her mom was dangerous. “I knew she would never physically hurt me,” she explains. “But I was terrified, even when she was in a good mood. At night, when I would hear her lightly snoring, I would feel this overwhelming sense of freedom, relief.”

Laura’s life was never at risk of course, she lived in a safe suburban neighborhood, had food to eat, clothes to wear. But she felt as if her life was at stake. Like all children whose parents display terrifying behavior, Laura carried the overwhelming biological fear that if her primary caregiver turned against her, she would not survive. After all, if the person upon whom you depend for food, shelter, and life itself, turns on you, how are you going to stay alive in the world? You feel as if your life depends on the adult’s goodwill, because when you were very small, how your caregiver treated you really was a matter of life or death.

As an adult, Laura “schooled” herself to believe that the early adversity she faced wasn’t that bad compared with that of other people who also grew up with alcoholic, angry, divorced, or depressed parents. She keeps telling herself that she’s over her childhood troubles.

But her body is far from over them. Laura lives with heart disease and a defibrillator in her chest. Like Michele, her anxiety sensors are set on high alert, and she doesn’t know how to turn them off.

The Rattled Cage

We might reasonably intuit that some types of childhood adversity are more damaging to us than others. For instance, we’d expect that the trauma that Kat experienced in knowing that her father murdered her mother would have a dramatically worse biological impact on her than Laura’s having been chronically put down by her depressive mom.

We’d certainly assume that Kat’s story would be more biologically damaging than that of Ellie, who was the second youngest of five children and grew up in a quiet suburban neighborhood outside Philadelphia. Ellie remembers having a very close relationship with her parents, but, as she got older, she says, “I knew something wasn’t right. My two oldest brothers were time bombs of violent emotion, just waiting to go off. Sitting at the dinner table with my parents, talking about politics, they’d start fighting each other over nothing at all, and the fights got ugly.”

Soon the boys were getting into trouble with alcohol and drugs, “and the police started showing up.” Ellie recalls, “I’d often hear my parents and my brothers screaming at each other at two in the morning. My mom and dad would come in my room and tell my little sister and me not to be scared, that everything was okay, but it was terrifying,” especially when her older brother ended up in jail.

Ellie got good grades, despite the stressors at home, and went to college in California on an athletic scholarship. But, after college, she began having suicidal thoughts and, at age twenty-four, was diagnosed with severe autoimmune psoriasis. “My body was attacking itself,” she says.

According to ACE research, growing up with a family member who is in jail is related to a much higher risk of poor health related outcomes as an adult.

Chronic unpredictable stress

Laura, John, Georgia, Kat, Michele, and Ellie tell six unique stories of childhood adversity. And yet their brains reacted to these different levels of trauma in a similar biological way. The developing brain reacts to different types and degrees of trauma so similarly because all the categories of Adverse Childhood Experience stressors have a very simple common denominator: they are all unpredictable. The child can’t predict exactly when, why, or from where the next emotional or physical hit is coming.

Researchers refer to stress that happens in unpredictable ways and at unpredictable times as “chronic unpredictable stress,” and they have been studying its effects on animal development for decades, long before Felitti and Anda’s investigation into ACEs first began.

In classic studies, investigators expose animals to different types of stressors for several weeks, to see how those stressful stimuli affect their behavior. In one experiment, McCarthy and her postdocs exposed male and female rats to three weeks of chronic unpredictable mild stress. Every day, rats were exposed to a few low grade stressors: their cage was rotated; they were given a five minute swim, their bedding was dampened; they went for a day without food; they were physically restrained for thirty minutes; or they were exposed to thirty minutes of strobe lights.

At the end of the three weeks, McCarthy’s team examined the rats to evaluate brain differences. In the group exposed to chronic unpredictable mild stress, she and her team found significant changes in the receptors in the brain’s hippocampus, an area of the brain associated with emotion, which would normally help modulate stress hormone production and put the brakes on feelings of stress and anxiety after a stressor has passed.

The rats who’d been exposed to chronic unpredictable stress weren’t able to turn off the stress response, but the control group that experienced no stress showed no brain changes.

However, when stress is completely predictable, even if it is more traumatic, such as giving a rat a regularly scheduled foot shock accompanied by a sharp, loud sound, the stress does not create these exact same brain changes. “Rats exposed to a much more traumatic stressor get used to it if it happens at the same time and in the same way every day,” says McCarthy. “They manage. They know it’s coming, then it’s over.” Moreover, she says, “They don’t show signs of these same brain changes, or inflammation, or illness.”

On the other hand, she adds, “if you introduce more moderate but unpredictable stressful experiences at a different time each day, with different levels of intensity, adding in different noises, such as loud clapping at unpredictable intervals, those rats show significant changes to the brain. And they get physically sick; they get ulcers.”

This is why researchers believe that it is the unpredictability of stress that is particularly damaging.

On a walking tour of her lab, McCarthy points out the metal stand on which rodents’ cages can be gently shaken for a short time. “Even the most mild unpredictable stressors, something as simple as gently shaking the cage, playing rock music, putting a new object in the cage that they aren’t used to, all these cause very specific changes in the brain when we do them without warning.”

The bottom line, McCarthy says, is that the brain can “tolerate severely stressful events if they are predictable, but you cannot tolerate even mild stressful events if they are very unpredictable.”

Yet even though researchers have known for years about the effects of chronic unpredictable stress on the adult brain, only recently have they examined what happens to the brains of children exposed to chronic unpredictable stressors.

The Difficulty of Not Knowing

Mary, now in her midfifties, grew up as the oldest of four kids in a small town in Oregon. Life with her artist parents was a lot like living with unpredictable cage rattling, shaking, and odd, loud noises. Mary’s dad had his own damaged childhood. He’d grown up never knowing who his own dad was, and his mom died when he was seven. His maternal grandparents adopted his brother, but not him because his parents hadn’t married, and he was seen as damaged goods. (His ACE Score was very high.)

Years later, when he was a father of four, he drank heavily, partied, and played cards. “I remember hearing my dad and friends, up all night drinking and swearing really loud in the living room outside my bedroom, even on school nights. I didn’t feel safe.” Mary has large, sympathetic eyes and shoulder length brown hair that she neatly tucks behind her ears with long, graceful fingers. “I can remember my mother yelling at him, ‘You need to make them leave. Your children can’t sleep!’ And he’d yell back, ‘I can’t make them leave, these are my friends!’ My sleep, and sense of being safe, weren’t important to him.”

Mary’s mother was managing her own anxiety that came with having four children and being stuck in a marriage with an alcoholic, so she, too, was emotionally absent. “I got bullied a lot in grade school,” Mary tells me. “I was scrawny and short and kids would terrorize me.” Her mom was preoccupied with an affair her dad was having and didn’t listen to Mary’s problems; eventually she took Mary and her younger siblings to the East Coast to live with her own mother.

“A part of me quite enjoyed that time away from all the partying and the tension in their marriage, the fighting,” says Mary.

After her parents got back together, at first Mary was happy and hopeful. But her dad was still drinking heavily. He’d get so drunk that “my mom would literally kick him out of bed and he’d come sleep with me.” Nothing happened, Mary says, “nothing like that.” But still, it was disconcerting to sometimes wake in the night at age ten to find her dad in bed with her, sleeping off another drunken stupor.

At school things hadn’t improved much. “We were still wearing dresses back then,” says Mary. “All the boys called me ‘Gladiator’ because when they’d tease me I’d go at them, I’d fight back.” That made the bullying worse. “They’d chase me and hold me down on the ground and forcibly pull off my underwear.”

Mary didn’t even think of telling her father about the bullying. “When he was drunk, he would spank us really hard. Once when my sister was in second grade, he pulled down her pants and spanked her in front of all his drunken friends.”

Mary’s sensors were always on high alert, getting ready for the next unpredictable, incoming emotional bomb. Her stress axis was constantly kicking into high gear; her immune system, in overdrive. By then, Mary had started to show signs of an autoimmune disorder called vitiligo, in which the body’s immune cells attack the pigmentation in the skin. Areas of her skin turned white, as if the skin had been bleached or burned in the past and new skin was trying to form over it.

“Our skin is our first line of defense against the world, the thing that’s supposed to keep us safe, secure our physical boundaries,” Mary says. “And yet my parents hadn’t set any boundaries to keep me or my siblings safe.” It was as if her skin were pleading for her parents to set those boundaries, the kind of safe zone parents are supposed to set for kids.

Even worse than the skin disorder, however, “were my constant stomachaches,” she recalls. “I’d have chronic constipation and cramping, and then terrible diarrhea, all the symptoms of irritable bowel, though we didn’t know what to call it back then.” Sometimes, she’d find herself getting physically jittery and nervous “seemingly for no reason. I’d just be standing there and I’d get these rushes of fear, ripping and prickling through my body.”

Over time, her father’s boundaryless behavior grew more bizarre. When Mary was fourteen, he cut out hundreds of naked bodies from a stack of old Playboys, took off their heads, and pasted their disembodied boobs, legs, butts, and crotches on the walls of the kitchen. Andrea, one of Mary’s few friends, told her parents about the “wallpaper.” “After that, Andrea wasn’t allowed at my house,” Mary says. “I started to realize that other kids weren’t comfortable around me because of my dad.”

When she was fifteen, her parents moved to a house in the country. “I think they were trying to salvage their marriage.” One crisp winter night, when Mary was coming out of the garage, one of her dad’s drunken friends was standing by his car in the driveway. “As I walked by to go in the house he stared at me hard and said, ‘You are so beautiful!’ Then he threw me into the backseat of his car and got on top of me. He stuck his tongue down my throat and was groping me.”

Mary forced him off and ran in to tell her dad, who was also drunk. “He told me to stop making such a big deal about it.”

And yet, at other times, Mary’s dad did show concern for her. Once, when Mary was in a car accident, “he got in the ambulance with me and cried the whole way to the hospital.” He was completely unpredictable.

By the time she was eighteen, Mary had developed “unwavering depression,” which would progress over the next thirty years, getting worse after she married and had her four children. She developed a severe lower back problem that worsened every year. And her autoimmune vitiligo started to cover her arms and neck.

“I fell into a postpartum depression after each birth, and after my fourth son, I was suicidal. My physical and emotional pain had snowballed. If I was driving without any of my kids in the car, I’d find myself thinking, ‘How can I crash this car into a tree in such a way that no one will know it’s suicide, and so that I’m not just impaired and a burden to my family afterward?”

And that was when, says Mary, “I realized something potent was haunting me; something was terribly wrong with how unsafe I felt in the world. I had these beautiful sons and I just didn’t feel okay inside in any way, shape, or form.”

To the developing brain, knowing what’s coming next matters most. This makes sense if you think back to how the stress response works optimally. You meet a bear in the woods and your body floods with adrenaline and cortisol so that you can decide quickly: do you run away or try to frighten away the bear? After you deal with the crisis, you recover, your stress hormones abate, and you go home with a great story.

McCarthy presents another situation. “What if that bear is circling the house and you can’t get away from it and you never know if it’s going to strike, or when, or what it will do next? There it is, threatening you every single day. You can’t fight or flee.” Then, she says, “Your emergency response system is set into overdrive over and over again. Your anxiety sensors are always going full blast.”

Even subtle, common forms of childhood stress, e.g., a hypercritical, narcissistic, or manic depressive parent can cause just as much damage as a parent who deals out angry, physical beatings or just disappears.

And in that sense, Kat’s story and Mary’s story are very similar to Laura’s, John’s, Georgia’s, Michele’s, and Ellie’s. All of them, even in adult life, felt that the bear was still out there, somewhere, circling in the woods, stalking, and might strike again any day, anytime.

According to Vincent Felitti, the one area in which a “yes” answer on the Adverse Childhood Experiences questionnaire has been correlated to a slightly higher level of adult negative health outcomes is in response to ACE question number 1, which addresses the issue of “chronic humiliation.” Would adults in the home often swear at you, insult you, put you down, or humiliate you?

This strong correlation between adverse health problems and unpredictable, chronic humiliation by a parent suggests that it is not knowing if you are safe from the “bear” that matters most.

There are a lot of bears out there. Depression, bipolar disease, alcohol, and other addictions are remarkably prevalent adult afflictions. According to the National Institute of Mental Health, over 18 percent of adults, or nearly forty four million Americans, suffer from a diagnosable mental health disorder in any given year. Twenty three million adult Americans suffer from an alcohol or drug addiction. Indeed, according to the original ACE Study, one in four people with Adverse Childhood Experiences had a parent who was addicted to alcohol.

Often, alcoholism and depression go hand in hand, addiction can be an unconscious effort to self medicate a mood disorder. But even when they are not working in tandem, mood disorders and alcoholism share one thing: both make adults behave in emotionally undependable ways. The parent who hugs you one day when picking you up from school might humiliate you in front of your friends the next afternoon. The sense of not knowing what’s coming next never goes away.

The Sadness Seed

Adversity in childhood can be the precursor to deep depression and anxiety later in life. A growing body of research shows that there is a close correlation between Adverse Childhood Experiences and emotional health disorders in adulthood. In Felitti and Anda’s Adverse Childhood Experiences Study, 18 percent of individuals with an ACE Score of 1 had suffered from clinical depression, and the likelihood rose sharply with each ACE Score. Thirty percent of those with an ACE Score of 3 and nearly 50 percent of those with an ACE Score of 4 or more had suffered from chronic depression.

Twelve and a half percent of respondents to the Adverse Childhood Experiences Study cite having an ACE Score of 4 or more.

For women, the correlation is even more disturbing. While 19 percent of men with an ACE Score of 1 suffered from clinical depression, 24 percent of women with that score did. Likewise, while 24 percent of men with a score of 2 developed adult clinical depression, 35 percent of women did. Thirty percent of men with a score of 3 developed clinical depression, compared to 42 percent of women who had three categories of Adverse Childhood Experiences. And 35 percent of men, versus nearly 60 percent of women, with a score of 4 or more suffered from chronic depression.

The strongest precursor of adult depression turned out to be Adverse Childhood Experiences that fell into the category of “childhood emotional abuse.”

Whether you are male or female, the loss of a parent in childhood triples your chances of depression in adulthood. Being raised by a mother who suffers from depression puts you at a higher risk of living with chronic pain as an adult. Children who experienced severe trauma before the age of sixteen are three times more likely to develop schizophrenia later in life.

Most disturbing are the statistics on suicide: while only 1 percent of those with an ACE Score of 0 have ever attempted suicide, almost one in five individuals with an ACE Score of 4 or more has tried to end his or her life. Indeed, a person with an ACE Score of 4 or more is, statistically, 1,220 percent more likely to attempt suicide than someone with an ACE Score of 0.

It certainly makes sense that childhood emotional trauma will spill out in our adulthood. Psychology and psychotherapy help us understand the link between our childhood wounds and adult emotional problems, and making this connection can help free us from the pain of our past.

But research tells us that often, childhood adversity leads to more deep seated changes within the brain, and that depression and mood dysregulation are also set in motion on a cellular and neurobiological level.

So what is causing neurobiological changes inside the brain itself?

How Early Adversity Changes the Shape and Size of the Brain

When a young child faces emotional adversity or stressors, cells in the brain release a hormone that actually shrinks the size of the brain’s developing hippocampus, altering his or her ability to process emotion and manage stress. Magnetic resonance imaging (MRI) studies show that the higher an individual’s childhood trauma score, the smaller the cerebral gray matter, or brain volume, is in key processing areas of the brain, including the prefrontal cortex, an area related to decision making and self regulatory skills; the amygdala, or fear processing center of the brain; and the sensory association cortices and cerebellum, both of which affect how we process and regulate emotions and moods.

MRIs also show that kids raised in orphanages have much smaller brains than those of others. That smaller brain volume may be due to a reduction in the brain’s gray matter which is made up of brain cells, or neurons, as well as white matter, which includes nerves (with coated, or myelinated, axons) that allow for the fast transmission of messages in the brain. Other studies show that this smaller sized amygdala in adults who’ve experienced childhood maltreatment shows marked “hyperactivity.” Frontal regions of the brain display “atypical activation” throughout daily life making individuals hyperreactive to even very small stressors.

The lnflamed Brain

“Early stress impacts the developing brain in a way that, until very recently, we just didn’t think was possible,” McCarthy says. “It turns out that chronic, early unpredictable stress can trigger a process of low grade inflammation within the brain itself.”

That is pretty revolutionary news. Until recently, most scientists thought that inflammation could not be generated by the brain. “We thought that the brain was what we call ‘immune-privileged,’ ” explains McCarthy. “Inflammation in the brain occurred only when there was an external event, such as a brain injury or head trauma, or an infection such as meningitis.”

