Category Archives: Depression

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

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.

*

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 functioning skills, decrements in IQ, and atypical patterns of emotional processing (Almas et al., 2012; Bos. Fox, Zeanah, & Nelson, 2009; Nelson et al., 2007; Tibu et al., 2016; Tottenham et al., 2011; Windsor et al., 2011). Institutional rearing also has wide ranging impacts on patterns of brain development, including neural structure and function (Gee et al., 2013; McLaughlin, Fox, Zeanah, & Nelson, 20] 1; McLaughlin, Sheridan, Winter, et al., 2014; Sheridan, Fox, Zeanah, McLaughlin, & Nelson, 2012; Tottenham et al., 2011).

Although children raised in institutional settings often experience deprivation in environmental inputs of many kinds, it is likely that the absence of a primary attachment figure in early development explains many of the downstream consequences of institutionalization on developmental outcomes. Indeed, recent evidence suggests that disruptions in attachment may be a causal mechanism linking institutional rearing with the onset of anxiety and depression in children. Specifically, in a randomized controlled trial of foster care as an intervention for orphaned children in Romania, improvements in attachment security were a mechanism underlying the preventive effects of the intervention on the onset of anxiety and depression in children (McLaughlin, Zeanah, Fox, & Nelson, 2012). By examining the developmental consequences of the absence of an expected input from the environment, namely, the presence of a primary attachment figure, studies of institutional rearing provide strong evidence for the centrality of the early attachment relationship in shaping numerous aspects of development.

Sensitive Periods

The integration of studies on typical and atypical development may be particularly useful in the identification of sensitive periods. Developmental psychopathology emphasizes the cumulative and hierarchical nature of development (Gottlieb, 1991a, 1991b; Sroufe, 2009; Sroufe, Egeland, & Kreutzer, I990; Werner & Kaplan, 1963). Learning and acquisition of competencies at one point in development provide the scaffolding upon which subsequent skills and competencies are built, such that capabilities from previous periods are consolidated and reorganized in a dynamic, unfolding process across time. The primary developmental tasks occurring at the time of exposure to a risk factor are thought to be the most likely to be interrupted or disrupted by the experience. Developmental deviations from earlier periods are then carried forward and have consequences for children’s ability to successfully accomplish developmental tasks in a later period (Cicchetti & Toth, 1998; Sroufe, 1997). In other words, early experiences constrain future learning of patterns or associations that represent departures from those that were previously learned (Kuhl, 2004).

This concept points to a critical area for future research on childhood adversity involving the identification of sensitive periods of emotional, cognitive, social, and neurobiological development when inputs from the environment are particularly influential. Sensitive periods have been identified both in sensory development and in the development of complex social-cognitive skills, including language (Hensch, 2005′, Kuhl. 2004).

Emerging evidence from cognitive neuroscience also suggests the presence of developmental periods when specific regions of the brain are most sensitive to the effects of stress and adversity (Andersen et al., 2008).

However, identification of sensitive periods has remained elusive in other domains of emotional and social development, potentially reflecting the fact that sensitive periods exist for fewer processes in these domains. However, determining how anomalous or atypical environmental inputs influence developmental processes differently based on the timing of exposure provides a unique opportunity to identify sensitive periods in development; in this way, research on adverse environments can inform our understanding of typical development by highlighting the environmental inputs that are necessary to foster adaptive development.

Identifying sensitive periods of emotional and social development requires detailed information on the timing of exposure to atypical or adverse environments, which is challenging to measure. To date, studies of institutional rearing have provided the best opportunity for studying sensitive periods in human emotional and social development, as it is straightforward to determine the precise period during which the child lived in the institutional setting.

Studies of institutional rearing have identified a sensitive period for the development of a secure attachment relationship at around 2 years of age; the majority of children placed into stable family care before that time ultimately develop secure attachments to a caregiver, whereas the majority of children placed after 2 years fail to develop secure attachments (Smyke et al., 2010).

Of interest, a sensitive period occurring around 2 years of age has also been identified for other domains, including reactivity of the autonomic nervous system and hypothalamic pituitary adrenal (HPA) axis to the environment and a neural marker of affective style (i.e., frontal electroencephalogram asymmetry; McLaughlin et al., 20] l; McLaughlin, Sheridan, et al., 2015), suggesting the importance of the early attachment relationship in shaping downstream aspects of emotional and neurobiological development.

The second concrete recommendation for future research is to integrate studies of typical development with those focused on understanding the impact of childhood adversity, in particular, research that can shed light on sensitive periods in emotional, social, cognitive, and neurobiological development is needed. Identifying the developmental processes that are disrupted by exposure to particular types of adverse environments will be facilitated by first characterizing the typical developmental trajectories of the processes in question. In turn, studies of atypical or adverse environments should be leveraged to inform our understanding of the types of environmental inputs that are required, and when, for particular systems to develop normally.

Given the inherent problems in retrospective assessment of timing of exposure to particular environmental experiences, longitudinal studies with repeated measurements of environmental experience and acquisition of developmental competencies are likely to be most informative. Alternatively, the occurrence of exogenous events like natural disasters, terrorist attacks, and changes in policies or the availability of resources (e.g., the opening of the casino on a Native American reservation; Costello, Compton, Keeler, & Angold, 2003) provides additional opportunities to study sensitive periods of development. Identifying sensitive periods is likely to yield critical insights into the points in development when particular capabilities are most likely to be influenced by environmental experience, an issue of central importance for understanding both typical and atypical development. Such information can be leveraged to inform decisions about the points in time when psychosocial interventions for children exposed to adversity are likely to be maximally efficacious.

Explaining Multifinality

The principle of multifinality is central to developmental psychopathology (Cicchetti, 1993). Multifinality refers to the process by which the same risk and/or protective factors may ultimately lead to different developmental outcomes (Cicchetti & Rogosch, 1996).

It has been repeatedly demonstrated that most forms of childhood adversity are associated with elevated risk for the onset of virtually all commonly occurring mental disorders (Green et al., 2010; McLaughlin, Green, et al., 2012). As noted earlier, recent evidence suggests that child maltreatment is associated with a latent liability for psychopathology that explains entirely the associations of maltreatment with specific mental disorders (Caspi et al., 2014; Keyes et al., 2012). However, the mechanisms that explain how child maltreatment, or other forms of adversity, influence a generalized liability to psychopathology have not been specified. To date, there have been few attempts to articulate a model explaining how childhood adversity leads to the diversity of mental disorders with which it is associated (i. e., multifinality). What are the mechanisms that explain this generalized vulnerability to psychopathology arising from adverse early experiences? Are these mechanisms shared across multiple forms of childhood adversity, or are they specific to particular types of adverse experience?

Identifying general versus specific mechanisms will require changes in the way we conceptualize and measure childhood adversity. Prior research has followed one of two strategies. The first involves studying individual types of childhood adversity, such as parental death, physical abuse, neglect, or poverty (Chase Lansdale, Cherlin, & Kieman, 1995; Dubowitz, Papas, Black, & Starr, 2002; Fristad, Jedel, Weller, & Weller, 1993; Mullen, Martin, Anderson, Romans, & Herbison, 1993; Noble, McCandliss, & Farah, 2007; Wolfe, Sas, & Wekerle, 1994). However, most individuals exposed to childhood adversity have experienced multiple adverse experiences (Dong et a1., 2004; Finkelhor, Ormrod, & Turner, 2007; Green et a1., 2010; McLaughlin, Green, et a1., 2012). This presents challenges for studies focusing on a single type of adversity, as it is unclear if any observed associations represent the downstream effects of the focal adversity in question (e.g., poverty) or the consequences of other co occurring experiences (e.g., exposure to violence) that might have different developmental consequences.