But, “That has turned out not to be the case. When we are chronically stressed, the brain responds by creating a state of neuro inflammation. And that neuro inflammation can be present at levels that, until very recently, we could not even detect.”

This type of inflammation develops due to a type of non neuronal brain cell known as microglia. Our microglial cells make up about one tenth of our brain cells. For years, researchers thought that these microglia cells were “just there to get rid of stuff we didn’t need,” explains McCarthy. “They were taking out the trash, so to speak?

Microglia play an integral role in pruning our brain’s neurons and in brain development. They are crucial to the normal processing of the brain all the time, continuously scanning their environment, determining, Are we good here? Or not so good? Are we safe? Or not safe?

Shake the cage. Flash the lights. The microglia in the brain take note, fast. They don’t like chronic, unpredictable stress. They don’t like it at all.

“Microglia go off kilter in the face of chronic unpredictable stress,” says McCarthy. “They get really worked up, they crank out neurochemicals that lead to neuro inflammation. And this below-the-radar state of chronic neuro inflammation can lead to changes that reset the tone of the brain for life.”

“It is very possible that when microglia go off kilter, they are actually pruning away neurons,” McCarthy says. That is, they are killing off brain cells that we need.

In a healthy brain, microglia control the number of neurons that the cerebral cortex needs, but unhappy microglia can excessively prune away cells in areas that would normally play a key role in basic executive functions, like reasoning and impulse control. They are essential in a healthy brain, but in the face of chronic unpredictable stress, they can start eating away at the brain’s synapses.

“In some cases, microglia are engulfing and destroying dying neurons, and they are taking out the trash, just as we always thought,” says McCarthy. “But in other cases, microglia are destroying healthy neurons and in that case, it’s more like murder.” This excessive pruning can lead to what McCarthy refers to as a “reset tone” in the brain. You might think of that stressed brain as a muscle that’s lost its tone and is atrophying. And that loss of gray and white matter can trigger depression, anxiety disorders, and even more extreme psychopathology such as schizophrenia and Alzheimer’s disease.

Microglia may also prune a special group of neurons in the hippocampus that are capable of regenerating. “We used to think that you could never make new neurons but one of the most revolutionary new findings in the last decade is the discovery that there are new neurons being born in the hippocampus all the time,” says McCarthy. The growth of new neurons is very important to adult mental health. “If something interferes with their growth, depression can set in.” Indeed research suggests, says McCarthy, that “microglia, when they are overly exuberant, may kill these new neurons as soon as they are born.”

Scientists have introduced healthy microglia back into the mouse brain. The results have been stunning: once mice brains are repopulated with microglia, all signs of depression completely disappear.

So much depends on the microglia in our brain being happy, unrattled. So much depends on our microglia not pruning away too many neurons.

We might hypothesize that “angry, worked-up microglia could impair the growth of healthy new neurons in the brain’s hippocampus,“ says McCarthy. “When healthy neurons in the hippocampus die, our emotional well-being would be impaired over the long term.”

Facing situation after situation of sudden and unpredictable stress in childhood can trigger microglia to prune away important neurons and initiate a state of neuroinflammation that resets the tone of the brain, creating the conditions for long lasting anxiety and depression.

A Perfect Storm: Childhood Stress, Brain Pruning, and Adolescence

When children come into adolescence, they naturally undergo a period of developmental pruning of neurons. When we are very young, we have an overproduction of neurons and synaptic connections. Some of them die off naturally to allow us to “turn down the noise in the brain,” says McCarthy, and to increase our mastery in skills that interest us. The brain prepares for becoming more specialized at the things we’re good at and interested in, while we lose what we don’t need.

But if, due to childhood stress, lots of neurons and synapses have already been pruned away, then when the natural pruning that occurs during adolescence begins to take place, and the brain starts to naturally prune neurons it doesn’t need so that a teenager can focus on building particular skills, baseball, singing, poetry, then suddenly, there may be too much pruning going on.

Dan Siegel, MD, child neuropsychiatrist and clinical professor at the University of California, Los Angeles (UCLA), is the pioneer of a growing field known as “interpersonal biology,” which integrates the fields of neuroscience and psychology. According to Siegel, “The stress of Adverse Childhood Experiences causes toxicity to the neurons and neural pathways that integrate different areas of the brain.” When adolescent pruning occurs in the integrated circuitry between the hippocampus, which is important in storing memories; the corpus callosum, which links the left and right hemispheres of the brain; and the prefrontal cortex, these brain changes, says Siegel, have a profound effect on our decision making abilities, self-regulatory processes, attention, emotional regulation, thoughts, and behavior.

When these integrated circuits are affected by adversity, or genetic vulnerability, or both, during preadolescence, says Siegel, and then puberty hits, “adolescent pruning pares down the existing but insufficient number of integrated fibers, which makes a child vulnerable to mood dysregulation. It is when this brain integration is impaired that a dysfunction in mood regulation may emerge.”

Imagine, hypothetically speaking, that all kids start with 4,000 neurons (that’s a made-up number, for illustration purposes). Now, let’s say that we have two five year old boys, Sam and Joe. Sam faces early adversity and Joe doesn’t. As Sam meets up with chronic unpredictable stress in his childhood, his neurons are slowly pruned away. By the time Sam is twelve, after a lot of stress-related neuronal pruning, he has 1,800 neurons left. He is still okay, functioning well; 1,800 neurons are enough (using our hypothetical numbers) to get by on, since kids start out with so many more than they need in the first place.

But then Sam and Joe both go through the adolescent period of neuronal pruning. Let’s say that Sam and Joe, like all kids, each lose a hypothetical 1,000 more neurons during adolescence. Sam, who grew up with early chronic unpredictable stress, begins to emerge with a notably different brain from Joe.

Suddenly, the difference between Sam’s brain and Joe’s trauma free brain becomes extreme. Joe, who’s grown up fairly adversity free, still has his 3,000 neurons, plenty to go forward and live a healthy and happy life.

Meanwhile, Sam is left with only 800 neurons.

And that makes all the difference. It is not enough for the brain to function in a healthy manner.

For kids who have already had pruning due to early stress, Siegel explains, “when average adolescent pruning occurs, what remains may be insufficient for mood to be kept in balance. If stressors are high, this pruning process may be even more intense, and more of the at risk circuits may be diminished in number and effectiveness.”

The child who faced Adverse Childhood Experiences will be more likely to develop depression, bipolar disorder, eating disorders, anxiety disorders, or poor executive function and decision making, many of which can lead to substance abuse. This may be why, statistically, so many young people first show signs of depression or bipolar disorders in high school, and in college, even kids who just a year or two earlier seemed absolutely fine.

Stephen’s parents, both investment bankers, were hardly around when he was growing up in New York City. Stephen ate dinner at night with his older sister and their nanny. When his parents came home around nine o’clock, a time when most kids were getting tucked into bed and kissed good night, they’d all sit down together at the kitchen table, and the nanny would give her daily report. She was an older woman who loved to “give a laundry list of what we’d done wrong.” Stephen “lived in fear of that moment. Especially for my sister.”

His sister, who was five years older, was “already expected to be a genius like our parents, by the time she was in fourth grade. If she brought home an eighty-five on a math test, my parents would drill her on math problems until eleven o’clock.” Then, they’d tell their friends at the next weekend party at our country house how “Alexis is already doing algebra!”

Stephen, as the baby, often got off lightly when he was young, and recalls feeling “that my parents loved me and wanted everything for me. But they were also terrifying.”

As Stephen got older, his parents stopped “treating me like the cute baby.” He did well academically and his standardized test scores were sometimes off the charts. “My parents decided that I must be the genius they’d been waiting for. I got their laser focus.”

But he soon started to feel that “I wasn’t as smart as my parents hoped I’d be.” When he was nine, Stephen started having acute asthma attacks. He was also “perpetually forgetful. I’d lose everything. I’d forget to bring my sweater or my Spanish book home. I’d leave my clarinet in the band room. It made my parents furious. They’d tell me, ‘Get it together! We don’t have time for your nonsense, Stephen!’ ”

Once, while staying at a plush lakeside resort, he walked into water with his flip-flops on to look for tadpoles. As he walked out, one flip-flop got stuck in the mud. “I tried to find it. I was digging in the muck. My dad just lost it. He stood on the edge of the lake yelling, ‘You lost your flip-flop? Really, Stephen? You can’t take a walk without losing your shoes? You think we’re going to just buy you another pair? We’re not buying you anything!’ ” On the ride home, Stephen had a full-blown asthma attack.

Stephen was also a “nonjock.” He liked to read more than he liked to play ball. “My dad started calling me ‘pretty boy.’ I’d come in the door from being at a concert with my friends and he’d say, ‘Hey, pretty boy, good time?’ He was pissed that I hadn’t spent the weekend on an athletic field the way he had when he was seventeen, the way his colleagues’ and friends’ kids were.”

As many adult children recall, “It wasn’t all bad. My dad taught me how to fish, how to sail, and how to analyze the financial pages of the newspaper. My mom left work to come to every single concert I was in when I played in the state youth orchestra. Sometimes when my dad was out of town, she’d let my sister and me snuggle in her bed and we’d watch movies and eat sandwiches from the deli downstairs. She’d tell me, ‘Your dad loves you so much, he’s just very stressed with work, it’s not about you, Stevie.’ She was not affectionate. But she tried.”

In high school Stephen, despite high test scores, couldn’t seem to manage his workload and get papers in on time, and was diagnosed with attention deficit disorder, high stakes performance anxiety, and depression. “I just stopped wanting to go out with my friends, or do anything. I wanted the world to just let me be.” Then he developed a condition known as alopecia areata, in which the immune system attacks the hair follicles and segments of hair fall out, leaving bald patches. “My hair started falling out in huge chunks.’ ”

Stephen went on to grad school, getting his PhD in psychology. Today, Stephen is forty-two, a high school counselor. He shaves his head so that he doesn’t have to deal with the recurring bald spots from alopecia. “For me, knowing what not to do with the kids I teach, I like to think that’s the gift my parents gave me. I can see when a kid is showing signs of anxiety or depression. I see how at this age, some kids who have been struggling to hold it together for so long just can’t anymore. Things start to fall apart, and they just can’t understand what’s happening to them. I was that kid.”

The research on neuro inflammation, pruning, and the brain helps to explain why adverse experiences in childhood are so highly correlated to depression and anxiety disorders in adulthood. It also sheds light on why, according to the National Institute of Mental Health (NIMH), depression affects eighteen million Americans. The World Health Organization recently cited depression as “the leading cause of disability worldwide,” responsible for more years of disability than cancer, HIV/AIDS, and cardiovascular and respiratory diseases combined.

This also may explain other brain based health disorders. For instance, a recent study of brain scans of people suffering from chronic fatigue syndrome, or CFS, myalgic encephalomyelitis, or ME, show higher levels of inflammation in specific parts of the brain, including the hippocampus and amygdala. The greater a patient’s level of self-reported CFS symptoms, the greater the degree of visible brain inflammation.

This may also help to account for why it is that those who faced Adverse Childhood Experiences are six times more likely to develop chronic fatigue in the first place.

The Walking Wounded

It’s impossible to estimate how many adults who experienced Adverse Childhood Experiences are getting by, day by day, unwittingly navigating a state of low grade neuro inflammation, functioning despite their “reset tone” in the brain, dealing with general low mood, depression, and anxiety.

This lowered “set point of well-being,” this generalized emotional misery, predicts with startling accuracy how likely we are to find ourselves as adults navigating mood fluctuations, anxiety, sadness, fear-reacting to life without resilience, rather than really living life fully.

It’s kind of the proverbial cat chasing its tail. Epigenetic changes in life cause inflammatory chemicals to increase. Chronic unpredictable stress sends microglia off kilter. Microglia murder neurons. Neurons die, synapses are less able to connect. Microglia proliferate and create a state of neuro inflammation. Essential gray matter areas of the brain lose volume and tone. White matter, the myelin in the brain that allows for synapses to connect between neurons is lost. This lack of brain tone impairs thought processes, making negative thoughts, fears, reactivity, and worries more likely over time. An Uberalert, fearful brain leads to increased negative reactions and thoughts, creating more inflammatory hormones and chemicals that lead to more microglial dysfunction and pruning and chronic inflammation in the brain. The cycle continues.

As McCarthy puts it, “Neuro inflammation becomes a runaway process.”

This, she says, “contributes to a chronic overreactivity. Things that most people would get over quickly would send someone with a low level of inflammation into a tailspin. They may not be able to sort out rational thought about what’s happening around them, is what’s happening right now good, or is it bad? They may be far more prone to see everything as bad.”

This is the new psychosocial theory of everything: our early emotional stories determine the body and brain’s operating system and how well they will be able to guard our optimal physical and emotional health all of our adult lives.

We take whatever reactive brain and increased sensitivity to stress we develop in childhood with us wherever we go, at any age. We’re likely to feel bad mentally and physically a lot of the time. That state of neuro inflammation means we are more likely to walk around in an irritable mood, be easily ticked off and annoyed.

Our relationships will suffer. We see hurt where none is intended. We’ll likely find the world more aggravating than gratifying. Our chances for a healthy, stable, and satisfying life narrow, and continue to narrow as the years go by. But we can take action to remove the early “fingerprints” that childhood adversity leaves on our neurobiology so that imprint does not stay with us.

The Really Good News

As scientists have learned more about how childhood adversity becomes biologically embedded, they have also learned how we can intervene in this process to reverse the damage of early stress, no matter whether we grew up in a happy, functional family or an often unhappy, dysfunctional one. And no matter what happened to us when we were young.

“The beauty of epigenetics is that it’s reversible, and the beauty of the brain is that it’s plastic,” says McCarthy:

“There are many ways that we can immuno-rehabilitate the brain to overcome early negative epigenetic changes so that we can respond normally to both pleasure and pain. The brain can restore itself.”

We can heal those early scars to get back to who it is we really are, who we might have been had we not faced so much adversity in the first place. But to do that, we first have to understand why we may be more prone to epigenetic changes than others in the first place, even though we are no less capable of epigenetic reversal and change.


from

Childhood Disrupted. How Your Biography Becomes Your Biology, and How You Can Heal

by Donna Jackson Nakazawa

get it at Amazon.com

Childhood Disrupted. How Your Biography Becomes Your Biology, and How You Can Heal – Donna Jackson Nakazawa * The Origins of Addiction. Evidence from the Adverse Childhood Experiences Study – Vincent J. Felitti, MD.

Chronic adversities change the architecture of a child’s brain, altering the expression of genes that control stress hormone output, triggering an overactive inflammatory stress response for life, and predisposing the child to adult disease.

“I felt myself a stranger at life’s party.”

New findings in neuroscience, psychology, and medicine have recently unveiled the exact ways in which childhood adversity biologically alters us for life. The past can tick away inside us for decades like a silent time bomb, until it sets off a cellular message that lets us know the body does not forget the past. Something that happened to you when you were five or fifteen can land you in the hospital thirty years later, whether that something was headline news, or happened quietly, without anyone else knowing it, in the living room of your childhood home.

No matter how old you are, or how old your children may be, there are scientifically supported and relatively simple steps that you can take to reboot the brain, create new pathways that promote healing, and come back to who it is you were meant to be.

Our findings are disturbing to some because they imply that the basic causes of addiction lie within us and the way we treat each other, not in drug dealers or dangerous chemicals. They suggest that billions of dollars have been spent everywhere except where the answer is to be found. Our findings indicate that the major factor underlying addiction is adverse childhood experiences that have not healed with time and that are overwhelmingly concealed from awareness by shame, secrecy, and social taboo.

“I wept, I saw how much people had suffered and I wept.” Robert Anda

“Our findings exceeded anything we had conceived. The correlation between having a difficult childhood and facing illness as an adult offered a whole new lens through which we could view human health and disease. Here was the missing piece as to what was causing so much of our unspoken suffering as human beings. Time does not heal all wounds. One does not ‘just get over’ something, not even fifty years later. Instead time conceals. And human beings convert traumatic emotional experiences in childhood into organic disease later in life.” Vincent Felitti

Adverse childhood experiences are the main determinant of the health and social well being of a nation.

This book explores how the experiences of childhood shape us into the adults we become. Cutting-edge research tells us that what doesn’t kill you doesn’t necessarily make you stronger. Far more often, the opposite is true: the early chronic unpredictable stressors, losses, and adversities we face as children shape our biology in ways that predetermine our adult health. This early biological blueprint depicts our proclivity to develop life altering adult illnesses such as heart disease, cancer, autoimmune disease, fibromyalgia, and depression. It also lays the groundwork for how we relate to others, how successful our love relationships will be, and how well we will nurture and raise our own children.

My own investigation into the relationship between childhood adversity and adult physical health began after I’d spent more than a dozen years struggling to manage several life limiting autoimmune illnesses while raising young children and working as a journalist. In my forties, I was paralyzed twice with an autoimmune disease known as Guillain-Barré syndrome, similar to multiple sclerosis, but with a more sudden onset. I had muscle weakness; pervasive numbness; a pacemaker for vasovagal syncope, a fainting and seizing disorder; white and red blood cell counts so low my doctor suspected a problem was brewing in my bone marrow; and thyroid disease.

Still I knew: I was fortunate to be alive, and I was determined to live the fullest life possible. If the muscles in my hands didn’t cooperate, I clasped an oversized pencil in my fist to write. If I couldn’t get up the stairs because my legs resisted, I sat down halfway up and rested. I gutted through days battling flulike fatigue, pushing away fears about what might happen to my body next; faking it through work phone calls while lying prone on the floor; reserving what energy I had for moments with my children, husband, and family life; pretending that our “normal” was really okay by me. It had to be, there was no alternative in sight.

Increasingly, I devoted my skills as a science journalist to helping women with chronic illness, writing about the intersection between neuroscience, our immune systems, and the innermost workings of our human hearts. I investigated the many triggers of disease, reporting on chemicals in our environment and foods, genetics, and how inflammatory stress undermines our health. I reported on how going green, eating clean, and practices like mind-body meditation can help us to recuperate and recover. At health conferences I lectured to patients, doctors, and scientists. My mission became to do all I could to help readers who were caught in a chronic cycle of suffering, inflammation, or pain to live healthier, better lives.

In the midst of that quest, three years ago, in 2012, I came across a growing body of science based on a groundbreaking public health research study, the Adverse Childhood Experiences Study, or ACE Study. The ACE Study shows a clear scientific link between many types of childhood adversity and the adult onset of physical disease and mental health disorders. These traumas include being verbally put down and humiliated; being emotionally or physically neglected; being physically or sexually abused; living with a depressed parent, a parent with a mental illness, or a parent who is addicted to alcohol or other substances; witnessing one’s mother being abused; and losing a parent to separation or divorce. The ACE Study measured ten types of adversity, but new research tells us that other types of childhood trauma, such as losing a parent to death, witnessing a sibling being abused, violence in one’s community, growing up in poverty, witnessing a father being abused by a mother, being bullied by a classmate or teacher, also have a longterm impact.

These types of chronic adversities change the architecture of a child’s brain, altering the expression of genes that control stress hormone output, triggering an overactive inflammatory stress response for life, and predisposing the child to adult disease. ACE research shows that 64 percent of adults faced one ACE in their childhood, and 40 percent faced two or more.

My own doctor at Johns Hopkins medical institutions confessed to me that she suspected that, given the chronic stress I’d faced in my childhood, my body and brain had been marinating in toxic inflammatory chemicals my whole life, predisposing me to the diseases I now faced.

My own story was a simple one of loss. When I was a girl, my father died suddenly. My family struggled and became estranged from our previously tight knit, extended family. I had been exceptionally close to my father and I had looked to him for my sense of being safe, okay, and valued in the world. In every photo of our family, I’m smiling, clasped in his arms. When he died, childhood suddenly ended, overnight. If I am honest with myself, looking back, I cannot recall a single “happy memory” from there on out in my childhood. It was no one’s fault. It just was. And I didn’t dwell on any of that. In my mind, people who dwelled on their past, and especially on their childhood, were emotionally suspect.

I soldiered on. Life catapulted forward. I created a good life, worked hard as a science journalist to help meaningful causes, married a really good husband, and brought up children I adored, children I worked hard to stay alive for. But other than enjoying the lovely highlights of a hard won family life, or being with close friends, I was pushing away pain.

I felt myself a stranger at life’s party. My body never let me forget that inside, pretend as I might, I had been masking a great deal of loss for a very long time. I felt myself to be “not like other people.”

Seen through the lens of the new field of research into Adverse Childhood Experiences, it suddenly seemed almost predictable that, by the time I was in my early forties, my health would deteriorate and I would be brought, in my case, quite literally, to my knees.

Like many people, I was surprised, even dubious, when I first learned about ACEs and heard that so much of what we experience as adults is so inextricably linked to our childhood experiences. I did not consider myself to be someone who had had Adverse Childhood Experiences. But when I took the ACES questionnaire and discovered my own ACE Score, my story also began to make so much more sense to me. This science was entirely new, but it also supported old ideas that we have long known to be true: “the child is father of the man.” This research also told me that none of us is alone in our suffering.

One hundred thirty three million Americans suffer from chronic illness and 116 million suffer from chronic pain. This revelation of the link between childhood adversity and adult illness can inform all of our efforts to heal. With this knowledge, physicians, health practitioners, psychologists, and psychiatrists can better understand their patients and find new insights to help them. And this knowledge will help us ensure that the children in our lives, whether we are parents, mentors, teachers, or coaches, don’t suffer from the long term consequences of these sorts of adversity.

To learn everything I could, I spent two years interviewing the leading scientists who research and study the effects of Adverse Childhood Experiences and toxic childhood stress. I combed through seventy research papers that comprise the ACE Study and hundreds of other studies from our nation’s best research institutions that support and complement these findings. And I followed thirteen individuals who suffered early adversity and later faced adult health struggles, who were able to forge their own lifechanging paths to physical and emotional healing.

In these pages, I explore the damage that Adverse Childhood Experiences can do to the brain and body; how these invisible changes contribute to the development of disease including autoimmune diseases, long into adulthood; why some individuals are more likely to be affected by early adversity than others; why girls and women are more affected than men; and how early adversity affects our ability to love and parent.

Just as important, I explore how we can reverse the effects of early toxic stress on our biology, and come back to being who we really are. I hope to help readers to avoid spending so much of their lives locked in pain.

Some points to bear in mind as you read these pages:

– Adverse Childhood Experiences should not be confused with the inevitable small challenges of childhood that create resilience. There are many normal moments in a happy childhood, when things don’t go a child’s way, when parents lose it and apologize, when children fail and learn to try again. Adverse Childhood Experiences are very different sorts of experiences; they are scary, chronic, unpredictable stressors, and often a child does not have the adult support needed to help navigate safely through them.

– Adverse Childhood Experiences are linked to a far greater likelihood of illness in adulthood, but they are not the only factor. All disease is multifactorial. Genetics, exposures to toxins, and infection all play a role. But for those who have experienced ACEs and toxic stress, other disease promoting factors become more damaging.

To use a simple metaphor, imagine the immune system as being something like a barrel. If you encounter too many environmental toxins from chemicals, a poor processed food diet, viruses, infections, and chronic or acute stressors in adulthood, your barrel will slowly fill. At some point, there may be one certain exposure, that last drop that causes the barrel to spill over and disease to develop.

Having faced the chronic unpredictable stressors of Adverse Childhood Experiences is a lot like starting life with your barrel half full. ACEs are not the only factor in determining who will develop disease later in life. But they may make it more likely that one will.

– The research into Adverse Childhood Experiences has some factors in common with the research on post-traumatic stress disorder, or PTSD. But childhood adversity can lead to a far wider range of physical and emotional health consequences than the overt symptoms of posttraumatic stress. They are not the same.

– The Adverse Childhood Experiences of extreme poverty and neighborhood violence are not addressed specifically in the original research. Yet clearly, growing up in unsafe neighborhoods where there is poverty and gang violence or in a war-torn area anywhere around the world creates toxic childhood stress, and that relationship is now being more deeply studied. It is an important field of inquiry and one I do not attempt to address here; that is a different book, but one that is no less important.

– Adverse Childhood Experiences are not an excuse for egregious behavior. They should not be considered a “blame the childhood” moral pass. The research allows us to finally tackle real and lasting physical and emotional change from an entirely new vantage point, but it is not about making excuses.

This research is not an invitation to blame parents. Adverse Childhood Experiences are often an intergenerational legacy, and patterns of neglect, maltreatment, and adversity almost always originate many generations prior to one’s own.

The new science on Adverse Childhood Experiences and toxic stress has given us a new lens through which to understand the human story; why we suffer; how we parent, raise, and mentor our children; how we might better prevent, treat, and manage illness in our medical care system; and how we can recover and heal on a deeper level than we thought possible.

And that last bit is the best news of all. The brain, which is so changeable in childhood, remains malleable throughout life. Today researchers around the world have discovered a range of powerful ways to reverse the damage that Adverse Childhood Experiences do to both brain and body. No matter how old you are, or how old your children may be, there are scientifically supported and relatively simple steps that you can take to reboot the brain, create new pathways that promote healing, and come back to who it is you were meant to be.

To find out about how many categories of ACEs you might have faced when you were a child or teenager, and your own ACE Score, turn the page and take the Adverse Childhood Experiences Survey for yourself.

TAKE THE ADVERSE CHILDHOOD EXPERIENCES (ACE) SURVEY

You may have picked up this book because you had a painful or traumatic childhood. You may suspect that your past has something to do with your current health problems, your depression, or your anxiety. Or perhaps you are reading this book because you are worried about the health of a spouse, partner, friend, parent, or even your own child, who has survived a trauma or suffered adverse experiences. In order to assess the likelihood that an Adverse Childhood Experience is affecting your health or the health of your loved one, please take a moment to fill out the following survey before you read this book.

ADVERSE CHILDHOOD EXPERIENCES SURVEY

Prior to your eighteenth birthday:

1. Did a parent or another adult in the household

often or very often . . . swear at you, insult you, put you down, or humiliate you? Or act in a way that made you afraid that you might be physically hurt?

Yes No, If yes, enter 1

2. Did a parent or another adult in the household

often or very often . . . push, grab, slap, or throw something at you? Or ever hit you so hard that you had marks or were injured?

Yes No, If yes, enter 1

3. Did an adult or person at least five years older than you

ever touch or fondle you or have you touch their body in a sexual way? Or attempt to touch you or touch you inappropriately or sexually abuse you?

Yes No, If yes, enter 1

4. Did you often or very often feel that

noone in your family loved you or thought you were important or special? Or feel that your family members didn’t look out for one another, feel close to one another, or support one another?

Yes No, If yes, enter 1

5. Did you often or very often

feel that you didn’t have enough to eat, had to wear dirty clothes, and had no one to protect you? Or that your parents were too drunk or high to take care of you or take you to the doctor if you needed it?

Yes No, If yes, enter 1

6. Was a biological parent ever lost to you

through divorce, abandonment, or another reason?

Yes No, If yes, enter 1

7. Was your mother or stepmother often or very often

pushed, grabbed, slapped, or have something thrown at her? Or was she sometimes, often, or very often kicked, bitten, hit with a fist, or hit with something hard? Or ever repeatedly hit over the course of at least a few minutes or threatened with a gun or knife?

Yes No, If yes, enter 1

8. Did you live with anyone who was

a problem drinker or alcoholic, or who used street drugs?

Yes No, If yes, enter 1

9. Was a household member

depressed or mentally ill, or did a household member attempt suicide?

Yes No, If yes, enter 1

10. Did a household member go to prison?

Yes No, If yes, enter 1

Add up your “Yes” answers: (this is your ACE Score)

Now take a moment and ask yourself how your experiences might be affecting your physical, emotional, and mental well-being. Is it possible that someone you love has been affected by Adverse Childhood Experiences they experienced? Are any children or young people you care for in adverse situations now?

Keep your Adverse Childhood Experiences Score in mind as you read the stories and science that follow, and keep your own experiences in mind, as well as those of the people you love. You may find this science to be the missing link in understanding why you or your loved one is having health problems. And this missing link will also lead to the information you will need in order to heal.

PART 1

How It Is We Become Who We Are

CHAPTER ONE

Every Adult Was Once a Child

If you saw Laura walking down the New York City street where she lives today, you’d see a well dressed forty six year old woman with auburn hair and green eyes who exudes a sense of “I matter here.” She looks entirely in charge of her life, as long as you don’t see the small ghosts trailing after her.

When Laura was growing up, her mom was bipolar. Laura’s mom had her good moments: she helped Laura with school projects, braided her hair, and taught her the name of every bird at the bird feeder. But when Laura’s mom suffered from depressive bouts, she’d lock herself in her room for hours. At other times she was manic and hypercritical, which took its toll on everyone around her. Laura’s dad, a vascular surgeon, was kind to Laura, but rarely around. He was, she says, “home late, out the door early, and then just plain out the doom”

Laura recalls a family trip to the Grand Canyon when she was ten. In a photo taken that day, Laura and her parents sit on a bench, sporting tourist whites. The sky is blue and cloudless, and behind them the dark, ribboned shadows of the canyon stretch deep and wide. It is a perfect summer day.

“That afternoon my mom was teaching me to identify the ponderosa pines,” Laura recalls. “Anyone looking at us would have assumed we were a normal, loving family.” Then, something seemed to shift, as it sometimes would. Laura’s parents began arguing about where to set up the tripod for their family photo. By the time the three of them sat down, her parents weren’t speaking. As they put on fake smiles for the camera, Laura’s mom suddenly pinched her daughter’s midriff around the back rim of her shorts, and told her to stop “staring off into space.” Then, a second pinch: “no wonder you’re turning into a butterball, you ate so much cheesecake last night you’re hanging over your shorts!”

If you look hard at Laura’s face in the photograph, you can see that she’s not squinting at the Arizona sun, but holding back tears.

When Laura was fifteen, her dad moved three states away with a new wife to be. He sent cards and money, but called less and less often. Her mother’s untreated bipolar disorder worsened. Laura’s days were punctuated with put downs that caught her off guard as she walked across the living room. “My mom would spit out something like, ‘You look like a semiwide from behind. If you’re ever wondering why no boy asks you out, that’s why!”’ One of Laura’s mother’s recurring lines was, “You were such a pretty baby, I don’t know what happened.” Sometimes Laura recalls, “My mom would go on a vitriolic diatribe about my dad until spittle foamed on her chin. I’d stand there, trying not to hear her as she went on and on, my whole body shaking inside.”

Laura never invited friends over, for fear they’d find out her secret: her mom “wasn’t like other moms.”

Some thirty years later, Laura says, “In many ways, no matter where I go or what I do, I’m still in my mother’s house.” Today, “If a car swerves into my lane, a grocery store clerk is rude, my husband and I argue, or my boss calls me in to talk over a problem, I feel something flip over inside. It’s like there’s a match standing inside too near a flame, and with the smallest breeze, it ignites.” Something, she says, “just doesn’t feel right. Things feel bigger than they should be. Some days, I feel as if I’m living my life in an emotional boom box where the volume is turned up too high.”

To see Laura, you would never know that she is “always shaking a little, only invisibly, deep down in my cells.”

Laura’s sense that something is wrong inside is mirrored by her physical health. In her mid thirties, she began suffering from migraines that landed her in bed for days at a time. At forty, Laura developed an autoimmune thyroid disease. At forty four, during a routine exam, Laura’s doctor didn’t like the sound of her heart. An EKG revealed an arrhythmia. An echocardiogram showed that Laura had a condition known as dilated cardiomyopathy. The left ventricle of her heart was weak; the muscle had trouble pumping blood into her heart. Next thing Laura knew, she was a heart disease patient, undergoing surgery. Today, Laura has a cardioverter defibrillator implanted in the left side of her chest to prevent heart failure. The two-inch scar from the implant is deceivingly small.

John’s parents met in Asia when his father was deployed there as an army officer. After a whirlwind romance, his parents married and moved to the United States. For as long as John can remember, he says, “my parents’ marriage was deeply troubled, as was my relationship with my dad. I consider myself to have been raised by my mom and her mom. I longed to feel a deeper connection with my dad, but it just wasn’t there. He couldn’t extend himself in that way.”

John occasionally runs his hands through his short blond hair, as he carefully chooses his words. “My dad would get so worked up and pissed off about trivial things. He’d throw out opinions that we all knew were factually incorrect, and just keep arguing.” If John’s dad said the capital of New York was New York City, it didn’t matter if John showed him it was Albany. “He’d ask me to help in the garage and I’d be doing everything right, and then a half hour into it I’d put the screwdriver down in the wrong spot and he’d start yelling and not let up. There was never any praise. Even when he was the one who’d made a mistake, it somehow became my fault. He could not be wrong about anything.”

As John got older, it seemed wrong to him that “my dad was constantly pointing out all the mistakes that my brother and I made, without acknowledging any of his own.” His dad chronically criticized his mother, who was, John says, “kinder and more confident.”