Increasing recognition of the co-occurring nature of adverse childhood experiences has resulted in a shift from focusing on single types of adversity to examining the associations between a number of adverse childhood experiences and developmental outcomes, the core strategy of the ACE approach (Arata, Langhinrichsen Roling, Bowers, & O’Brien, 2007; Dube et al., 2003; Edwards et a1., 2003; Evans et al., 2013). There has been a proliferation of research utilizing this approach in recent years, and it has proved useful in documenting the importance of childhood adversity as a risk factor for a wide range of negative mental health outcomes. However, this approach implicitly assumes that very different kinds of experiences ranging from violence exposure to material deprivation (e.g., food insecurity) to parental loss influence psychopathology through similar mechanisms. Although there is likely to be some overlap in the mechanisms linking different forms of adversity to psychopathology, the count approach oversimplifies the boundaries between distinct types of environmental experience that may have unique developmental consequences.

An alternative approach that is likely to meet with more success involves identifying dimensions of environmental experience that underlie multiple forms of adversity and are likely to influence development in similar ways. In recent work, my colleague Margaret Sheridan and I have proposed two such dimensions that cut across multiple forms of adversity: threat and deprivation (McLaughlin, Sheridan, & Lambert, 2014; Sheridan & McLaughlin, 2014).

Threat involves exposure to events involving harm or threat of harm, consistent with the definition of trauma in the Diagnostic and Statistical Manual of Mental Disorders (5th ed.; American Psychiatric Association, 2013). Threat is a central dimension underlying multiple commonly studied forms of adversity, including physical abuse, sexual abuse, some forms of emotional abuse (i.e., that involve threats of physical violence and coercion), exposure to domestic violence, and other forms of violent victimization in home, school, or community settings.

Deprivation, in contrast, involves the absence of expected cognitive and social inputs from the environmental stimuli, resulting in reduced opportunities for learning. Deprivation in expected environmental inputs is common to multiple forms of adversity including emotional and physical neglect, institutional rearing, and poverty. Critically, we do not propose that exposure to deprivation and threat occurs independently for children, as these experiences are highly co-occurring, or that these are the only important dimensions of experience involved in childhood adversity.

Instead we propose, first, that these are two important dimensions that can be measured separately and, second, that the mechanisms linking these experiences to the onset of psychopathology are likely to be at least partially distinct (McLaughlin, Sheridan, & Lambert, 2014; Sheridan & McLaughlin, 2014). I describe some of these key mechanisms in the transdiagnostic model presented later. Recently, others have argued for the importance of taking this type of dimensional approach as well (Hamby & Grych, 2013; Humphreys & Zeanah, 2015).

Specific recommendations are for future research to (a) identify key dimensions of environmental experience that might differentially influence developmental outcomes and (b) measure multiple such dimensions in studies of childhood adversity to distinguish between general and specific underlying mechanisms linking different forms of adversity to psychopathology. Fine grained measurement of the dimensions of threat and deprivation has often not been conducted within the same study.

Studies focusing on specific types of exposure (e.g., abuse) without measuring or adjusting for co-occurring exposures (e.g., neglect) are unable to distinguish between common and specific mechanisms linking different dimensions of adverse experiences to psychopathology. The only way to determine whether such specificity exists is to measure and model these dimensions of experience together in future studies.

Characterizing the Interplay of Risk and Protective Factors

Although psychopathology is common among children exposed to a wide range of adverse environments, many children exhibit adaptation and resilience following adversity (Masten, 2001; Masten, Best, & Garmezy, 1990). For example, studies of resilience suggest that children who have a positive relationship with a caring and competent adult; are good at learning. problem solving, and self regulation; are socially engaging; and have positive self image are more likely to exhibit positive adaptation after exposure to adversity than children without these characteristics (Luthar, Cicchetti. & Becker, 2000; Masten. 2001; Masten et al.. 1990).

However, in contrast to the consistent pattern of associations between childhood adversity and psychopathology, evidence for protective factors varies widely across studies, and in most cases children exposed to adversity exhibit adaptive functioning in some domains but not others: even within a single domain, children may be functioning well at one point in time but not at others (Luthar et al.. 2000). This is not surprising given that the degree to which a particular factor is protective depends heavily upon context, including the specific risk factors with which it is interacting (Cicchetti & Lynch. 1993; Sameroff. Gutman, & Peck, 2003).

For example. authoritative parenting has been shown to be associated with adaptive outcomes for children raised in stable contexts that are largely free of significant adversity (Steinberg, Elmen, & Mounts, 1989; Steinberg, Lamborn, Dornbusch. & Darling. 1992; Steinberg, Mounts, Lambom. & Dombusch, I991); in contrast, authoritarian parenting appears to be protective for children being raised in environments characterized by low resources and/or high degrees of violence and other threats (Flouri, 2007; Gonzales, Cauce. Friedman. & Mason, 1996).

The degree to which variation in specific genetic polymorphisms moderates the impact of childhood adversity on development outcomes is also highly variable across studies; although genetic variation clearly contributes to developmental trajectories of adaptation and maladaptation following childhood adversity, this topic has been reviewed extensively elsewhere (Heim & Binder. 2012: McCrory, De Brito, & Viding. 2010; Uher & McGuffrn, 20l0) and is not discussed further. This complexity has contributed to the widely variable findings regarding protective factors and resilience.

Progress in identifying protective factors that buffer children from maladaptive outcomes following childhood adversity might be achieved by shifting the focus from downstream outcomes to more proximal mechanisms known to underlie the relationship between adverse childhood experiences and psychopathology. Research on resiliency has often focused on distal outcomes, such as the absence of psychopathology, the presence of high quality peer relationships, or good academic performance as markers of adaptive functioning in children with exposure to adversity (Bolger, Patterson, & Kupersmidt. 1999; Collishaw et al., 2007; Fergusson & Lynskey, 1996; Luthar, 1991).

Just as there are numerous mechanisms through which exposure to adverse environments lead to psychopathology and other downstream outcomes, there are likely to be a wide range of mechanisms through which protective factors buffer children from maladaptation following childhood adversity. Indeed. modern conceptualizations of resilience describe it as a developmental process that unfolds over time as an ongoing transaction between a child and the multiple contexts in which he or she is embedded (Luthar et al., 2000)

Rather than examining protective factors that buffer children from developing psychopathology following adverse childhood experiences, an alternative approach is to focus on factors that moderate the association of childhood adversity with the developmental processes that serve as mechanisms linking adversity with psychopathology (e.g., emotion regulation, executive functioning) or that moderate the link between these developmental processes and the onset of psychopathology. Deconstructing the pathways linking childhood adversity to psychopathology allows moderators to be examined separately at different stages of these pathways and may yield greater information about how protective factors ultimately exert their effects on downstream outcomes. including psychopathology.