When John was twelve, he interjected himself into the fights between his parents. One Christmas Eve, when he was fifteen, John awoke to the sound of “a scream and a commotion. I realized it was my mother screaming. I jumped out of bed and ran into my parents’ room, shouting, ‘What the hell is going on here?’ My mother sputtered, ‘He’s choking me!’ My father had his hands around my mother’s neck. I yelled at him: ‘You stay right here! Don’t you dare move! Mom is coming with me!’ I took my mother downstairs. She was sobbing. I was trying to understand what was happening, trying to be the adult between them.”

Later that Christmas morning, John’s father came down the steps to the living room where John and his mom were sleeping. “No one explained,” he says. “My little brother came downstairs and we had Christmas morning as if nothing had happened.”

Not long after, John’s grandmother, “who’d been an enormous source of love for my mom and me,” died suddenly. John says, “It was a terrible shock and loss for both of us. My father couldn’t support my mom or me in our grieving. He told my mom, ‘You just need to get over it!’ He was the quintessential narcissist. If it wasn’t about him, it wasn’t important, it wasn’t happening.”

Today, John is a boyish forty. He has warm hazel eyes and a wide, affable grin that would be hard not to warm up to. But beneath his easy, open demeanor, John struggles with an array of chronic illnesses.

By the time John was thirty three, his blood pressure was shockingly high for a young man. He began to experience bouts of stabbing stomach pain and diarrhea and often had blood in his stool. These episodes grew more frequent. He had a headache every day of his life. By thirty four, he’d developed chronic fatigue, and was so wiped out that sometimes he struggled to make it through an entire day at work.

For years, John had loved to go hiking to relieve stress, but by the time he was thirty five, he couldn’t muster the physical stamina. “One day it hit me, I’m still a young man and I’ll never go hiking again.’ ”

John’s relationships, like his physical body, were never quite healthy. John remembers falling deeply in love in his early thirties. After dating his girlfriend for a year, she invited him to meet her family. During his stay with them, John says, “I became acutely aware of how different I was from kids who grew up without the kind of shame and blame I endured.” One night, his girlfriend, her sisters, and their boyfriends all decided to go out dancing. “Everyone was sitting around the dinner table planning this great night out and I remember looking around at her family and the only thing going through my mind were these words: ‘I do not belong here.’ Everyone seemed so normal and happy. I was horrified suddenly at the idea of trying to play along and pretend that I knew how to be part of a happy family.”

So John faked “being really tired. My girlfriend was sweet and stayed with me and we didn’t go. She kept asking what was wrong and at some point I just started crying and I couldn’t stop. She wanted to help, but instead of telling her how insecure I was, or asking for her reassurance, I told her I was crying because I wasn’t in love with her.”

John’s girlfriend was, he says, “completely devastated.” She drove John to a hotel that night. “She and her family were shocked. No one could understand what had happened.” Even though John had been deeply in love, his fear won out. “I couldn’t let her find out how crippled I was by the shame and grief I carried inside.”

Bleeding from his inflamed intestines, exhausted by chronic fatigue, debilitated and distracted by pounding headaches, often struggling with work, and unable to feel comfortable in a relationship, John was stuck in a universe of pain and solitude, and he couldn’t get out.

Georgia’s childhood seems far better than the norm: she had two living parents who stayed married through thick and thin, and they lived in a stunning home with walls displaying Ivy League diplomas; Georgia’s father was a well-respected, Yale-educated investment banker. Her mom stayed at home with Georgia and two younger sisters. The five of them appear, in photos, to be the perfect family.

All seemed fine, growing up, practically perfect.

“But I felt, very early on, that something wasn’t quite right in our home, and that no one was talking about it,” Georgia says. “Our house was saturated by a kind of unease all the time. You could never put your finger on what it was, but it was there.”

Georgia’s mom was “emotionally distant and controlling,” Georgia recalls. “If you said or did something she didn’t like, she had a way of going stone cold right in front of you she’d become what I used to think of as a moving statue that looked like my mother, only she wouldn’t look at you or speak to you.” The hardest part was that Georgia never knew what she’d done wrong. “I just knew that l was shut out of her world until whenever she decided I was worth speaking to again.”

For instance, her mother would “give my sisters and me a tiny little tablespoon of ice cream and then say, ‘You three will just have to share that.’ We knew better than to complain. If we did, she’d tell us how ungrateful we were, and suddenly she wouldn’t speak to us.”

Georgia’s father was a borderline alcoholic and “would occasionally just blow up over nothing,” she says. “One time he was changing a light bulb and he just started cursing and screaming because it broke. He had these unpredictable eruptions of rage. They were rare but unforgettable.” Georgia was so frightened at times that “I’d run like a dog with my tail between my legs to hide until it was safe to come out again.”

Georgia was “so sensitive to the shifting vibe in our house that I could tell when my father was about to erupt before even he knew. The air would get so tight and I’d know, it’s going to happen again.” The worst part was that “We had to pretend my father’s outbursts weren’t happening. He’d scream about something minor, and then he’d go take a nap. Or you’d hear him strumming his guitar in his den.”

Between her mother’s silent treatments and her dad’s tirades, Georgia spent much of her childhood trying to anticipate and move out of the way of her parents’ anger. She had the sense, even when she was nine or ten, “that their anger was directed at each other. They didn’t fight, but there was a constant low hum of animosity between them. At times it seemed they vehemently hated each other.” Once, fearing that her inebriated father would crash his car after an argument with her mother, Georgia stole his car keys and refused to give them back.

Today, at age forty nine, Georgia is reflective about her childhood. “I internalized all the emotions that were storming around me in my house, and in some ways it’s as if I’ve carried all that external angst inside me all my life.” Over the decades, carrying that pain has exacted a high toll. At first, Georgia says, “My physical pain began as a low whisper in my body.” But by the time she entered Columbia graduate school to pursue a PhD in classics, “I’d started having severe back problems. I was in so much physical pain, I could not sit in a chair. I had to study lying down.” At twenty six, Georgia was diagnosed with degenerative disc disease. “My body just started screaming with its pain.”

Over the next few years, in addition to degenerative disc disease, Georgia was diagnosed with severe depression, adrenal fatigue, and finally, fibromyalgia. “I’ve spent my adult life in doctors’ clinics and trying various medications to relieve my pain,” she says. “But there is no relief in sight.”

Laura’s, John’s, and Georgia’s life stories illustrate the physical price we pay, as adults, for childhood adversity. New findings in neuroscience, psychology, and medicine have recently unveiled the exact ways in which childhood adversity biologically alters us for life.

This groundbreaking research tells us that the emotional trauma we face when we are young has farther reaching consequences than we might have imagined.

Adverse Childhood Experiences change the architecture of our brains and the health of our immune systems, they trigger and sustain inflammation in both body and brain, and they influence our overall physical health and longevity long into adulthood.

These physical changes, in turn, prewrite the story of how we will react to the world around us, and how well we will work, and parent, befriend, and love other people throughout the course of our adult lives.

This is true whether our childhood wounds are deeply traumatic, such as witnessing violence in our family, as John did; or more chronic living room variety humiliations, such as those Laura endured; or more private but pervasive familial dysfunctions, such as Georgia’s.

All of these Adverse Childhood Experiences can lead to deep biophysical changes in a child that profoundly alter the developing brain and immunology in ways that also change the health of the adult he or she will become.

Scientists have come to this startling understanding of the link between Adverse Childhood Experiences and later physical illness in adulthood thanks, in large part, to the work of two individuals: a dedicated physician in San Diego, and a determined medical epidemiologist from the Centers for Disease Control (CDC). Together, during the 1980s and 1990s, the same years when Laura, John, and Georgia were growing up, these two researchers slowly uncovered the stunning scientific link between Adverse Childhood Experiences and later physical and neurological inflammation and life changing adult health outcomes.

The Philosophical Physicians

In 1985 physician and researcher Vincent J. Felitti, MD, chief of a revolutionary preventive care initiative at the Kaiser Permanente Medical Program in San Diego, noticed a startling pattern: adult patients who were obese also alluded to traumatic incidents in their childhood. Felitti came to this realization almost by accident.

In the mid 1980s, a significant number of patients in Kaiser Permanente’s obesity program were, with the help and support of Felitti and his nurses, successfully losing hundreds of pounds a year nonsurgically, a remarkable feat. The program seemed a resounding success, up until a large number of patients who were losing substantial amounts of weight began to drop out.

The attrition rate didn’t make sense, and Felitti was determined to find out what was going on. He conducted face-to-face interviews with 286 patients. In the course of Felitti’s one-on-one conversations, a striking number of patients confided that they had faced trauma in their childhood; many had been sexually abused. To these patients, eating was a solution: it soothed the anxiety, fear, and depression that they had secreted away inside for decades. Their weight served, too, as a shield against unwanted physical attention, and they didn’t want to let it go.

Felitti’s conversations with this large group of patients allowed him to perceive a pattern, and a new way of looking at human health and well-being, that other physicians just were not seeing. It became clear to him that, for his patients, obesity, “though an obvious physical sign,” was not the core problem to be treated, “any more than smoke is the core problem to be treated in house fires.”

In 1990, Felitti presented his findings at a national obesity conference. He told the group of physicians gathered that he believed “certain of our intractable public health problems” had root causes hidden “by shame, by secrecy, and by social taboos against exploring certain areas of life experience.”….

*

from

Childhood Disrupted. How Your Biography Becomes Your Biology, and How You Can Heal

by Donna Jackson Nakazawa

get it at Amazon.com


The Origins of Addiction: Evidence from the Adverse Childhood Experiences Study

Vincent J. Felitti, MD

Department of Preventive Medicine Kaiser Permanente Medical Care Program

”In my beginning is my end.” T.S. Elliot, “Four Quartets”

ABSTRACT:

A population based analysis of over 17,000 middle class American adults undergoing comprehensive, biopsychosocial medical evaluation indicates that three common categories of addiction are strongly related in a proportionate manner to several specific categories of adverse experiences during childhood. This, coupled with related information. suggests that the basic cause of addiction is predominantly experience dependent during childhood and not substance dependent. This challenge to the usual concept of the cause of addictions has significant implications for medical practice and for treatment programs.

Purpose: My intent is to challenge the usual concept of addiction with new evidence from a population based clinical study of over 17,000 adult, middle class Americans.

The usual concept of addiction essentially states that the compulsive use of ‘addictive’ substances is in some way caused by properties intrinsic to their molecular structure’. This view confuses mechanism with cause. Because any accepted explanation of addiction has social. medical. therapeutic, and legal implications, the way one understands addiction is important. Confusing mechanism with basic cause quickly leads one down a path that is misleading. Here, new data is presented to stimulate rethinking the basis of addiction.

Background: The information I present comes from the Adverse Childhood Experiences (ACE) Study. The ACE Study deals with the basic causes underlying the 10 most common causes of death in America; addiction is only one of several outcomes studied.

In the mid 1980s, physicians in Kaiser Permanente’s Department of Preventive Medicine in San Diego discovered that patients successfully losing weight in the Weight Program were the most likely to drop out. This unexpected observation led to our discovery that overeating and obesity were often being used unconsciously as protective solutions to unrecognized problems dating back to childhood.” Counterintuitively, obesity provided hidden benefits: it often was sexually, physically, or emotionally protective.

Our discovery that public health problems like obesity could also be personal solutions, and our finding an unexpectedly high prevalence of adverse childhood experiences in our middle class adult population, led to collaboration with the Centers for Disease Control (CDC) to document their prevalence and to study the implications of these unexpected clinical observations. I am deeply indebted to my colleague, Robert F. Anda MD, who skillfully designed the Adverse Childhood Experiences (ACE) Study in an epidemiologically sound manner, and whose group at CDC analyzed several hundred thousand pages of patient data to produce the data we have published.

Many of our obese patients had previously been heavy drinkers, heavy smokers, or users of illicit drugs. Of what relevance are these observations; do they imply some unspecified innate tendency to addiction? Is addiction genetic, as some have proposed for alcoholism? Is addiction a biomedical disease. a personality disorder. or something different? Are diseases and personality disorders separable. or are they ultimately related? What does one make of the dramatic recent findings in neurobiology that seem to promise a neurochemical explanation for addiction? Why does only a small percent of persons exposed to addictive substances become compulsive users?

Although the problem of narcotic addiction has led to extensive legislative attempts at eradication, its prevalence has not abated over the past century. However. the distribution pattern of narcotic use within the population has radically changed. attracting significant political attention and governmental actions The inability to control addiction by these major, well intended governmental efforts has drawn thoughtful and challenging commentary from a number of different viewpoints.

In our detailed study of over 17.000 middle class American adults of diverse ethnicity, we found that the compulsive use of nicotine, alcohol, and injected street drugs increases proportionally in a strong, graded dose response manner that closely parallels the intensity of adverse life experiences during childhood. This of course supports old psychoanalytic views and is at odds with current concepts, including those of biological psychiatry, drug treatment programs, and drug eradication programs.

Our findings are disturbing to some because they imply that the basic causes of addiction lie within us and the way we treat each other, not in drug dealers or dangerous chemicals. They suggest that billions of dollars have been spent everywhere except where the answer is to be found.

Study design: Kaiser Permanente (KP) is the largest prepaid. non profit. healthcare delivery system in the United States; there are 500,000 KP members in San Diego, approximately 30% of the greater metropolitan population. We invited 26,000 consecutive adults voluntarily seeking comprehensive medical evaluation in the Department of Preventive Medicine to help us understand how events in childhood might later affect health status in adult life. Seventy percent agreed, understanding the information obtained was anonymous and would not become part of their medical records.

Our cohort population was 80% white including Hispanic, 10% black, and 10% Asian. Their average age was 57 years; 74% had been to college. 44% had graduated college; 49.5% were men.

In any four year period, 81% of all adult Kaiser Health Plan members seek such medical evaluation; there is no reason to believe that selection bias is a significant factor in the Study. The Study was carried out in two waves. to allow mid point correction if necessary. Further details of Study design are described in our initial publication.

The ACE Study compares adverse childhood experiences against adult health status, on average a half century later. The experiences studied were eight categories of adverse childhood experience commonly observed in the Weight Program. The prevalence of each category is stated in parentheses. The categories are:

1. recurrent and severe physical abuse (11%)

2. recurrent and severe emotional abuse (11%)

3. contact sexual abuse (22%)

growing up in a household with:

4. an alcoholic or drug user (25%)

5. a member being imprisoned (3%)

6. a mentally ill, chronically depressed, or institutionalized member (19%)

7. the mother being treated violently (12%)

8. both biological parents not being present (22%)

The scoring system is simple: exposure during childhood or adolescence to any category of ACE was scored as one point. Multiple exposures within a category were not scored: one alcoholic within a household counted the same as an alcoholic and a drug user; if anything, this tends to understate our findings. The ACE Score therefore can range from 0 to 8. Less than half of this middle class population had an ACE Score of 0; one in fourteen had an ACE Score of 4 or more.

In retrospect, an initial design flaw was not scoring subtle issues like low level neglect and lack of interest in a child who is otherwise the recipient of adequate physical care. This omission will not affect the interpretation of our First Wave findings, and may explain the presence of some unexpected outcomes in persons having ACE Score zero. Emotional neglect was studied in the Second Wave.

The ACE Study contains a prospective arm: the starting cohort is being followed forward in time to match adverse childhood experiences against current doctor office visits, emergency depanment visits, pharmacy costs, hospitalizations, and death. Publication of these analyses soon will begin.

Findings: Our overall findings. presented extensively in the American literature, demonstrate that:

– Adverse childhood experiences are surprisingly common. although typically concealed and unrecognized.

– ACEs still have a profound effect 50 years later, although now transformed from psychosocial experience into organic disease, social malfunction, and mental illness.

– Adverse childhood experiences are the main determinant of the health and social well being of the nation.

Our overall findings challenge conventional views, some of which are clearly defensive. They also provide opportunities for new approaches to some of our most difficult public health problems. Findings from the ACE Study provide insights into changes that are needed in pediatrics and adult medicine, which expectedly will have a significant impact on the cost and effectiveness of medical care.

Our intent here is to present our findings only as they relate to the problem of addiction, using nicotine, alcohol, and injected illicit drugs as examples of substances that are commonly viewed as ‘addicting‘. If we know why things happen and how, then we may have a new basis for prevention.

Smoking

Smoking tobacco has come under heavy opposition in the United States, particularly in southern California where the ACE Study was carried out. Whereas at one time most men and many women smoked, only a minority does so now; it is illegal to smoke in office buildings, public transportation, restaurants, bars, and in most areas of hotels.

When we studied current smokers, we found that smoking had a strong, graded relationship to adverse childhood experiences Figure 1 illustrates this clearly. The p value for this and all other data displays is .001 or better.

This stepwise 250% increase in the likelihood of an ACE Score 6 child being a current smoker, compared to an ACE Score 0 child. is generally not known. This simple observation has profound implications that illustrate the psychoactive benefits of nicotine; this information has largely been lost in the public health onslaught against smoking but is important in understanding the intractable nature of smoking in many people.

When we match the prevalence of adult chronic bronchitis and emphysema against ACEs, we again see a strong dose response relationship. We thereby proceed from the relationship of adverse childhood experiences to a health risk behavior to their relationship with an organic disease. In other words, Figure 2 illustrates the conversion of emotional stressors into an organic disease, through the intermediary mechanism of an emotionally beneficial (although medically unsafe) behavior.

Alcoholism

One’s own alcoholism is not easily or comfortably acknowledged; therefore. when we asked our Study cohort if they had ever considered themselves to be alcoholic, we felt that Yes answers probably understated the truth, making the effect even stronger than is shown. The relationship of self acknowledged alcoholism to adverse childhood experiences is depicted in Figure 3. Here we see that more than a 500% increase in adult alcoholism is related in a strong, graded manner to adverse childhood experiences.

Injection of illegal drugs

In the United States the most commonly injected street drugs are heroin and methamphetamine. Methamphetamine has the interesting property of being closely related to amphetamine, the first anti depressant introduced by Ciba Pharmaceuticals in 1932.

When we studied the relation of injecting illicit drugs to adverse childhood experiences, we again found a similar dose response pattern; the likelihood of injection of street drugs increases strongly and in a graded fashion as the ACE Score increases (Figure 4). At the extremes of ACE Score. the figures for injected drug use are even more powerful. For instance, a male child with an ACE Score of 6, when compared to a male child with an ACE Score of 0, has a 46 fold (4.600%) increase in the likelihood of becoming an injection drug user sometime later in life.

Discussion

Although awareness of the hazards of smoking is now near universal. and has caused a significant reduction in smoking, in recent years the prevalence of smoking has remained largely unchanged. In fact. the association between ACE score and smoking is stronger in age cohorts born after the Surgeon General’s Report on Smoking.

Do current smokers now represent a core of individuals who have a more profound need for the psychoactive benefits of nicotine than those who have given up smoking? Our clinical experience and data from the ACE Study suggest this as a likely possibility. Certainly, there is good evidence of the psychoactive benefits of nicotine for moderating anger anxiety, and hunger.

Alcohol is well accepted as a psychoactive agent. This obvious explanation of alcoholism is now sometimes rejected in favor of a proposed genetic causality. Certainly, alcoholism may be familial, as is language spoken. Our findings support an experiential and psychodynamic explanation for alcoholism, although this may well be moderated by genetic and metabolic differences between races and individuals.

Analysis of our Study data for injected drug use shows a powerful relation to ACEs. Population Attributable Risk (PAR) analysis shows that 78% of drug injection by women can be attributed to adverse childhood experiences. For men and women combined, the PAR is 67%. Moreover, this PAR has been constant in four age cohorts whose birth dates span a century; this indicates that the relation of adverse childhood experiences to illicit drug use has been constant in spite of major changes in drug availability and in social customs, and in the introduction of drug eradication programs.

American soldiers in Vietnam provided an important although overlooked observation. Many enlisted men in Vietnam regularly used heroin. However, only 5% of those considered addicted were still using it 10 months after their return to the US.” Treatment did not account for this high recovery rate.

Why does not everyone become addicted when they repeatedly inject a substance reputedly as addicting as heroin? If a substance like heroin is not inherently addicting to everyone, but only to a small minority of human users, what determines this selectivity? Is it the substance that is intrinsically addicting, or do life experiences actually determine its compulsive use? Surely its chemical structure remains constant.

Our findings indicate that the major factor underlying addiction is adverse childhood experiences that have not healed with time and that are overwhelmingly concealed from awareness by shame, secrecy, and social taboo.

The compulsive user appears to be one who, not having other resolutions available, unconsciously seeks relief by using materials with known psychoactive benefit, accepting the known long term risk of injecting illicit, impure chemicals. The ACE Study provides population based clinical evidence that unrecognized adverse childhood experiences are a major, if not the major, determinant of who turns to psychoactive materials and becomes ‘addicted’.

Given that the conventional concept of addiction is seriously flawed, and that we have presented strong evidence for an alternative explanation, we propose giving up our old mechanistic explanation of addiction in favor of one that explains it in terms of its psychodynamics: unconscious although understandable decisions being made to seek chemical relief from the ongoing effects of old trauma, often at the cost of accepting future health risk.

Expressions like ‘self destructive behavior’ are misleading and should be dropped because, while describing the acceptance of long term risk, they overlook the importance of the obvious short term benefits that drive the use of these substances.

This revised concept of addiction suggests new approaches to primary prevention and treatment. The current public health approach of repeated cautionary warnings has demonstrated its limitations, perhaps because the cautions do not respect the individual when they exhort change without understanding.

Adverse childhood experiences are widespread and typically unrecognized. These experiences produce neurodevelopmental and emotional damage, and impair social and school performance. By adolescence, children have a sufficient skill and independence to seek relief through a small number of mechanisms, many of which have been in use since biblical times: drinking alcohol, sexual promiscuity, smoking tobacco, using psychoactive materials, and overeating. These coping devices are manifestly effective for their users, presumably through their ability to modulate the activity of various neurotransmitters. Nicotine, for instance. is a powerful substitute for the neurotransmitter acetylcholine. Not surprisingly, the level of some neurotransmitters varies genetically between individuals.

It is these coping devices, with their short term emotional benefits, that often pose long term risks leading to chronic disease; many lead to premature death. This sequence is depicted in the ACE Pyramid (Figure 5). The sequence is slow, often unstoppable, and is generally obscured by time, secrecy, and social taboo. Time does not heal in most of these instances. Because cause and effect usually lie within a family, it is understandably more comforting to demonize a chemical than to look within. We find that addiction overwhelmingly implies prior adverse life experiences.

The sequence in the ACE Pyramid supports psychoanalytic observations that addiction is primarily a consequence of adverse childhood experiences. Moreover, it does so by a population based study, thereby escaping the potential selection bias of individual case reports.

Addiction is not a brain disease, nor is it caused by chemical imbalance or genetics. Addiction is best viewed as an understandable, unconscious, compulsive use of psychoactive materials in response to abnormal prior life experiences, most of which are concealed by shame, secrecy, and social taboo.

Our findings show that childhood experiences profoundly and causally shape adult life‘ ‘Chemical imbalances’. whether genetically modulated or not, are the necessary intermediary mechanisms by which these causal life experiences are translated into manifest effect. It is important to distinguish between cause and mechanism. Uncertainty and confusion between the two will lead to needless polemics and misdirected efforts for preventing or treating addiction, whether on a social or an individual scale.

Our findings also make it clear that studying any one category of adverse experience, be it domestic violence. childhood sexual abuse, or other forms of family dysfunction is a conceptual error. None occur in vacuum; they are part of a complex systems failure: one does not grow up with an alcoholic where everything else in the household is fine.

Treatment

If we are to improve the current unhappy situation, we must in medical settings routinely screen at the earliest possible point for adverse childhood experiences. It is feasible and acceptable to carry out mass screening for ACEs in the context of comprehensive medical evaluation. This identifies cases early and allows treatment of basic causes rather than vainly treating the symptom of the moment. We have screened over 450, 000 adult members of Kaiser Health Plan for these eight categories of adverse childhood experiences. Our initial screening is by an expanded Review of Systems questionnaire; patients certainly do not spontaneously volunteer this information. ‘Yes’ answers then are pursued with conventional history taking: “I see that you were molested as a child. Tell me how that has affected you later in your life.”

Such screening has demonstrable value. Before we screened for adverse childhood experiences, our standardized comprehensive medical evaluation led to a 12% reduction in medical visits during the subsequent year. Later, in a pilot study, an on site psychoanalyst conducted a one time interview of depressed patients; this produced a 50% reduction in the utilization of this subset during the subsequent year. However, the reduction occurred only in those depressed patients who were high utilizers of medical care because of somatization disorders.

Recently, we evaluated our current approach by a neural net analysis of the records of 135,000 patients who were screened for adverse childhood experiences as part of our redesigned comprehensive medical evaluation. This entire cohort showed an overall reduction of 35% in doctor office visits during the year subsequent to evaluation.

Our experience asking these questions indicates that the magnitude of the ACE problem is so great that primary prevention is ultimately the only realistic solution. Primary prevention requires the development of a beneficial and acceptable intrusion into the closed realm of personal and family experience. Techniques for accomplishing such change en masse are yet to be developed because each of us, fearing the new and unknown as a potential crisis in self esteem, often adjusts to the status quo. However, one possible approach to primary prevention lies in the mass media: the story lines of movies and television serials present a major therapeutic opportunity, unexploited thus far, for contrasting desirable and undesirable parenting skills in various life situations.

Because addiction is experience dependent and not substance dependent, and because compulsive use of only one substance is actually uncommon, one also might restructure treatment programs to deal with underlying causes rather than to focus on substance withdrawal. We have begun using this approach with benefit in our Obesity Program, and plan to do so with some of the more conventionally accepted addictions.

Conclusion

The current concept of addiction is ill founded. Our study of the relationship of adverse childhood experiences to adult health status in over 17,000 persons shows addiction to be a readily understandable, although largely unconscious, attempt to gain relief from well concealed prior life traumas by using psychoactive materials. Because it is difficult to get enough of something that doesn’t quite work, the attempt is ultimately unsuccessful, apart from its risks. What we have shown will not surprise most psychoanalysts, although the magnitude of our observations is new, and our conclusions are sometimes vigorously challenged by other disciplines.

The evidence supporting our conclusions about the basic cause of addiction is powerful and its implications are daunting. The prevalence of adverse childhood experiences and their long term effects are clearly a major determinant of the health and social well being of the nation. This is true whether looked at from the standpoint of social costs, the economics of health care, the quality of human existence, the focus of medical treatment, or the effects of public policy.

Adverse childhood experiences are difticult issues, made more so because they strike close to home for many of us. Taking them on will create an ordeal of change, but will also provide for many the opportunity to have a better life.


Adverse Childhood Experiences Study

Wikipedia

The Adverse Childhood Experiences Study (ACE Study) is a research study conducted by the American health maintenance organization Kaiser Permanente and the Centers for Disease Control and Prevention. Participants were recruited to the study between 1995 and 1997 and have been in long-term follow up for health outcomes. The study has demonstrated an association of adverse childhood experiences (ACEs) (aka childhood trauma) with health and social problems across the lifespan. The study is frequently cited as a notable landmark in epidemiological research, and has produced many scientific articles and conference and workshop presentations that examine ACEs.

Background

In the 1980s, the dropout rate of participants at Kaiser Permanente’s obesity clinic in San Diego, California, was about 50%; despite all of the dropouts successfully losing weight under the program. Vincent Felitti, head of Kaiser Permanente’s Department of Preventive Medicine in San Diego, conducted interviews with people who had left the program, and discovered that a majority of 286 people he interviewed had experienced childhood sexual abuse. The interview findings suggested to Felitti that weight gain might be a coping mechanism for depression, anxiety, and fear.

Felitti and Robert Anda from the Centers for Disease Control and Prevention (CDC) went on to survey childhood trauma experiences of over 17,000 Kaiser Permanente patient volunteers. The 17,337 participants were volunteers from approximately 26,000 consecutive Kaiser Permanente members. About half were female; 74.8% were white; the average age was 57; 75.2% had attended college; all had jobs and good health care, because they were members of the Kaiser health maintenance organization. Participants were asked about 10 types of childhood trauma that had been identified in earlier research literature:

– Physical abuse

– Sexual abuse

– Emotional abuse

– Physical or emotional neglect

– Exposure to domestic violence

– Household substance abuse

– Household mental illness

– Family member (attempted) suicide

– Parental separation or divorce

– Incarcerated household member

In one way or another, all ten questions speak to family dysfunction.

Findings

The ACE Pyramid represents the conceptual framework for the ACE Study, which has uncovered how adverse childhood experiences are strongly related to various risk factors for disease throughout the lifespan, according to the Centers for Disease Control and Prevention.

According to the United States’ Substance Abuse and Mental Health Services Administration, the ACE study found that:

Adverse childhood experiences are common. For example, 28% of study participants reported physical abuse and 21% reported sexual abuse. Many also reported experiencing a divorce or parental separation, or having a parent with a mental and/or substance use disorder.

Adverse childhood experiences often occur together. Almost 40% of the original sample reported two or more ACEs and 12.5% experienced four or more. Because ACEs occur in clusters, many subsequent studies have examined the cumulative effects of ACEs rather than the individual effects of each.

Adverse childhood experiences have a dose response relationship with many health problems. As researchers followed participants over time, they discovered that a person’s cumulative ACEs score has a strong, graded relationship to numerous health, social, and behavioral problems throughout their lifespan, including substance use disorders. Furthermore, many problems related to ACEs tend to be comorbid, or co-occurring.

About two-thirds of individuals reported at least one adverse childhood experience; 87% of individuals who reported one ACE reported at least one additional ACE. The number of ACEs was strongly associated with adulthood high-risk health behaviors such as smoking, alcohol and drug abuse, promiscuity, and severe obesity, and correlated with ill-health including depression, heart disease, cancer, chronic lung disease and shortened lifespan.

Compared to an ACE score of zero, having four adverse childhood experiences was associated with a seven fold (700%) increase in alcoholism, a doubling of risk of being diagnosed with cancer, and a four-fold increase in emphysema; an ACE score above six was associated with a 30-fold (3000%) increase in attempted suicides.

The ACE study’s results suggest that maltreatment and household dysfunction in childhood contribute to health problems decades later. These include chronic diseases, such as heart disease, cancer, stroke, and diabetes, that are the most common causes of death and disability in the United States. The study’s findings, while relating to a specific population within the United States, might reasonably be assumed to reflect similar trends in other parts of the world, according to the World Health Organization. The study was initially published in the American Journal of Preventive Medicine.

Subsequent surveys

The ACE Study has produced more than 50 articles that look at the prevalence and consequences of ACEs. It has been influential in several areas. Subsequent studies have confirmed the high frequency of adverse childhood experiences, or found even higher incidences in urban or youth populations.

The original study questions have been used to develop a 10-item screening questionnaire. Numerous subsequent surveys have confirmed that adverse childhood experiences are frequent.

The CDC runs the Behavioral Risk Factor Surveillance System (BRFSS), an annual survey conducted by individual state health departments in all 50 states. An expanded survey instrument in several states found each state to be similar. Some states have collected additional local data. Adverse childhood experiences were even more frequent in studies in urban Philadelphia, and in a survey of young mothers (mostly younger than 19). Internationally, an Adverse Childhood Experiences International Questionnaire (ACE-IQ) is undergoing validation testing. Surveys of adverse childhood experiences have been conducted in Romania, the Czech Republic, the Republic of Macedonia, Norway, the Philippines, the United Kingdom, Canada, China and Jordan.

Child Trends used data from the 2011/12 National Survey of Children’s Health (NSCH) to analyze ACEs prevalence in children nationally, and by state. The NSCH’s list of “adverse family experiences” includes a measure of economic hardship and shows that this is the most common ACE reported nationally.

Neurobiology of Stress

Cognitive and neuroscience researchers have examined possible mechanisms that might explain the negative consequences of adverse childhood experiences on adult health. Adverse childhood experiences can alter the structural development of neural networks and the biochemistry of neuroendocrine System and may have long term effects on the body, including speeding up the processes of disease and aging and compromising immune systems.

Allostatic load refers to the adaptive processes that maintain homeostasis during times of toxic stress through the production of mediators such as adrenalin, cortisol and other chemical messengers. According to researcher Bruce S McEwen, who coined the term:

“These mediators of the stress response promote adaptation in the aftermath of acute stress, but they also contribute to allostatic overload, the wear and tear on the body and brain that result from being ‘stressed out.‘ This conceptual framework has created a need to know how to improve the efficiency of the adaptive response to stressors while minimizing overactivity of the same systems, since such overactivity results in many of the common diseases of modern life. This framework has also helped to demystify the biology of stress by emphasizing the protective as well as the damaging effects of the body’s attempts to cope with the challenges known as stressors.”

Additionally, epigenetic transmission may occur due to stress during pregnancy or during interactions between mother and newborns. Maternal stress, depression, and exposure to partner violence have all been shown to have epigenetic effects on infants.