Accordingly, a fourth recommendation is that future research should focus on identifying protective factors that buffer children from the negative consequences of adversity at two levels: (a) factors that modify the association between childhood adversity and the maladaptive patterns of emotional, cognitive, social, and neurobiological development that serve as intermediate phenotypes linking adversity with psychopathology. and (b) factors that moderate the influence of intennediate phenotypes on the emergence of psychopathology, leading to divergent trajectories of adaptation across children.

To understand resilience, we first need to understand the developmental processes that are disrupted following exposure to adversity and how certain characteristics either prevent or compensate for those developmental disruptions or reduce their impact on risk for psychopathology.

A TRANSDIAGNOSTIC MODEL OF CHILDHOOD ADVERSITY AND PSYCHOPATHOLOGY

The remainder of the article outlines a transdiagnostic model of mechanisms linking childhood adversity with youth psychopathology. Two core developmental mechanisms are proposed that, in part, explain patterns of multitinality: emotional processing and executive functioning.

The model builds on a framework described by Nolen Hoeksema and Watkins (2011) for identifying transdiagnostic processes. Of importance, the model is not intended to be comprehensive in delineating all mechanisms linking childhood adversity with psychopathology but rather focuses on two candidate mechanisms linking childhood adversity to multiple forms of psychopathology. At the same time, these mechanisms are also specific in that each is most likely to emerge following exposure to specific dimensions of adverse early experience.

The model is specific with regard to the underlying dimensions of adverse experience considered and identifies several key moderators that might explain divergent developmental trajectories among children following exposure to adversity. Future research is needed to expand this framework to incorporate other key dimensions of the adverse environmental experience, developmental mechanisms linking those dimensions of adversity with psychopathology, and moderators of those associations.

Distal Risk Factors

Within the proposed model, core dimensions of environmental experience that underlie multiple forms of adversity are conceptualized as distal risk factors for psychopathology, Specifically, experiences of threat and deprivation constitute the first component of the proposed transdiagnostic model of childhood adversity and psychopathology.

Experiences of threat and deprivation meet each of Nolen Hoeksema and Watkins’s (2011) criteria for a distal risk factor. They represent environmental conditions largely outside the control of the child that are linked to the onset of psychopathology only through intervening causal mechanisms that represent more proximal risk factors. Although they are probabilistically related to psychopathology, exposure to threat and deprivation do not invariably lead to mental disorders. These experiences influence proximal risk factors primarily through learning mechanisms that ultimately shape patterns of information processing, emotional responses to the environment, and higher order control processes that influence both cognitive and emotional processing.

Proximal Risk Factors

The developmental processes that are altered following exposure to adverse environmental experiences represent proximal risk factors, or intermediate phenotypes, linking them to the onset of psychopathology. These proximal risk factors represent the second component of the proposed transdiagnostic model. Nolen Hoeksema and Watkins (2011) argued that proximal risk factors are within person factors that mediate the relationship between distal risk factors, including aspects of environmental context that are difficult to modify, such as childhood adversity, and the emergence of psychopathology. Proximal risk factors directly influence symptoms and are temporally closer to symptom onset and often easier to modify than distal risk factors (Nolen Hoeksema & Watkins, 2011).

Identifying modifiable within person factors that link adverse environmental experiences with the onset of symptoms is the key to developing interventions to prevent the onset of psychopathology in children who have experienced adversity.

The model includes two primary domains of proximal risk factors: emotional processing and executive functioning.

Emotional processing refers to information processing of emotional stimuli (e.g., attention, memory), emotional reactivity, and both automatic (e.g., habituation, fear extinction) and effortful (e.g., cognitive reappraisal) forms of emotion regulation. These processes all represent responses to emotional stimuli, and many involve interactions of cognition with emotion.

Executive functions comprise a set of cognitive processes that support the ability to learn new knowledge and skills; hold in mind goals and information; and create and execute complex, future oriented plans. Executive functioning comprises the ability to hold information in mind and focus on currently relevant information (working memory), inhibit actions and information not currently relevant (inhibition). and switch flexibly between representations or goals (cognitive flexibility; Miyake & Friedman. 2012; Miyake, Friedman, Rettinger, Shah, & Hegarty, 2001).

Together these skills allow the creation and execution of future oriented plans and the inhibition of behaviors that do not serve these plans, providing the foundation for healthy decision making and self regulation. Many of the diverse mechanisms linking childhood adversity to psychopathology are subsumed within these two broad domains.

Emotional processing, stable patterns of emotional processing, emotional responding to the environment, and emotion regulation represent the first core domain of proximal risk factors. Experiences of uncontrollable threat are associated with strong learning of specific contingencies and overgeneralization of that learning to novel contexts, which facilitates the processing of salient emotional cues in the environment (e.g., biased attention to threat). Given the importance of quickly identifying potential threats in the environment for children growing up in environments characterized by legitimate danger, these learning processes should produce information processing biases that promote rapid identification of potential threats. Indeed, evidence suggests that children with abuse histories, an environment characterized by high levels of threat, exhibit attention biases toward facial displays of anger, identify anger with little perceptual information, have difficulty disengaging from angry faces, and display anticipatory monitoring of the environment following interpersonal displays of anger (Pollak, Cicchetti, Hornung, & Reed, 2000; Pollak & Sinha, 2002; Pollak & Tolley Schell, 2003; Pollak, Vardi, Putzer Bechner, & Curtin, 2005; Shackman, Shackman, & Pollak, 2007).

Given the relevance of anger as a signal of potential threat, these findings suggest that exposure to threatening environments results in stable patterns of information processing that facilitate threat identification and maintenance of attention to threat cues. These attention biases are specific to children who have experienced violence; for example, children who have been neglected (i.e., an environment characterized by deprivation in social and cognitive inputs) experience difficulty discriminating facial expressions of emotion but do not exhibit attention biases toward threat (Pollak, Klorrnan, Thatcher, & Cicchetti, 2001; Pollak et al., 2005).

In addition to attention biases, children who have been the victims of violence are also more likely to generate attributions of hostility to others in socially ambiguous situations (Dodge, Bates, & Pettit, 1990; Dodge, Pettit, Bates, & Valente, 1995; Weiss, Dodge, Bates, & Petit, 1992), a pattern of social information processing tuned to be overly sensitive to potential threats in the environment. Finally, some evidence suggests that exposure to threatening environments is associated with memory biases for overgeneral autobiographical memories in both children and adults (Crane et al., 2014; Williams et al., 2007).

Children with trauma histories also exhibit meaningful differences in patterns of emotional responding that are consistent with these patterns of information processing. For example, children who have experienced interpersonal violence exhibit greater activation in the amygdala and other nodes of the salience network (e.g., anterior insula, putamen, thalamus) to a wide range of negative emotional stimuli (McCrory et al., 2013; McCrory et al., 2011; McLaughlin, Peverill, Gold, Alves, & Sheridan, 2015), suggesting heightened salience of information that could predict threat.

These findings build on earlier work using evoked response potentials documenting amplified neural response to angry faces in children who were physically abused (Pollak, Cicchetti, Klorman, & Brumaghim, 1997; Pollak et al., 2001) and suggests that exposure to threatening experiences heightens the salience of negative emotional information, due to the potential relevance for detecting novel threats.