Implementing practices

As knowledge about the prevalence and consequences of adverse childhood experiences increases, trauma informed and resilience building practices based on the research is being implemented in communities, education, public health departments, social services, faith-based organizations and criminal justice. A few states are considering legislation.

Communities

As knowledge about the prevalence and consequences of ACEs increases, more communities seek to integrate trauma informed and resilience building practices into their agencies and systems. Tarpon Springs, Florida, became the first trauma informed community in 2011. Trauma informed initiatives in Tarpon Springs include trauma awareness training for the local housing authority, changes in programs for ex-offenders, and new approaches to educating students with learning difficulties.

Education

Children who are exposed to adverse childhood experiences may become overloaded with stress hormones, leaving them in a constant state of arousal and alertness to environmental and relational threats. Therefore, they may have difficulty focusing on school work, and consolidating new memory, making it harder for them to learn at school.

Approximately one in three or four children have experienced significant ACEs. A study by the Area Health Education Center of Washington State University found that students with at least three ACEs are three times as likely to experience academic failure, six times as likely to have behavioral problems, and five times as likely to have attendance problems. These students may have trouble trusting teachers and other adults, and may have difficulty creating and maintaining relationships.

The trauma informed school movement aims to train teachers and staff to help children self-regulate, and to help families that are having problems that result in children’s normal response to trauma, rather than simply jumping to punishment. It also seeks to provide behavioral consequences that will not retraumatize a child. Punishment is often ineffective, and better results can often be achieved with positive reinforcement. Out of school suspensions can be particularly bad for students with difficult home lives; forcing students to remain at home may increase their distrust of adults.

Trauma sensitive, or compassionate, schooling has become increasingly popular in Washington, Massachusetts, and California. Lincoln High School in Walla Walla, Washington, adapted a trauma informed approach to discipline and reduced its suspensions by 85%. Rather than standard punishment, students are taught to recognize their reaction to stress and learn to control it.

Spokane, Washington, schools conducted a research study that demonstrated that academic risk was correlated with students’ experiences of traumatic events known to their teachers. The same school district has begun a study to test the impact of trauma informed intervention programs, in an attempt to reduce the impact of toxic stress.

In Brockton, Massachusetts, a community wide meeting led to a trauma informed approach being adopted by the Brockton School District. So far, all of the district’s elementary schools have implemented trauma informed improvement plans, and there are plans to do the same in the middle school and high school. About one-fifth of the district teachers have participated in a course on teaching traumatized students. Police alert schools when they have arrested someone or visited at a student’s address.

Massachusetts state legislation has sought to require all schools to develop plans to create “safe and supportive schools”.

At El Dorado, an elementary school in San Francisco, California, trauma-informed practices were associated with a suspension reduction of 89%.

Social services

Social service providers, including welfare systems, housing authorities, homeless shelters, and domestic violence centers are adopting trauma informed approaches that help to prevent ACEs or minimize their impact. Utilizing tools that screen for trauma can help a social service worker direct their clients to interventions that meet their specific needs. Trauma informed practices can also help social service providers look at how trauma impacts the whole family.

Trauma informed approaches can improve child welfare services by 1) openly discussing trauma and 2) addressing parental trauma.

The New Hampshire Division for Children Youth and Families (DCYF) is taking a trauma informed approach to their foster care services by educating staff about childhood trauma, screening children entering foster care for trauma, using trauma informed language to mitigate further traumatization, mentoring birth parents and involving them in collaborative parenting, and training foster parents to be trauma informed.

In Albany, New York the HEARTS Initiative has led to local organizations developing trauma informed practice. Senior Hope Inc, an organization serving adults over the age of 50, began implementing the 10 question ACE survey and talking with their clients about childhood trauma. The LaSalle School, which serves orphaned and abandoned boys, began looking at delinquent boys from a trauma informed perspective and began administering the ACE questionnaire to their clients.

Housing authorities are also becoming trauma informed. Supportive housing can sometimes recreate control and power dynamics associated with clients’ early trauma. This can be reduced through trauma informed practices, such as training staff to be respectful of clients’ space by scheduling appointments and not letting themselves into clients’ private spaces, and also understanding that an aggressive response may be trauma related coping strategies.

The housing authority in Tarpon Springs provided trauma awareness training to staff so they could better understand and react to their clients’ stress and anger resulting from poor employment, health, and housing.

A survey of 200 homeless individuals in California and New York demonstrated that more than 50% had experienced at least four ACEs. In Petaluma, California, the Committee on the Shelterless (COTS) uses a trauma informed approach called Restorative Integral Support (RIS) to reduce intergenerational homelessness. RIS increases awareness of and knowledge about ACEs, and calls on staff to be compassionate and focus on the whole person. COTS now consider themselves ACE informed and focus on resiliency and recovery.

Health care services

Screening for or talking about ACEs with parents and children can help to foster healthy physical and psychological development and can help doctors understand the circumstances that children and their parents are facing. By screening for ACEs in children, pediatric doctors and nurses can better understand behavioral problems.

Some doctors have questioned whether some behaviors resulting in attention deficit hyperactivity disorder (ADHD) diagnoses are in fact reactions to trauma. Children who have experienced four or more ACEs are three times as likely to take ADHD medication when compared with children with less than four ACEs.

Screening parents for their ACEs allows doctors to provide the appropriate support to parents who have experienced trauma, helping them to build resilience, foster attachment with their children, and prevent a family cycle of ACEs. Trauma informed pediatric care also allows doctors to develop a more trusting relationship with parents, opening the lines of communication.

At Monteflore Medical Center ACEs screenings will soon be implemented in 22 pediatric clinics. In a pilot program any child with one parent who has an ACE score of four or higher is offered enrollment and receive a variety of services. For families enrolled in the program parents report fewer ER visits and children have healthier emotional and social development, compared with those not enrolled.

Public health

Most American doctors as of 2015 do not use ACE surveys to assess patients. Objections to doing so include that there are no randomized controlled trials that show that such surveys can be used to actually improve health outcomes, there are no standard protocols for how to use the information gathered, and that revisiting negative childhood experiences could be emotionally traumatic. Other obstacles to adoption include that the technique is not taught in medical schools, is not billable, and the nature of the conversation makes some doctors personally uncomfortable.

Some public health centers see ACEs as an important way, especially for mothers and children, to target health interventions for individuals during sensitive periods of development early in their life, or even in utero.

For example, Jefferson Country Public Health clinic in Port Townsend, Washington, now screens pregnant women, their partners, parents of children with special needs, and parents involved with CPS for ACEs. With regard to patient counseling, the clinic treats ACEs like other health risks such as smoking or alcohol consumption.

Resiliency

Resilience is not a trait that people either have or do not have. It involves behaviors, thoughts and actions that can be learned and developed in anyone.

According to the American Psychological Association (2017) resilience is the ability to adapt in the face of adversity, tragedy, threats or significant stress such as family and relationship problems, serious health problems or workplace and financial stressors. Resilience refers to bouncing back from difficult experiences in life. There is nothing extraordinary about resilience. People often demonstrate resilience in times of adversity. However, being resilient does not mean that a person will not experience difficulty or distress as emotional pain is common for people when they suffer from a major adversity or trauma. In fact, the path to resilience often involves considerable emotional pain.

Resilience is labeled as a protective factor. Having resilience can benefit children who have been exposed to trauma and have a higher ACE score. Children who can learn to develop it, can use resilience to build themselves up after trauma. A child who has not developed resilience will have a harder time coping with the challenges that can come in adult life. People and children who are resilient, embrace the thinking that adverse experiences do not define who they are. They also can think about past events in their lives that were traumatic and, try to reframe them in a way that is constructive. They are able to find strength in their struggle and ultimately can overcome the challenges and adversity that was faced in childhood.

In childhood, resiliency can come from having a caring adult in a child’s life. Resiliency can also come from having meaningful moments such as an academic achievement or getting praise from teachers or mentors. In adulthood, resilience is the concept of self-care. If you are taking care of yourself and taking the necessary time to reflect and build on your experiences, then you will have a higher capacity for taking care of others.

Adults can also use this skill to counteract some of the trauma they have experienced. Self-care can mean a variety of things. One example of selfcare, is knowing when you are beginning to feel burned out and then taking a step back to rest and recuperate yourself. Another component of self-care is practicing mindfulness or engaging in some form of meditation. If you are able to take the time to reflect upon your experiences, then you will be able to build a greater level of resiliency moving forward.

All of these strategies put together can help to build resilience and counteract some of the childhood trauma that was experienced. With these strategies children can begin to heal after experiencing adverse childhood experiences. This aspect of resiliency is so important because it enables people to find hope in their traumatic past.

When first looking at the ACE study and the different correlations that come with having 4 or more traumas, it is easy to feel defeated. It is even possible for this information to encourage people to have unhealthy coping behaviors. Introducing resilience and the data that supports its positive outcome in regards to trauma, allows for a light at the end of a tunnel. It gives people the opportunity to be proactive instead of reactive when it comes to addressing the traumas in their past.

Criminal justice

Since research suggests that incarcerated individuals are much more likely to have been exposed to violence and suffer from posttraumatic stress disorder (PTSD), a trauma informed approach may better help to address some of these criminogenic risk factors and can create a less traumatizing criminal justice experience. Programs, like Seeking Safety, are often used to help individuals in the criminal justice system learn how to better cope with trauma, PTSD, and substance abuse.

Juvenile courts better help deter children from crime and delinquency when they understand the trauma many of these children have experienced.

The criminal justice system itself can also retraumatize individuals. This can be prevented by creating safer facilities where correctional and police officers are properly trained to keep incidents from escalating. Partnerships between police and mental health providers can also reduce the possible traumatizing effects of police intervention and help provide families with the proper mental health and social services.

The Women’s Community Correctional Center of Hawaii began a Trauma Informed Care Initiative that aims to train all employees to be aware and sensitive to trauma, to screen all women in their facility for trauma, to assess those who have experienced trauma, and begin providing trauma informed mental health care to those women identified.

Faith based Organizations

Some faith based organizations offer spiritual services in response to traumas identified by ACE surveys. For example, the founder of ACE Overcomers combined the epidemiology of ACEs, the neurobiology of toxic stress and principles of the Christian Bible into a workbook and 12-week course used by clergy in several states.

Another example of this integration of faith based principles and ACEs science is the work of Intermountain Residential’s chaplain, who has created a curriculum called “Bruised Reeds and Smoldering Wicks” a six week study meant to introduce the science behind ACEs and early childhood trauma within the context of Christian theology and ministry practice. Published in 2017, it has been used by ministry professionals in 30 states, the District of Columbia, and two Canadian provinces.

Faith based organizations also participate in the online group ACES Connection Network.

The Faith and Health Connection Ministry also applies principles of Christian theology to address childhood traumas.

Legislation

Vermont has passed a bill, Act 43(H.508), an act relating to building resilience for individuals experiencing adverse childhood experiences which acknowledges the life span effects of ACEs on health outcomes, seeks wide use of ACE screening by health providers and aims to educate medical and health school students about ACEs.

“Vermont first state to propose bill to screen for ACEs in health care”, ACEs Connection, 18 March 2014

Previously Washington State passed legislation to set up a public-private partnership to further community development of trauma informed and resilience building practices that had begun in that state; but it was not adequately funded.

On August 18, 2014, California lawmakers unanimously passed ACR No. 155, which encourages policies reducing children’s exposure to adverse experiences.

Recent Massachusetts legislation supports a trauma informed school movement as part of The Reduction of Gun Violence bill (No. 4376). This bill aims to create “safe and supportive schools” through services and initiatives focused on physical, social, and emotional safety.

Childhood Adversity Can Change Your Brain. How People Recover From Post Childhood Adversity Syndrome – Donna Jackson Nakazawa * Future Directions in Childhood Adversity and Youth Psychopathology – Katie A. McLaughlin.

Childhood Adversity: exposure during childhood or adolescence to environmental circumstances that are likely to require significant psychological, social, or neurobiological adaptation by an average child and that represent a deviation from the expectable environment.

Early emotional trauma changes who we are, but we can do something about it.

The brain and body are never static; they are always in the process of becoming and changing.

Findings from epidemiological studies indicate clearly that exposure to childhood adversity powerfully shapes risk for psychopathology.

This research tells us that what doesn’t kill you doesn’t necessarily make you stronger; far more often, the opposite is true.

Donna Jackson Nakazawa

If you’ve ever wondered why you’ve been struggling a little too hard for a little too long with chronic emotional and physical health conditions that just won’t abate, feeling as if you’ve been swimming against some invisible current that never ceases, a new field of scientific research may offer hope, answers, and healing insights.

In 1995, physicians Vincent Felitti and Robert Anda launched a large scale epidemiological study that probed the child and adolescent histories of 17,000 subjects, comparing their childhood experiences to their later adult health records. The results were shocking: Nearly two thirds of individuals had encountered one or more Adverse Childhood Experiences (ACEs), a term Felitti and Anda coined to encompass the chronic, unpredictable, and stress inducing events that some children face. These included growing up with a depressed or alcoholic parent; losing a parent to divorce or other causes; or enduring chronic humiliation, emotional neglect, or sexual or physical abuse. These forms of emotional trauma went beyond the typical, everyday challenges of growing up.

The number of Adverse Childhood Experiences an individual had had predicted the amount of medical care she’d require as an adult with surprising accuracy:

– Individuals who had faced 4 or more categories of ACEs were twice as likely to be diagnosed with cancer as individuals who hadn’t experienced childhood adversity.

– For each ACE Score a woman had, her risk of being hospitalized with an autoimmune disease rose by 20 percent.

– Someone with an ACE Score of 4 was 460 percent more likely to suffer from depression than someone with an ACE Score of 0.

– An ACE Score greater than or equal to 6 shortened an individual’s lifespan by almost 20 years.

The ACE Study tells us that experiencing chronic, unpredictable toxic stress in childhood predisposes us to a constellation of chronic conditions in adulthood. But why? Today, in labs across the country, neuroscientists are peering into the once inscrutable brain-body connection, and breaking down, on a biochemical level, exactly how the stress we face when we’re young catches up with us when we’re adults, altering our bodies, our cells, and even our DNA. What they’ve found may surprise you.

Some of these scientific findings can be a little overwhelming to contemplate. They compel us to take a new look at how emotional and physical pain are intertwined.

1. Epigenetic Shifts

When we’re thrust over and over again into stress inducing situations during childhood or adolescence, our physiological stress response shifts into overdrive, and we lose the ability to respond appropriately and effectively to future stressors 10, 20, even 30 years later. This happens due to a process known as gene methylation, in which small chemical markers, or methyl groups, adhere to the genes involved in regulating the stress response, and prevent these genes from doing their jobs.

As the function of these genes is altered, the stress response becomes re-set on ”high” for life, promoting inflammation and disease.

This can make us more likely to overreact to the everyday stressors we meet in our adult life, an unexpected bill, a disagreement with a spouse, or a car that swerves in front of us on the highway, creating more inflammation. This, in turn, predisposes us to a host of chronic conditions, including autoimmune disease, heart disease, cancer, and depression.

Indeed, Yale researchers recently found that children who’d faced chronic, toxic stress showed changes “across the entire genome,” in genes that not only oversee the stress response, but also in genes implicated in a wide array of adult diseases. This new research on early emotional trauma, epigenetic changes, and adult physical disease breaks down longstanding delineations between what the medical community has long seen as “physical” disease versus what is “mental” or “emotional.”

2. Size and Shape of the Brain

Scientists have found that when the developing brain is chronically stressed, it releases a hormone that actually shrinks the size of the hippocampus, an area of the brain responsible of processing emotion and memory and managing stress. Recent magnetic resonance imaging (MRI) studies suggest that the higher an individual’s ACE Score, the less gray matter he or she has in other key areas of the brain, including the prefrontal cortex, an area related to decision making and self regulatory skills, and the amygdala, or fear-processmg center. Kids whose brains have been changed by their Adverse Childhood Experiences are more likely to become adults who find themselves over-reacting to even minor stressors.

3. Neural Pruning

Children have an overabundance of neurons and synaptic connections; their brains are hard at work, trying to make sense of the world around them. Until recently, scientists believed that the pruning of excess neurons and connections was achieved solely in a “use-it-or-lose-it” manner, but a surprising new player in brain development has appeared on the scene: non-neuronal brain cells, known as microglia, which make up one-tenth of all the cells in the brain, and are actually part of the immune system, participate in the pruning process. These cells prune synapses like a gardener prunes a hedge. They also engulf and digest entire cells and cellular debris, thereby playing an essential housekeeping role.

But when a child faces unpredictable, chronic stress of Adverse Childhood Experiences, microglial cells “can get really worked up and crank out neurochemicals that lead to neuroinflammation,” says Margaret McCarthy, PhD, whose research team at the University of Maryland Medical Center studies the developing brain. “This below-the-radar state of chronic neuroinflammation can lead to changes that reset the tone of the brain for life.”

That means that kids who come into adolescence with a history of adversity and lack the presence of a consistent, loving adult to help them through it may become more likely to develop mood disorders or have poor executive functioning and decision-making skills.

4. Telomeres

Early trauma can make children seem “older,” emotionally speaking, than their peers. Now, scientists at Duke University; the University of California, San Francisco; and Brown University have discovered that Adverse Childhood Experiences may prematurely age children on a cellular level as well. Adults who’d faced early trauma show greater erosion in what are known as telomeres, the protective caps that sit on the ends of DNA strands, like the caps on Shoelaces, to keep the genome healthy and intact. As our telomeres erode, we’re more likely to develop disease, and our cells age faster.

5. Default Mode Network

Inside each of our brains, a network of neurocircuitry, known as the “default mode network,” quietly hums along, like a car idling in a driveway. It unites areas of the brain associated with memory and thought integration, and it’s always on standby, ready to help us to figure out what we need to do next. “The dense connectivity in these areas of the brain help us to determine what’s relevant or not relevant, so that we can be ready for whatever our environment is going to ask of us,” explains Ruth Lanius, neuroscientist professor of psychiatry, and director of the Post Traumatic Stress (PTSD) Research Unit at the University of Ontario.

But when children face early adversity and are routinely thrust into a state of fight-or-flight, the default mode network starts to go offline; it’s no longer helping them to figure out what’s relevant, or what they need to do next.

According to Lanius, kids who’ve faced early trauma have less connectivity in the default mode network, even decades after the trauma occurred. Their brains don’t seem to enter that healthy idling position, and so they may have trouble reacting appropriately to the world around them.

6. Brain-Body Pathway

Until recently, it’s been scientifically accepted that the brain is ”immune-privileged,” or cut off from the body’s immune system. But that turns out not to be the case, according to a groundbreaking study conducted by researchers at the University of Virginia School of Medicine. Researchers found that an elusive pathway travels between the brain and the immune system via lymphatic vessels. The lymphatic system, which is part of the circulatory system, carries lymph, a liquid that helps to eliminate toxins, and moves immune cells from one part of the body to another. Now we know that the immune system pathway includes the brain.

The results of this study have profound implications for ACE research. For a child who’s experienced adversity, the relationship between mental and physical suffering is strong: the inflammatory chemicals that flood a child’s brain when she’s chronically stressed aren’t confined to the brain alone; they’re shuttled from head to toe.

7. Brain Connectivity

Ryan Herringa, neuropsychiatrist and assistant professor of child and adolescent psychiatry at the University of Wisconsin, found that children and teens who’d experienced chronic childhood adversity showed weaker neural connections between the prefrontal cortex and the hippocampus. Girls also displayed weaker connections between the prefrontal cortex and the amygdala. The prefrontalcortex-amygdala relationship plays an essential role in determining how emotionally reactive we’re likely to be to the things that happen to us in our day-to-day life, and how likely we are to perceive these events as stressful or dangerous.

According to Herringa:

“If you are a girl who has had Adverse Childhood Experiences and these brain connections are weaker, you might expect that in just about any stressful situation you encounter as life goes on, you may experience a greater level of fear and anxiety.”

Girls with these weakened neural connections, Herringa found, stood at a higher risk for developing anxiety and depression by the time they reached late adolescence. This may, in part, explain why females are nearly twice as likely as males to suffer from later mood disorders.

This science can be overwhelming, especially to those of us who are parents. So, what can you do if you or a child you love has been affected by early adversity?

The good news is that, just as our scientific understanding of how adversity affects the developing brain is growing, so is our scientific insight into how we can offer the children we love resilient parenting, and how we can all take small steps to heal body and brain. Just as physical wounds and bruises heal, just as we can regain our muscle tone, we can recover function in under-connected areas of the brain. The brain and body are never static; they are always in the process of becoming and changing.

Donna Jackson Nakazawa

8 Ways People Recover From Post Childhood Adversity Syndrome

New research leads to new approaches with wide benefits.

In this infographic, I show the link between Adverse Childhood Experiences, later physical adult disease, and what we can do to heal.

Cutting edge research tells us that experiencing childhood emotional trauma can play a large role in whether we develop physical disease in adulthood. In Part 1 of this series we looked at the growing scientific link between childhood adversity and adult physical disease. This research tells us that what doesn’t kill you doesn’t necessarily make you stronger; far more often, the opposite is true.

Adverse Childhood Experiences (ACES), which include emotional or physical neglect; harm developing brains, predisposing them to autoimmune disease, heart disease, cancer, debression, and a number of other chronic conditions, decades after the trauma took place.

Recognizing that chronic childhood stress can play a role, along with genetics and other factors, in developing adult illnesses and relationship challenges, can be enormously freeing. If you have been wondering why you’ve been struggling a little too hard for a little too long with your emotional and physical wellbeing, feeling as if you’ve been swimming against some invisible current that never ceases this “aha” can come as a welcome relief. Finally, you can begin to see the current and understand how it’s been working steadily against you all of your life.

Once we understand how the past can spill into the present, and how a tough childhood can become a tumultuous, challenging adulthood, we have a new possibility of healing. As one interviewee in my new book, Childhood Disrupted: How Your Biography Becomes Your Biology, and How You Can Heal, said, when she learned about Adverse Childhood Experiences for the first time, “Now I understand why I’ve felt all my life as if I’ve been trying to dance without hearing any music.” Suddenly, she felt the possibility that by taking steps to heal from the emotional wounds of the past she might find a new layer of healing in the present.

There is truth to the old saying that knowledge is power. Once you understand that your body and brain have been harmed by the biological impact of early emotional trauma, you can at last take the necessary, science based steps to remove the fingerprints that early adversity left on your neurobiology. You can begin a journey to healing, to reduce your proclivity to inflammation, depression, addiction, physical pain, and disease.

Science tells us that biology does not have to be destiny. ACEs can last a lifetime but they don’t have to. We can reboot our brains. Even if we have been set on high reactive mode for decades or a lifetime, we can still dial it down. We can respond to life’s inevitable stressors more appropriately and shift away from an overactive inflammatory response. We can become neurobiologically resilient. We can turn bad epigenetics into good epigenetics and rescue ourselves.

Today, researchers recognize a range of promising approaches to help create new neurons (known as neurogenesis), make new synaptic connections between those neurons (known as synaptogenesis), promote new patterns of thoughts and reactions, bring underconnected areas of the brain back online, and reset our stress response so that we decrease the inflammation that makes us ill.

We have the capacity, within ourselves, to create better health. We might call this brave undertaking “the neurobiology of awakening.”

There can be no better time than now to begin your own awakening, to proactively help yourself and those you love, embrace resilience, and move forward toward growth, even transformation.

Here are 8 steps to try:

1. Take the ACE Questionnaire

The single most important step you can take toward healing and transformation is to fill out the ACE Questionnaire for yourself and share your results with your health, care practitioner. For many people, taking the 10-question survey “helps to normalize the conversation about Adverse Childhood Experiences and their impact on our lives,” says Vincent Felitti, co-founder of the ACE Study. “When we make it okay to talk about what happened, it removes the power that secrecy so often has.”

You’re not asking your healthcare practitioner to act as your therapist, or to change your prescriptions; you’re simply acknowledging that there might be a link between your past and your present. Ideally, given the recent discoveries in the field of ACE research, your doctor will also acknowledge that this link is plausible, and add some of the following modalities to your healing protocol.

2. Begin Writing to Heal.

Think about writing down your story of childhood adversity, using a technique psychologists call “writing to heal.” James Pennebaker, professor of psychology at the University of Texas, Austin, developed this assignment, which demonstrates the effects of writing as a healing modality. He suggests: “Over the next four days, write down your deepest emotions and thoughts about the emotional upheaval that has been influencing your life the most. in your writing, really let go and explore the event and how it has affected you. You might tie this experience to your childhood, your relationship with your parents, people you have loved or love now…Write continuously for twenty minutes a day.”

When Pennebaker had students complete this assignment, their grades went up. When adults wrote to heal, they made fewer doctors’ visits and demonstrated changes in their immune function. The exercise of writing about your secrets, even if you destroy what you’ve written afterward, has been shown to have positive health effects.

3. Practice Mindfulness Meditation.

A growing body of research indicates that individuals who’ve practiced mindfulness meditation and Mindfulness Based Stress Reduction (MBSR) show an increase in gray matter in the same parts of the brain that are damaged by Adverse Childhood Experiences and shifts in genes that regulate their physiological stress response.

According to Trish Magyari, LCPC, a mindfulness-based psychotherapist and researcher who specializes in trauma and illness, adults abuse who took part in a “trauma-sensitive” MBSR program, had less anxiety and depression, and demonstrated fewer PTSD symptoms, even two years after taking the course.

Many meditation centers offer MBSR classes and retreats, but you can practice anytime in your own home. Choose a time and place to focus on your breath as it enters and leaves your nostrils; the rise and fall of your chest; the sensations in your hands or through the whole body; or sounds within or around you. If you get distracted, just come back to your anchor.

There are many medications you can take that dampen the sympathetic nervous system (which ramps up your stress response when you come into contact with a stressor), but there aren’t any medications that boost the parasympathetic nervous system (which helps to calm your body down after the stressor has passed).

Your breath is the best natural calming treatment, and it has no side effects.

4. Yoga

When children face ACEs, they often store decades of physical tension from a fight, flight, or freeze state of mind in their bodies. PET scans show that yoga decreases blood flow to the amygdala, the brain’s alarm center, and increases blood flow to the frontal lobe and prefrontal cortex, which help us to react to stressors with a greater sense of equanimity.

Yoga has also be found to increase levels of GABA, or gamma aminobutyric acid, a chemical that improves brain function, promotes calm, and helps to protect us against depression and anxiety.

5. Therapy

Sometimes, the long lasting effects of childhood trauma are just too great to tackle on our own. In these cases, says Jack Kornfield, psychologist and meditation teacher, “meditation is not always enough.” We need to bring unresolved issues into a therapeutic relationship, and get backup in unpacking the past.

When we partner with a skilled therapist to address the adversity we may have faced decades ago, those negative memories become paired with the positive experience of being seen by someone who accepts us as we are, and a new window to healing opens.

Part of the power of therapy lies in an allowing safe person. A therapist’s unconditional acceptance helps us to modify the circuits in our brain that tell us that we can’t trust anyone, and grow new, healthier neural connections.

It can also help us to heal the underlying, cellular damage of traumatic stress, down to our DNA. In one study, patients who underwent therapy showed changes in the integrity of their genome, even a year after their regular sessions ended.

6. EEG Neurofeedback

Electroencephalographic (EEG) Neurofeedback is a clinical approach to healing childhood trauma in which patients learn to influence their thoughts and feelings by watching their brain’s electrical activity in real-time, on a laptop screen. Someone hooked up to the computer via electrodes on his scalp might see an image of a field; when his brain is under-activated in a key area, the field, which changes in response to neural activity, may appear to be muddy and gray, the flowers wilted; but when that area of the brain reactivates, it triggers the flowers to burst into color and birds to sing. With practice, the patient learns to initiate certain thought patterns that lead to neural activity associated with pleasant images and sounds.

You might think of a licensed EEG Neurofeedback therapist as a musical conductor, who’s trying to get different parts of the orchestra to play a little more softly in some cases, and a little louder in others, in order to achieve harmony. After just one EEG Neurofeedback session, patients showed greater neural connectivity and improved emotional resilience, making it a compelling option for those who’ve suffered the long lasting effects of chronic, unpredictable stress in childhood.

7. EMDR Therapy

Eye Movement Desensitization and Reprocessing (EMDR) is a potent form of psychotherapy that helps individuals to remember difficult experiences safely and relate those memories in ways that no longer cause pain in the present.

Here’s how it works:

EMDR-certified therapists help patients to trigger painful emotions. As these emotions lead the patients to recall specific difficult experiences, they are asked to shift their gaze back and forth rapidly, often by following a pattern of lights or a wand that moves from right to left, right to left, in a movement that simulates the healing action of REM sleep.

The repetitive directing of attention in EMDR induces a neurobiological state that helps the brain to re-integrate neural connections that have been dysregulated by chronic, unpredictable stress and past experiences. This re-integration can, in turn, lead to a reduction in the episodic, traumatic memories we store in the hippocampus, and downshift the amygdala’s activity. Other studies have shown that EMDR increases the volume of the hippocampus,

EMDR therapy has been endorsed by the World Health Organization as one of only two forms of psychotherapy for children and adults in natural disasters and war settings.

8. Rally Community Healing

Often, ACEs stem from bad relationships, neglectful relatives, schoolyard bullies, abusive partners, but the right kinds of relationships can help to make us whole again. When we find people who support us, when we feel “tended and befriended,” our bodies and brains have a better shot at healing. Research has found that having strong social ties improves outcomes for women with breast cancer, multiple sclerosis, and other diseases. In part, that’s because positive interactions with others boost our production of oxytocin, a feel-good hormone that dials down the inflammatory stress response.

If you’re at a loss for ways to connect, try a mindfulness meditation community or an MBSR class, or pass along the ACE Questionnaire or even my newest book, Childhood Disrupted: How Your Biography Becomes Your Biology, and How You Can Heal, to family and friends to spark important, meaningful conversations.

You’re Not Alone

Whichever modalities you and your physician choose to implement, it’s important to keep in mind that you’re not alone. When you begin to understand that your feelings of loss, shame, guilt, anxiety, or grief are shared by so many others, you can lend support and swap ideas for healing.

When you embrace the process of healing despite your Adverse Childhood Experiences, you don’t just become who you might have been if you hadn’t encountered childhood suffering in the first place. You gain something better, the hard earned gift of life wisdom, which you bring forward into every arena of your life. The recognition that you have lived through hard times drives you to develop deeper empathy, seek more intimacy, value life’s sweeter moments, and treasure your connectedness to others and to the world at large. This is the hard won benefit of having known suffering.

Best of all, you can find ways to start right where you are, no matter where you find yourself.

Future Directions in Childhood Adversity and Youth Psychopathology

Katie A. McLaughlin, Department of Psychology, University of Washington

Abstract

Despite long standing interest in the influence of adverse early experiences on mental health, systematic scientific inquiry into childhood adversity and developmental outcomes has emerged only recently. Existing research has amply demonstrated that exposure to childhood adversity is associated with elevated risk for multiple forms of youth psychopathology.

In contrast. knowledge of developmental mechanisms linking childhood adversity to the onset of Psychopathology, and whether those mechanisms are general or specific to particular kinds of adversity, remains cursory.

Greater understanding of these pathways and identification of protective factors that buffer children from developmental disruptions following exposure to adversity is essential to guide the development of interventions to prevent the onset of psychopathology following adverse childhood experiences,

This article provides recommendations for future research in this area. In particular, use of a consistent definition of childhood adversity, integration of studies of typical development with those focused on childhood adversity, and identification of distinct dimensions of environmental experience that differentially influence development are required to uncover mechanisms that explain how childhood adversity is associated with numerous psychopathology outcomes (i.e., multifinality) and identify moderators that shape divergent trajectories following adverse childhood experiences.

A transdiagnostic model that highlights disruptions in emotional processing and poor executive functioning as key mechanisms linking childhood adversity with multiple forms of psychopathology is presented as a starting point in this endeavour. Distinguishing between general and specific mechanisms linking childhood adversity with psychopathology is needed to generate empirically informed interventions to prevent the long term consequences of adverse early environments on children’s development.

The lasting influence of early experience on mental health across the lifespan has been emphasized in theories of the etiology of psychopathology since the earliest formulations of mental illness. In particular, the roots of mental disorder have often been argued to be a consequence of adverse environmental experiences occurring in childhood. Despite this long standing interest, systematic scientific inquiry into the effects of childhood adversity on health and development has emerged only recently.

Prior work on childhood adversity focused largely on individual types of adverse experiences, such as death of a parent, divorce, sexual abuse, or poverty, and research on these topics evolved as relatively independent lines of inquiry. The transition to considering these types of adversities as indicators of the same underlying construct was prompted, in part, by the findings of a seminal study examining childhood adversity as a determinant of adult physical and mental health and advances in theoretical conceptualizations of stress. Specifically. findings from the Adverse Childhood Experiences (ACE) Study documented high levels of cooccurrence of multiple forms of childhood adversity and strong associations of exposure to adverse childhood experiences with a wide range of adult health outcomes (Dong et al., 2004; Edwards, Holden, Felitti, & Anda, 2003; Felitti et al., 1998).