Heightened amygdala response to negative emotional cues could also reflect fear learning processes, whereby previously neutral stimuli that have become associated with traumatic events begin to elicit conditioned fear responses, or the result of deficits in automatic emotion regulation processes like fear extinction and habituation, which are mediated through connections between the ventromedial prefrontal cortex and amygdala. Recent findings of poor resting state functional connectivity between the ventromedial prefrontal cortex and amygdala among female adolescents with abuse histories provide some evidence for this latter pathway (Herringa et al., 2013).

In addition to heightened neural responses in regions involved in salience processing, consistent associations between exposure to threatening environments and elevations in self reported emotional reactivity to the environment have been observed in our lab and elsewhere (Glaser, Van Os, Portegijs. & Myin Genneys, 2006; Heleniak, Jenness, Van Der Stoep, McCauley, & McLaughlin, in press; McLaughlin, Kubzansky et al., 2010).

Atypical physiological responses to emotional cues have also been documented consistently among children who have experienced trauma, although the specific pattern of findings has varied across studies depending on the specific physiological measures and emotion eliciting paradigms employed. We recently applied a theoretical model drawn from social psychology on adaptive and maladaptive responses to stress to examine physiological responses to stress among maltreated youths. We observed a pattern of increased vascular resistance and blunted cardiac output reactivity among youths who had been physically or sexually abused relative to participants with no history of violence exposure (McLaughlin, Sheridan, Alves, & Mendes, 2014). This pattern of autonomic nervous system reactivity reflects an inefficient cardiovascular response to stress that has been shown in numerous studies to occur when individuals are in a state of heightened threat and is associated with threat appraisals and maladaptive cognitive and behavioral responses to stress (J amieson, Mendes, Blackstock, & Schmader, 2010; Jamieson, Nock, & Mendes, 2012; Mendes, Blascovich, Major. & Seery, 200l; Mendes, Major, McCoy, & Blascovich, 2008). Using data from a large population based cohort of adolescents, we recently replicated the association between childhood trauma exposure and blunted cardiac output reactivity during acute stress (Heleniak, Riese, Ormel, & McLaughlin, 2016).

Together, converging evidence across multiple levels of analysis indicates that exposure to trauma is associated with a persistent pattern of information processing involving biased attention toward potential threats in the environment, heightened neural and subjective responses to negative emotional cues, and a pattern of autonomic nervous system reactivity consistent with heightened threat perception. This heightened reactivity to negative emotional cues may make it more difficult for children who have been exposed to threatening enviromnents to regulate emotional responses. Indeed, a recent study from my lab found that when trying to regulate emotional responses using cognitive reappraisal, children who had been abused recomited regions of the prefrontal cortex involved in effortful control to a greater degree than children who had never experienced violence (McLaughlin, Peverill, et a1., 2015). This pattern suggests that attempts to modulate emotional responses to negative cues require more cognitive resources for children with abuse histories, meaning that effective regulation may break down more easily in the face of stress. Evidence that the negative emotional effects of stressful events are heightened among those with maltreatment histories is consistent with this possibility (Glaser et a1., 2006; McLaughlin, Conron, et al., 2010).

In addition to alterations in patterns of emotional reactivity to environmental cues, child trauma has been associated with maladaptive patterns of responding to distress. For example, exposure to threatening environments early in development is associated with habitual engagement in rumination, a response style characterized by passive focus on feelings of distress along with their causes and consequences without attempts to actively resolve the causes of distress (Nolen Hoeksema, Wisco, & Lyubomirsky, 2008). High reliance on rumination as a strategy for responding to distress has been observed in adolescents and adults who were abused as children (Conway. Mendelson, Giannopoulos, Csank. & Holm, 2005; Heleniak et al., in press; Sarin & Nolen Hoeksema, 2010). Adolescents who experienced victimization by peers (McLaughlin, Hatzenbuehler, & Hilt, 2009), and both adolescents and adults exposed to a wide range of negative life events (McLaughlin & Hatzenbuehler, 2009; Michl, McLaughlin, Shepherd, & Nolen Hoeksema, 2013), although the latter findings are not specific to threat per se.

Although evidence for disruptions in emotional processing come primarily from studies examining children exposed to environments characterized by high degrees of threat, deprived environments are also likely to have downstream effects on emotional development that are at least partially unique from those associated with threat. As noted previously, children who have been neglected experience difficulties discriminating facial displays of emotion (Pollak et al., 2001: Pollak et al., 2005), although some studies of neglected children have found few differences in neural responses to facial emotion in early childhood (Moulson, Fox, Zeanah, & Nelson, 2009; Slopen, McLaughlin, Fox, Zeanah, & Nelson, 2012). However, recent work suggests that children raised in deprived early environments exhibit elevated amygdala response to facial emotion and a mature pattem of functional connectivity between the amygdala and mPFC during emotional processing tasks (Gee et al., 2013; Tottenham et al., 201 1). Finally, children who were neglected or raised in deprived institutions tend to exhibit blunted physiological responses to stress, including in the autonomic nervous system and HPA axis (Gunnar, Frenn, Wewerka, & Van Ryzin, 2009; McLaughlin, Sheridan, et al., 2015).

Much of the existing work on childhood adversity and emotional responding has focused on responses to negative emotional cues. However, a growing body of evidence also suggests that responses to appetitive and rewarding cues are disrupted in children exposed to adversity. For example, children raised in deprived early environments exhibit blunted ventral striatal response to the anticipation of reward (Mehta et al., 2010), and a similar pattern has been observed in a sample of adults exposed to abuse during childhood (Dillon et al., 2009). In a recent study, an increase in ventral striatum response to happy emotional faces occurred from childhood to adolescence in typically developing children but not in children reared in deprived institutions (Goff et al., 2013). In recent work in our lab, we have also observed blunted reward learning among children exposed to institutional rearing (Sheridan, McLaughlin, et al., 2016).

Although the mechanisms underlying the link between diverse forms of childhood adversity and responsiveness to reward have yet to be clearly identified, it has been suggested that repeated activation of the HPA axis in early childhood can attenuate expression of brain derived neurotrophic factor, which in turn regulates the mesolimbic dopamine system that underlies reward learning (Goff & Tottenham, 2014). These reductions in brain derived neurotrophic factor expression may contribute to a pattern of blunted ventral striatum response to reward anticipation or receipt.

Alternatively, given the central role of the mesolimbic dopamine system in attachment related behavior (Strathearn, 2011), the absence or unpredictability of an attachment figure in early development may reduce opportunities for learning about the rewarding nature of affiliative interactions and social bonds; the absence of this type of stimulus reward learning early in development, when sensitive and responsive caregiving from a primary attachment figure is an expected environmental input, may ultimately contribute to biased processing of rewarding stimuli later in development. If social interactions in early life are either absent or unrewarding, expectations about the hedonic value of social relationships and other types of rewards might be altered in the long term, culminating in attenuated responsiveness to anticipation of reward. Future research is needed to identify the precise mechanisms through which adverse early environments ultimately shape reward learning and responses to rewarding stimuli.

Links between emotional processing and psychopathology

An extensive and growing body of work suggests that disruptions in emotional processing, emotional responding, and emotion regulation represent transdiagnostic factors associated with virtually all commonly occurring forms of psychopathology (Aldao, Nolen Hoeksema, & Schweizer, 2010). Specifically, attention biases to threat and overgeneral autobiographical memory biases have been linked to anxiety and depression, respectively, in numerous studies (Bar Haim, Lamy, Bakermans Kranenburgh, Pergamin, & Van Ijzendoorn, 2007; Williams et al., 2007), and attributions of hostility and other social information processing biases associated with trauma exposure are associated with risk for the onset of conduct problems and aggression (Dodge et al., 1990; Dodge et 211., 1995; Weiss et al., 1992).

Heightened emotional responses to negative environmental cues are associated with both internalizing and externalizing psychopathology in laboratory based paradigms examining self reported emotional and physiological responses to emotional stimuli (Boyce et al., 2001; Carthy, Horesh, Apter, Edge. & Gross, 2010: Hankin, Badanes, Abela, & Watamura, 2010′, McLaughlin, Kubzansky. et al., 2010; McLaughlin, Sheridan, Alves, et al., 2014; Rao. Hammen, Ortiz, Chen, & Poland, 2008), MRI studies examining neural response to facial emotion (Sebastian et al., 2012; Siegle, Thompson, Caner, Steinhauer, & Thase, 2007; Stein, Simmons, Feinstein, & Paulus, 2007; Suslow et al., 2010; Thomas et al.. 2001), and experience sampling studies that measure emotional responses in real world situations (Myin Germeys et al., 2003; Silk. Steinberg, & Morris. 2003).

Habitual engagement in rumination has also been linked to heightened risk for anxiety, depression, eating disorders, and problematic substance use (McLaughlin & Nolen Hoeksema, 20l 1: Nolen Hoeksema, 2000; Nolen Hoeksema, Stice, Wade, & Bohon, 2007). Together, evidence from numerous studies examining emotional processing at multiple levels of analysis suggests that disruptions in emotional processing are a key transdiagnostic factor in psychopathology that may explain patterns of multifinality following exposure to threatening early environments.

Executive functioning

Disruption in executive functioning represent the second key proximal risk factor in the model. A growing body of evidence suggests that environmental deprivation is associated with lasting alterations in executive functioning skills. Poor executive functioning, including problems with working memory, inhibitory control, planning ability, and cognitive flexibility, has consistently been documented among children raised in deprived environments ranging from institutional settings to low socioeconomic status [3138) families.

Children raised in institutional settings exhibit a range of deficits in cognitive functions including general intellectual ability (Nelson et al., 2007‘, O’Connor, Rutter, Beckett, Keaveney, & Kreppner, 2000), expressive and receptive language (Albers, Johnson, Hostetter, Iverson, & Miller, 1997; Windsor et al., 201 I), and executive function skills (Bos et al., 2009; Tibu et al., 2016). In contrast to other domains of cognitive ability, however, deficits in executive functioning and marked elevations in the prevalence of attention deficit hyperactivity disorder (ADHD), which is characterized by executive functioning problems, are persistent over time even after placement into a stable family environment (Bos et al., 2009; Tibu et al., 2016; Zeanah et al., 2009).

Similar patterns of executive functioning deficits have also been observed among children raised in low SES families, including problems with working memory, inhibitory control, and cognitive flexibility (Blair, 2002; Farah et al., 2006; Noble et al., 2007; Noble, Norman, & Farah, 2005; Raver, Blair, Willoughby, & The Family life Project Key Investigators, 2013), as well as deficits in language abilities (Fernald, Marchman, & Weisleder, 2013; Weisleder & Femald, 2013). Poor cognitive flexibility among children raised in low SES environments has been observed as early as infancy (Clearfield & Niman, 2012). Relative to children who have been abused, children exposed to neglect are at greater risk for cognitive deficits (Hildyard & Wolfe, 2002) similar to those observed in poverty and institutionalization (Dubowitz et al., 2002; Spratt et al., 2012).

The lateral PFC is recruited during a wide variety of executive functioning tasks, including working memory (Wager & Smith, 2003), inhibition (Aron, Robbins, & Poldrack, 2004), and cognitive flexibility (Rougier, Noelle, Braver, Cohen, & O’Reilly, 2005), and is one of the brain regions most centrally involved in executive functioning. In addition to exhibiting poor performance on executive functioning tasks, children from low SES families also have different patterns of lateral PFC recruitment during these tasks as compared to children from middle class families (Kishiyama, Boyce, Jimenez, Perry, & Knight, 2009; Sheridan, Sarsour, Jutte, D’Esposito, & Boyce, 2012). A similar pattern of poor inhibitory control and altered lateral PFC recruitment during an inhibition task has also been observed in children raised in institutional settings (Mueller et al., 2010).

These studies provide some clues about where to look with regards to the types of environmental inputs that might be necessary for the development of adaptive executive functions. In particular, environmental inputs that are absent or atypical among children raised in institutional settings. as well as among children raised in poverty, are promising candidates. Institutional rearing is associated with an absence of environmental inputs of numerous kinds, including the presence of an attachment figure, variation in daily routines and activities, access to age appropriate enriching cognitive stimulation from books, toys, and interactions with adults, and complex language exposure (Smyke et al., 2007; Zeanah et al., 2003).

Some of these dimensions of environmental experience have also been shown to be deprived among children raised in poverty, including access to cognitively enriching activities, including access to books, toys, and puzzles; learning opportunities outside the home (e.g., museums) and within the context of the parent-child relationship (e.g., parental encouragement of learning colors, words, and numbers, reading to the child); and variation in environmental complexity and stimulation as well as the amount and complexity of language input (Bradley, Convyn, Burchinal, McAdoo, & C01], 200]; Bradley, Corwyn, MCAdoo. & C011, 2001; Dubowitz et al., 2002; Garrett, Ng’andu, & Ferron, 1994; Hart & Risley, 1995; Hoff, 2003; Linver, Brooks Gunn, & Kohen, 2002).

Together, these distinct lines of research suggest that enriching cognitive activities and exposure to complex language might provide the scaffolding that children require to develop executive functions. Some indirect evidence supports this notion. For example, degree of environmental stimulation in the home and amount and quality of maternal language each predict the development of language skills in early childhood (Farah et al., 2008; Hoff, 2003), and children raised in both institutional settings and low SES families exhibit deficits in expressive and receptive language (Albers et al., 1997; Hoff, 2003; Noble et al., 2007; Noble et al., 2005; Windsor et al., 2011), in addition to problems with executive functioning skills. Moreover, a recent study found that atypical patterns of PFC activation during executive function tasks among children from low SES families is explained by degree of complex language exposure in the home (Sheridan et al., 2012). Finally, children raised in bilingual environments appear to have improved performance on executive function tasks (Carlson & Meltzoff, 2008).

These findings suggest that the environmental inputs that are required for language development (i.e., complex language directed at the child) may also be critical for the development of executive function skills. Language provides an opportunity to develop multiple such skills ranging from working memory (e.g., holding in mind the first part of a sentence as you wait for the speaker to finish), inhibitory control (e.g., waiting your turn in a conversation), and cognitive flexibility (e.g,, switching between grammatical and syntactic rules).