Around the same time, the concept of allostatic load was introduced as a comprehensive neurobiological model of the effects of stress (McEwen, 1998, 2000). Allostatic load provided a framework for explaining the neurobiological mechanisms linking a variety of adverse social experiences to health. Together, these discoveries sparked renewed interest in the childhood determinants of physical and mental health. Since that time there has been a veritable explosion of research into the impact of childhood adversity on developmental outcomes, including psychopathology.

CHILDHOOD ADVERSITY AND PSYCHOPATHOLOGY

Over the past two decades, hundreds of studies have examined the associations between exposure to childhood adversity and risk for psychopathology (Evans, Li, & Whipple, 2013). Here, I briefly review this evidence, focusing specifically on findings from epidemiological studies designed to allow inferences to be drawn at the population level. These studies have documented five general patterns with regard to childhood adversity and the distribution of mental disorders in the population.

First, despite differences across studies in the prevalence of specific types of adversity, all population based studies indicate that exposure to childhood adversity is common. The prevalence of exposure to childhood adversity is estimated at about 50% in the U.S. population across numerous epidemiological surveys (Green et al., 2010; Kessler, Davis, & Kendler, 1997; McLaughlin, Conron, Koenen, & Gilman, 2010; McLaughlin, Green et al., 2012). Remarkably similar prevalence estimates have been documented in other high income countries, as well as in low and middle income countries worldwide (Kessler et al., 2010).

Second, individuals who have experienced childhood adversity are at elevated risk for developing a lifetime mental disorder compared to individuals without such exposure, and the odds of developing a lifetime mental disorder increase as exposure to adversity increases (Edwards et al., 2003; Green et al., 2010; Kessler et al., 1997; Kessler et al., 2010; McLaughlin, Conron, etal., 2010; McLaughlin, Green, et al., 2012).

Third, exposure to childhood adversity confers vulnerability to psychopathology that persists across the life course. Childhood adversity exposure is associated not only with risk of mental disorder onset in childhood and adolescence (McLaughlin, Green, et al., 2012) but also with elevated odds of developing a first onset mental disorder in adulthood, which persists after adjustment for mental disorders beginning at earlier stages of development (Green et al., 2010; Kessler et al., 1997; Kessler et al., 2010).

Fourth, the associations of childhood adversity with different types of commonly occurring mental disorders are largely nonspecific. Individuals who have experienced childhood adversity experience greater odds of developing mood, anxiety, substance use, and disruptive behavior disorders, with little meaningful variation in the strength of associations across disorder classes (Green et al., 2010; Kessler et al., 1997; Kessler et al., 2010; McLaughlin, Green, et al., 2012).

Recent epidemiological findings suggest that the associations of child maltreatment, a commonly measured form of adversity, with lifetime mental disorders operate entirely through a latent liability to experience internalizing and externalizing psychopathology with no direct effects on specific mental disorders that are not explained by this latent vulnerability (Caspi et al., 2014; Keyes et al., 2012).

Finally, exposure to childhood adversity explains a substantial proportion of mental disorder onsets in the population, both in the United States and cross nationally (Afifi et al., 2008′, Green et a1., 2010; Kessler et al., 2010; McLaughlin, Green, et al., 2012). This reflects both the high prevalence of exposure to childhood adversity and the strong association of childhood adversity with the onset of psychopathology.

Together, findings from epidemiological studies indicate clearly that exposure to childhood adversity powerfully shapes risk for psychopathology in the population.

As such, it is time for the field to move beyond these types of basic descriptive studies to research designs aimed at identifying the underlying developmental mechanisms linking childhood adversity to psychopathology. Although ample research has been conducted examining mechanisms linking individual types of adversity to psychopathology (e.g., sexual abuse; Trickett, Noll, & Putnam, 2011), far less is known about which of these mechanisms are common across different types of adversity versus specific to particular types of experiences. Greater understanding of these pathways, as well as the identification of protective factors that buffer children from disruptions in emotional, cognitive, social, and neurobiological development following exposure to adversity, is essential to guide the development of interventions to prevent the onset of psychopathology in children exposed to adversity, a critical next step for the field.

However, persistent issues regarding the definition and measurement of childhood adversity must be addressed before meaningful progress on mechanisms, protective factors, and prevention of psychopathology following childhood adversity will be possible.

FUTURE DIRECTIONS IN CHILDHOOD ADVERSITY AND YOUTH PSYCHOPATHOLOGY

This article has two primary goals. The first is to provide recommendations for future research on childhood adversity and youth psychopathology. These recommendations relate to the definition and measurement of childhood adversity, the integration of studies of typical development with those on childhood adversity, and the importance of distinguishing between general and specific mechanisms linking childhood adversity to psychopathology.

The second goal is to provide a transdiagnostic model of mechanisms linking childhood adversity and youth psychopathology that incorporates each of these recommendations.

Defining Childhood Adversity

Childhood adversity is a construct in search of a definition. Despite the burgeoning interest and research attention devoted to childhood adversity, there is a surprising lack of consistency with regard to the definition and measurement of the construct. Key issues remain unaddressed in the literature regarding the definition of childhood adversity and the boundary conditions of the construct. To what does the construct of childhood adversity refer? What types of experiences qualify as childhood adversity and what types do not?

Where do we draw the line between normative experiences of stress and those that qualify as an adverse childhood experience? How does the construct of childhood adversity differ from other constructs that have been linked to psychopathology risk, including stress, toxic stress. and trauma? It will be critical to gain clarity on these definitional issues before more complex questions regarding mechanisms and protective factors can be systematically examined.

Even in the seminal ACE Study that spurred much of the recent research into childhood adversity, a concrete definition of adverse childhood experience is not provided. The original article from the study argues for the importance of understanding the lasting health effects of child abuse and “household dysfunction,” the latter of which is never defined specifically (Felitti et al., 1998). The CDC website for the ACE Study indicates that the ACE score. a count of the total number of adversities experienced. is designed to assess ”the total amount of stress experienced during childhood.”

Why has a concrete definition of childhood adversity remained elusive? As I see it, there is a relatively simple explanation for this notable gap in the literature. Childhood adversity is difficult to define but fairly obvious to most observers. making the construct an example of the classic standard of you know it when you see it. Although this has allowed a significant scientific knowledge base on childhood adversity to emerge within a relatively short period, the lack of an agreed upon definition of the construct represents a significant impediment to future progress in the field.

How can we begin to build scientific consensus on the definition of childhood adversity? Critically, we must come to an agreement about what childhood adversity is and what it is not. Adversity is defined as “a state or instance of serious or continued difficulty or misfortune; a difficult situation or condition; misfortune or tragedy” (“Adversity,” 2015).

This provides a reasonable starting point. Adversity is an environmental event that must be serious (i.e., severe) or a series of events that continues overtime (i.e.. chronic).

Building on Scott Monroe‘s (2008) definition of life stress and models of experience expectant brain development (Baumrind, 1993; Fox. Levitt, & Nelson. 2010), I propose that childhood adversity should be defined as experiences that are likely to require significant adaptation by an average child and that represent a deviation from the expectable environment. The expectable environment refers to a wide range of species typical environmental inputs that the human brain requires to develop normally. These include sensory inputs (e.g., variation in patterned light information that is required for normal development of the visual system), exposure to language, and the presence of a sensitive and responsive caregiver (Fox et al., 2010).

As I have argued elsewhere (McLaughlin, Sheridan, & Lambert, 2014; Sheridan & McLaughlin, 2014), deviations from the expectable environment often take two primary forms: an absence of expected inputs (e. g., limited exposure to language or the absence of a primary caregiver), or the presence of unexpected inputs that represent significant threats to the physical integrity or well being of the child (e.g., exposure to violence).

A similar approach to classifying key forms of child adversity has been articulated by others as well (Farah et al., 2008; Humphreys & Zeanah, 2015). These experiences can either be chronic (e.g.. prolonged neglect) or involve single events that are severe enough to represent a deviation from the expectable environment (e.g., sexual abuse).

Together, this provides a working definition of childhood adversity: exposure during childhood or adolescence to environmental circumstances that are likely to require significant psychological, social, or neurobiological adaptation by an average child and that represent a deviation from the expectable environment.

This definition provides some clarity about what childhood adversity is not. The clearest boundary condition involves the developmental timing of exposure; experiences classified as childhood adversity must occur prior to adulthood, either during childhood or adolescence. Most research on childhood adversity has taken a broad definition of childhood, including events occurring during either childhood or adolescence. Although the demarcation between adolescence and adulthood is itself a point of debate, relative consensus exists regarding the onset of adult roles as the end of adolescence (Steinberg, 2014).

Second. childhood adversity refers to an event or ongoing events in the environment. Childhood adversity thus refers only to specific environmental circumstances or events and not to an individual child’s response to those circumstances.

Third, childhood adversity refers to environmental conditions that are likely to require significant psychological, social, or neurobiological adaptation by an average child; therefore, events that represent transient or minor hassles should not qualify.

What types of events should be considered severe enough to warrant classification as adversity? Although there is no absolute rule or formula that can be used to distinguish circumstances or events requiring significant adaptation from those that are less severe or impactful, childhood adversity should include conditions or events that are likely to have a meaningful and lasting impact on developmental processes for most children who experience them. In other words, experiences that could alter fundamental aspects of development in emotional, cognitive, social, or neurobiological domains are the types of experiences that should qualify as adversity.

Studies of childhood adversity should clearly define the study specific decision rules used to distinguish between adversity and more normative stressors.

Finally, environmental circumstances or stressors that do not represent deviations from the expectable environment should not be classified as childhood adversity. In other words. childhood adversity should not include any and all stressors that occur during childhood or adolescence. Two examples of childhood stressors that would likely not qualify as childhood adversity based on this definition, because they do not meet the condition of representing a deviation from the expectable environment, are moving to a new school and death of an elderly grandparent. Each of these childhood stressors should require adaptation by an average child. and could influence mental health and development. However, neither represents a deviation from the expectable childhood environment and therefore does not meet the proposed definition of childhood adversity.

A key question for the field is whether the definition of childhood adversity should be narrow or broad. This question will determine whether other common forms of adversity or stress should be considered as indicators of childhood adversity. For example, many population based studies have included parental psychopathology and divorce as forms of adversity (Felitti et al., 1998; Green et al.. 2010). Given the high prevalence of psychopathology and divorce in the population, consideration of any form of parental psychopathology or any type of divorce as a form of adversity results in a fairly broad definition of adversity; certainly, not all cases of parental psychopathology or all divorces result in significant adversity for children. A more useful approach might be to consider only those cases of parental psychopathology or divorce that result in parenting behavior that deviates from the expectable environment (i. e., consistent unavailability, unresponsiveness, or insensitive care) or that generate other types of significant adversity for children (e.g., economic adversity, emotional abuse, etc.) as meeting the threshold for childhood adversity. Providing these types of boundary conditions is important to prevent the construct of childhood adversity from meaning everything and nothing at the same time.

Finally, how does childhood adversity differ from related constructs, including stress, toxic stress, and trauma that can also occur during childhood? What is unique about the construct of childhood adversity that is not captured in definitions of these similar constructs?

First, how is childhood adversity different from stress? The prevailing conceptualization of life stress defines the construct as the adaptation of an organism to specific circumstances that change over time (Monroe, 2008). This definition includes three primary components that interact with one another: environment (the circumstance or event that requires adaptation by the organism), organism (the response to the environmental stimulus), and time (the interactions between the organism and the environment over time; Monroe, 2008). In contrast, childhood adversity refers only to the first of these three components, the environmental aspect of stress.

Second. how is adversity different from toxic stress, a construct recently developed by Jack Shonkoff and colleagues (Shonkoff & Garner, 2012)? Toxic stress refers to the second component of stress just described, the response of the organism. Specifically, toxic stress refers to exaggerated, frequent, or prolonged activation of physiological stress response systems in response to an accumulation of multiple adversities over time in the absence of protection from a supportive caregiver (Shonkoff & Garner, 2012). The concept of toxic stress is conceptually similar to the construct of allostatic load as defined by McEwen (2000) and focuses on a different aspect of stress than childhood adversity.

Finally, how is childhood adversity distinct from trauma? Trauma is defined as exposure to actual or threatened death. serious injury, or sexual violence, either by directly experiencing or witnessing such events or by learning of such events occurring to a close relative or friend (American Psychiatric Association, 2013). Traumatic events occurring in childhood represent one potential form of childhood adversity, but not all types of childhood adversity are traumatic. Examples of adverse childhood experiences that would not be considered traumatic are neglect; poverty; and the absence of a stable, supportive caregiver.

The first concrete recommendation for future research is that the field must utilize a consistent definition of childhood adversity. A useful definition must have clarity about what childhood adversity is and what it is not, provide guidance about decision rules for applying the definition in specific contexts, and increase consistency in the measurement and application of childhood adversity across studies. The definition proposed here that childhood adversity involves experiences that are likely to require significant adaptation by an average child and that represent a deviation from the expectable environment-represents a starting point in this endeavor, although consideration of alterative definitions and scholarly debate about the relative merits of different definitions is encouraged.

Integrating Studies of Typical and Atypical Development

A developmental psychopathology perspective emphasizes the reciprocal and integrated nature of our understanding of normal and abnormal development (Cicchetti, 1996′, Cicchetti & Lynch, 1993; Lynch & Cicchetti, 1998). Normal developmental patterns must be characterized to identify developmental deviations, and abnormal developmental outcomes shed light on the normal developmental processes that lead to maladaptation when disrupted (Cicchetti, 1993; Sroufe, 1990). Maladaptive outcomes, including psychopathology, are considered to be the product of developmental processes (Sroufe, 1997, 2009). This implies that in order to uncover mechanisms linking childhood adversity to psychopathology, the developmental trajectory of the candidate emotional, cognitive, social, or neurobiological process under typical circumstances must first be characterized before examining how exposure to an adverse environment alters that trajectory. This approach has been utilized less frequently than would be expected in the literature on childhood adversity.

Recent work from Nim Tottenham’s lab on functional connectivity between the amygdala and medial prefrontal cortex (mPFC) highlights the utility of this strategy. In an initial study, Gee, Humphreys, et a1. (2013) demonstrated age related changes in amygdala-mPFC functional connectivity in a typically developing sample of children during a task involving passive viewing of fearful and neutral faces. Specifically, they observed a developmental shift from a pattern of positive amygdala-mPFC functional connectivity during early and middle childhood to a pattern of negative connectivity (i.e., higher mPFC activity, lower amygdala activity) beginning in the prepubertal period and continuing throughout adolescence (Gee. Humphreys, et al., 2013). Next, they examined how exposure to institutional rearing in infancy influenced these age related changes, documenting a more mature pattern of negative functional connectivity among young children with a history of institutionalization (Gee, Gabard Dumam, et a1., 2013).

Utilizing this type of approach is important not only to advance knowledge of developmental mechanisms underlying childhood adversity-psychopathology associations but also to leverage research on adverse environmental experiences to inform our understanding of typical development. Specifically, as frequently argued by Cicchetti (Cicchetti & Toth, 2009), research on atypical or aberrant developmental processes can provide a window into typical development not available through other means, This is particularly relevant in studies of some forms of childhood adversity that involve an absence of expected inputs from the environment, such as institutional rearing and child neglect (McLaughlin. Sheridan, & Lambert, 2014; Sheridan & McLaughlin, 2014). Examining the developmental consequences associated with deprivation in a particular type of input from the environment (e.g., the presence of an attachment figure, exposure to complex language) can provide insights into the types of environmental inputs that are required for a system or set of competencies to develop normally.

Evidence on the developmental trajectories of children raised in institutional settings provides an illustrative example. Institutions for abandoned and orphaned children vary widely, but a common feature across them is the absence of an attachment figure who provides sensitive and responsive care for each child (Smyke et al., 2007; Tottenham, 2012; Zeanah et al., 2003). Developmental research on children raised in institutional settings has provided ample evidence about the importance of the attachment relationship in early development for shaping numerous aspects of development, Unsurprisingly, most children raised in institutions fail to develop a secure attachment relationship to a caregiver; this is particularly true if children remain in institutional care past the age of 2 years (Smyke, Zeanah, Fox, Nelson, & Guthrie, 2010; Zeanah, Smyke, Koga, Carlson, & The Bucharest Early Intervention Project Core Group, 2005).

Children reared in institutional settings also exhibit social skills deficits, delays in language development, lasting disruptions in executive func