Lack of consistent rules, routines, structure, and parental scaffolding behaviors may be another mechanism explaining deficits in executive functioning among children from low SES families. This lack of environmental predictability is more common among low SES than middle class families (Deater Deckard, Chen, Wang, & Bell, 2012; Evans, Gonnella, Mareynyszyn, Gentile, & Salpekar, 2005; Evans & Wachs, 2009). The absence of consistent rules, routines, and contingencies in the environment may interfere with children’s ability to learn abstract rules and to develop the capacity for self regulation. Indeed, higher levels of parental scaffolding, or provision of support to allow the child to solve problems autonomously, has been prospectively linked with the development of better executive function skills in early childhood (Bemier, Carlson. & Whipple, 2010; Hammond, Muller, Carpendale, Bibok, & Lieberrnann Finestone, 2012; Landry, Miller Loncar, Smith, & Swank, 2002).

These findings suggest that environmental unpredictability is an additional mechanism linking low SES environments to poor executive functioning in children. However, given the highly structured and routinized nature of most institutional settings, environmental unpredictability is an unlikely explanation for executive functioning deficits among institutionally reared children.

Deficits in executive functioning skills have sometimes been observed in children with exposure to trauma (DePrince, Weinzierl, & Combs, 2009; Mezzacappa, Kindlon, & Earls, 2001) as well as children with high levels of exposure to stressful life events (Hanson et al., 2012), although some studies have found associations between trauma exposure and working memory but not inhibition or cognitive flexibility (Augusti & Melinder. 2013).

There are two possible explanations for these findings.

First, for children exposed to threat, it may be that deficits in executive functions emerge primarily in emotional contexts, such that the heightened perceptual sensitivity and reactivity to emotional stimuli in children exposed to threat draws attention to emotional stimuli (Shackman et al., 2007), making it more difficult to hold other stimuli in mind, effectively inhibit responses to emotional stimuli, or flexibly allocate attention to nonemotional stimuli. Indeed. in a recent study in my lab, we observed that exposure to trauma (both maltreatment and community violence) was associated with deficits in inhibitory control only in the context of emotional stimuli (i.e., a Stroop task involving emotional faces) and not when stimuli were neutral (i.e., shapes), and had no association with cognitive flexibility (Lambert. King, Monahan, & McLaughlin, 2016). In contrast, deprivation exposure was associated with deficits in inhibition to both neutral and emotional stimuli and poor cognitive flexibility. Although this suggests there may be specificity in the association of trauma exposure with executive functions, greater research is needed to understand these links.

Second, studies examining exposure to trauma seldom measure indicies of deprivation, nor do they adjust for deprivation exposure (just as studies of deprivation rarely assess or control for trauma exposure). Disentangling the specific effects of these two types of experiences on executive functioning processes is a critical goal for future research.

Links between executive functioning and psychopathology

Executive functioning deficits are a central feature of ADHD (Martinussen, Hayden, Hogg Johnson, & Tannock, 2005′, Sergeant, Geurts. & Oosterlaan, 2002; Willcutt, Doyle, Nigg, Faraone, & Pennington, 2005). Problems with executive functions have also been observed in children with externalizing psychopathology, including conduct disorder and oppositional defiant disorder, even after accounting for comorbid ADHD (Hobson, Scott, & Rubia, 2011). They are also associated with elevated risk for the onset of substance use problems and other types of risky behavior (Crews & Boettiger, 2009; Patrick, Blair, & Maggs, 2008), including criminal behavior (Moffitt et al., 2011) and the likelihood of becoming incarcerated (Yechiam et a1., 2008).

Although executive functioning deficits figure less prominently in theoretical models of the etiology of internalizing psychopathology, when these deficits emerge in the context of emotional processing (e.g., poor inhibition of negative emotional information) they are more strongly linked to internalizing problems, including depression (Goeleven, De Raedt, Baert, & Koster, 2006; Joorman & Gotlib, 2010). Executive functioning deficits also contribute to other proximal risk factors, such as rumination (Joorman, 2006), that are well established risk factors for depression and anxiety disorders. Patterns of executive functioning in childhood have lasting implications for health and development beyond effects on psychopathology. Recent work suggests that executive functioning measured in early childhood predicts a wide range of outcomes in adulthood in the domains of health, SES, and criminal behavior. over and above the effects of IQ (Moffrtt et al., 2011).

Mechanisms Linking Distal Risk Factors to Proximal Risk Factors

How do experiences of threat and deprivation come to influence proximal risk factors? Learning mechanisms are the most obvious pathways linking these experiences with changes in emotional processing and executive functioning. although other mechanisms (e. g., the development of stable beliefs and schemes) are also likely to play an important role. Specifically, the impact of threatening and deprived early environments on the development of patterns of emotional processing and emotional responding may be mediated, at least in part, through emotional learning pathways. The associative learning mechanisms and neural circuitry underlying fear learning and reward learning have been well characterized in both animals and humans and reviewed elsewhere (Delgado, Olsson, & Phelps, 2006; Flagel et al., 2011; Johansen, Cain, Ostroff, & LeDoux. 20l l; O’Doherty‘ 2004).

Exposure to threatening or deprived environments early in development results in the presence (i.e., in the case of threats) or absence (i.e., in the case of deprivation) of opportunities for emotional learning: these learning experiences, in turn, have lasting downstream effects on emotional processing. Specifically, early learning histories can influence the salience of environmental stimuli as either potential threats or incentives, shape the magnitude of emotional responses to environmental stimuli, particularly those that represent either threat or reward, and alter motivation to avoid threats or pursue rewards. Thus, fear learning mechanisms and their downstream consequences explain, in part, the association of threatening environments with alterations in emotional processing (McLaughlin et al., 2014; Sheridan & McLaughlin. 2014).

Similarly, the effects of deprived early environments on emotional processing are likely to be partially explained through reward learning pathways. Pathways linking threatening early environments to habitual patterns of responding to distress, such as rumination, may also involve learning mechanisms including both observational (e.g., modeling responses utilized by caregivers) and instrumental (e.g., reinforcement of passive responses to distress when emotional displays are met with dismissive or punishing reactions from caregivers) learning.

Learning mechanisms may also be a central mechanism in the association between deprived early environments and the development of executive functioning. In particular, deprived environments such as institutional rearing. neglect, and poverty are characterized by the absence of learning opportunities, which is thought to directly contribute to later difficulties with complex higher order cognition. Specifically. reduced opportunities for learning due to the absence of complex and varied stimulus response contingencies or the presence of consistent rules, routines, and structures that allow children to learn concrete and abstract rules may influence the development of both cognitive and behavioral aspects of self regulation.

Moderators of the Link Between Distal and Proximal Risk Factors

Children vary markedly in their sensitivity to environmental context. Advances in theoretical conceptualizations of individual differences in sensitivity to context can be leveraged to understand variability in developmental processes among children exposed to adverse environments. A growing body of evidence suggests that certain characteristics make children particularly responsive to environmental influences; such factors confer not only vulnerability in the context of adverse environments but also benefits in the presence of supportive environments (Belsky, Bakermans Kranenburg, & Van Ijzendoom, 2007; Belsky & Pluess, 2009; Boyce & Ellis, 2005; Ellis, Essex, & Boyce, 2005). Highly reactive temperament, vagal tone, and genetic polymorphisms that regulate the dopaminergic and serotonergic system have been identified as markers of plasticity and susceptibility to both negative and positive environmental influences (Belsky & Pluess, 2009). These plasticity markers represent potential moderators of the link between childhood adversity and disruptions in emotional processing and executive functioning.

Developmental timing of exposure to adversity also plays a meaningful role in moderating the impact of childhood adversity on emotional processing and executive functioning For example, in recent work we have shown that early environmental deprivation has a particularly pronounced impact on the development of stress response systems during the first 2 years of life (McLaughlin et al., ZOIS). These findings suggest the possibility of an early sensitive period during which the environment exerts a disproportionate effect on the development of neurobiological systems that regulate responses to stress. As noted in the beginning of this article, additional research is needed to identify developmental periods of heightened plasticity in specific subdomains of emotional processing and executive functioning and to determine the degree to which disruptions in these domains vary as a function of the timing of exposure to childhood adversity.

Moderators of Trajectories From Proximal Risk Factors to Psychopathology

A key component of Nolen Hoeksema and Watkins‘s (2011) transdiagnostic model of psychopathology involves moderators that determine the specific type of psychopathology that someone with a particular proximal risk factor will develop. Specifically, their model argues that ongoing environmental context and neurobiological factors can moderate the impact of proximal risk factors on psychopathology by raising concerns or themes that are acted upon by proximal risk factors and by shaping responses to and altering the reinforcement value of particular types of stimuli.

For example. the nature of ongoing environmental experiences might determine whether someone with an underlying vulnerability (e.g.. neuroticism) develops anxiety or depression. Specifically, a person with high neuroticism who experiences a stressor involving a high degree of threat or danger (e.g., a mugging or a car accident) might develop an anxiety disorder, whereas a person with high neuroticism who experiences a loss (e.g.. an unexpected death of a loved one) might develop major depression (Nolen Hoeksema & Watkins. 2011).

Neurobiological factors that influence the reinforcement value of certain stimuli (e.g., alcohol and other substances. food, social rejection) can also serve as moderators. For example, individual differences in rejection sensitivity might determine whether a child who is bullied develops an anxiety disorder. Although a review of these factors is beyond the scope of the current article, greater understanding of the role of ongoing environmental context as a moderator of the link between proximal risk factors and the emergence of psychopathology has relevance for research on childhood adversity. In particular, environmental factors that buffer against the emergence of psychopathology in children with disruptions in emotional processing and executive functioning can point to potential targets for preventive interventions for children exposed to adversity.

CONCLUSION

Exposure to childhood adversity represents one of the most potent risk factors for the onset of psychopathology. Recognition of the strong and pervasive influence of childhood adversity on risk for psychopathology throughout the life course has generated a burgeoning field of research focused on understanding the links between adverse early experience, developmental processes, and mental health. This article provides recommendations for future research in this area. In particular, future research must develop and utilize a consistent definition of childhood adversity across studies, as it is critical for the field to agree upon what the construct of childhood adversity represents and what types of experiences do and do not qualify.

Progress in identifying developmental mechanisms linking childhood adversity to psychopathology requires integration of studies of typical development with those focused on childhood adversity in order to characterize how experiences of adversity disrupt developmental trajectories in emotion, cognition, social behavior. and the neural circuits that support these processes, as well as greater efforts to distinguish between distinct dimensions of adverse environmental experience that differentially influence these domains of development. Greater understanding of the developmental pathways linking childhood adversity to the onset of psychopathology can inform efforts to identify protective factors that buffer children from the negative consequences of adversity by allowing a shift in focus from downstream outcomes like psychopathology to specific developmental processes that serve as intermediate phenotypes (i.e., mechanisms) linking adversity with psychopathology.

Progress in these domains will generate clinically useful knowledge regarding the mechanisms that explain how childhood adversity is associated with a wide range of psychopathology outcomes (i.e., multifinality) and identify moderators that shape divergent trajectories following adverse childhood experiences. This knowledge can be leveraged to develop and refine empirically informed interventions to prevent the long term consequences of adverse early environments on children’s development. Greater understanding of modifiable developmental processes underlying the associations of diverse forms of childhood adversity with psychopathology will provide critical information regarding the mechanisms that should be specifically targeted by intervention. Determining whether these mechanisms are general or specific is essential, as it is unlikely that a one size fits all approach to intervention will be effective for preventing the onset of psychopathology following all types of childhood adversity. Identifying processes that are disrupted following specific forms of adversity, but not others, will allow interventions to be tailored to address the developmental mechanisms that are most relevant for children exposed to particular types of adversity. Identification of moderators that buffer children either from disruptions in core developmental domains or from developing psychopathology in the presence of developmental disruptions, for example, among children with heightened emotional reactivity or poor executive functioning, will provide additional targets for intervention.

Finally, uncovering sensitive periods when emotional, cognitive, and neurobiological processes are most likely to be influenced by the environment will provide key information about when interventions are most likely to be successful. Together, these advances will help the field to generate innovative new approaches for preventing the onset of psychopathology among children who have experienced adversity.

Meditation can work for everybody – Eric Klein * The Buddha Pill: Can Meditation Change You? – Dr Miguel Farias and Dr Catherine Wikholm.

“When the body can be still, the mind can be still. Spirituality is what you do with those fires that burn within you.” Sister Elaine

Seven Reasons Why Meditation Doesn’t Work, And how to fix them.

by Eric Klein

We didn’t have air conditioning, when we were living in Chicago in the 1970s. So, on hot, humid summer nights, Devi and I would ride our bikes to the shores of Lake Michigan. After securing our bikes, we‘d head for the water.

The water was nice and cool. But, to enjoy it we had to move through the twigs, paper cups, and assorted debris that had accumulated at the water’s edge.

It’s the same with meditation. The deep waters of your inner mind are pure, clear, and refreshing. But, to get there you need to move through some inner. . . um. . . debris.

This debris isn’t life threatening. Just a bit messy. It’s made up of ideas, memories, sensations, misconceptions, and reasons. Reasons why meditation doesn’t work at least for you.

Here are some of the common reasons that people give. You may find some of them familiar, if you’ve gone for a swim in the waters of meditation. Even if you’ve just dipped your toe in.

1) “Meditation is self-centered.”

As meditation has become more mainstream, pictures of people (slim, beautiful people) sitting in lotus postures show up in all kinds of advertising for spas, exotic vacations, skin cream, perfume, and jewelry.

It’s easy to get the impression that meditation is just the latest fashion accessory. Like a big spiritual mirror that you gaze into while putting on organic makeup to cover any imperfections.

But, meditation is the opposite. Meditation is about taking your self much less seriously and much more lightly. And in the process opening more fully and creatively to life.

The practice of meditation reveals that most of what’s scurrying around in the mind isn’t that significant much less real. And that all the ideas about the self are more limiting than liberating. Meditation frees you from being overly preoccupied with protecting and preserving the self.

Through practice, you discover that there really is no hard and fast line between “me” and “life”.

You discover that you are part of life, not apart from life in any way. Thus, the practice of meditation shifts you from self centered to lite centered living. Whether your attention is turned within or without it’s all life.

2) “I don’t have time to meditate.”

The scattered mind never has time for what matters most. It’s busy, busy, busy. Driven by emotion fueled thoughts. The day is filled to overflowing with activities, demands, meetings, and requirements. There’s barely time to sit down for a meal much less to spend a few moments in silence and stillness.

In the mad rush to get more done, the mind becomes more fragmented and speedy.

When things do slow down like in a traffic jam or on a grocery line it’s intolerable. The mind rails against the waste of time and against slowing down. “There’s too much to do!!” it cries.

But, everyone has exactly the same amount of time each day: 1440 minutes.

It’s the experience of time that differs. The more scattered and sped up the mind the more time seems to slip through your fingers like sand. Through meditation, the mind learns to slow down. As it does so, the feeling of pressure lifts. And with it another veil lifts as well.

The veil that concealed the richness of the moment, lifts. Through meditation you touch and are touched by the richness of the present moment. You experience fullness of time which reveals that this moment yes this very moment) is always enough.

3) “My back hurts when I meditate.”

This is likely a technical, postural issue that can be handled with some simple information about how to sit. Here are some practical guidelines.

You can sit on the floor or on a chair.

The key is to keep your spine straight but not still. Allow the chin to be parallel to the ground. When seated on the floor, elevate your body on a firm cushion or folded blanket. This reduces strain on the back. Experiment with different heights of cushion.

If you sit on a chair, make sure it is firm and not too cushiony. You don’t want to sink into it. You want to sit upright.

Once you have assumed a seated posture find your physical center of gravity.

You do this by gently rocking from side to side. As you rock from left to right, feel into the core of your body. You will notice a physical sensation I call passing through the center of gravity as your body shifts from side to side.

Slow down the shifting and feel more deeply into that center of gravity as you pass through. Then reduce the side to side movement and gradually settle your body so that it is aligned along the center of gravity. Do this all by feeling inwardly and sensing that place of balance.

As you settle the body in the center of gravity feel your spine gently lengthening. The back of your skull lifts slightly and the chin is parallel to the ground. The base of the body is grounded.

Your posture is aligned along the center of gravity and the spine is effortlessly extended. Place eyes gaze gently at the root of the nose between the eyebrows

Sitting is a skill that becomes easier with practice.

4) “I’m not religious.”

It’s easy to assume that meditation is religious. When you think about monks, yogis, nuns, and other professionally religious people, concepts like meditation come to mind. And it’s true, that meditation or similar practices have been central to those on a religious quest.

But, does that mean that meditation is religious? Not really. Religions are based on articles of faith, on beliefs.

Meditation requires no beliefs. It’s based on practice and results. In this way, meditation is more like a science experiment than a religious exercise. You don’t need to believe anything in order to conduct an experiment. You just need to follow the protocol. Do the practice. It’s a self validating process. Follow the steps and see the results.

The practitioners who developed the meditation methods used their minds and bodies as laboratories. They conducted experiments in consciousness. They recorded their results. And passed them onto their students for validation testing.

Some of these experiments have stood the test of time. People have conducted these meditation experiments for thousands of years, with reliable results. It’s these tested and validated practices that have been passed from teacher to student for thousands of years.

So, whether you’re religious or not, doesn’t matter in terms of meditation. If you are religious, meditation will enrich your understanding of your faith. If you’re not, you‘ll discover that which is deeper than believing or not believing.

5) “My mind won’t get quiet.”

If you stop the average person on the street and ask them, “Is your mind basically quiet or filled with thoughts?” most will tell you, “Basically quiet.” But, sit them down on a meditation cushion for a few minutes without anything to distract them and bam most people are shocked to discover how noisy it is in there.

It’s not that meditation made their minds noisy. Rather, the practice revealed the noise that was already there. This revelation of the running, ranting mind is a movement forward on the path. Many people drop the practice at this point thinking, “I can’t meditate.” But, they are meditating! The practice is working by revealing the actual state of the conditioned mind. Don’t stop now. The key is to keep practicing. To stay with the process which will lead to the quieting of the mind chatter.

The mind isn’t quieted by willing or by effort. You can’t quiet the mind through will power. That would be like pushing down on a spring. The harder you push the more the spring pushes back. You quiet the mind in the same way that you allow a glass of muddy water to become clear. You just let the particles settle. When you don’t stir up the water the mud settles on its own.

It’s the same in meditation.

Meditation lets the mud, the noisy thoughts settle. The glass of muddy water becomes clear as gravity draws the mud together. The mind becomes clear as you shift from thinking about thoughts to being aware of what is arising. Just by being aware, present, and mindful of the activity of the mind it settles down.

6) “Meditation is . . . boring.”

I remember when my parents would take me, as a child, to watch the sunset. I didn’t get it. I couldn’t see the beauty. To me, the sunset was boring.

Being bored is a symptom of not paying attention. If you pay attention deeply to anything it becomes very, very interesting. Meditation, which is the practice of cultivating deep attention, dissolves boredom. As the mud of the mind settles, as you discover the richness of the present moment even something as simple as a breath becomes the doorway to gratitude, wonder, and joy.

But, on the other hand, meditation is actually quite boring. I mean, you’re sitting there breathing in and breathing out. What could be more boring? In, out, in, out. Or you’re repeating the same mantra over and over. It is kind of boring by design. As the surface mind gets bored, it settles down.

And in that settling, an awareness of all encompassing, and ever present silence emerges. A sense of undisturbed stillness. This stillness and silence infuse everything with aliveness and presence. Not boring at all”

7) “I don’t want to be weird.”

There are two reasons that practicing meditation can feel weird. One is neurological, the other more psychological.

Let’s start neurologically: doing anything unfamiliar can feel weird. Your neurological patterns get used to doing things a certain way. Putting your left leg in your pants before your right ones Brushing one side of your teeth before the other. Sitting in a certain chair and in a certain posture) to watch television. The list goes on.

So, when you change a pattern of behavior even in a positive direction it feels weird. Inside your brain, new neurons are firing.

New connections are being made. And old connections, old patterns, are being restrained. Subjectively it feels weird. The new neurological circuits aren’t totally grooved in yet. so you’re clumsy at the new pattern. And this clumsiness is where the weird feeling can turn more psychological.

Being clumsy can be embarrassing (even if you’re all by yourself). Even if you’re sitting there by yourself with your eyes closed you can still be “watching” what you’re doing and wondering, “Am I doing this right? Is this weird?”

Have you ever danced in front of the mirror? If you judge what your dancing it’s no fun. To enjoy the experience, you need to cut loose from any fixed ideas of what dancing should look like and even more so what you should look like.

It’s the same with meditation. Whether you want to or not, you have an idea about the kind of person who meditates. If you don’t think of yourself as that kind of person then when you meditate, you’ll feel weird. You’ll get in your own way.

But, if you relax, take a breath, and realize that your ideas about meditation are just that ideas. You don’t have to live up to these self imposed ideas of meditation. You can just cut loose and enjoy the process. When you do, you find a whole new and wonderful kind of weirdness.

But, one of the blessings of meditation is finding out that you indeed are weird. You’re weird in the best possible sense of the word. Because, the most ancient meaning of the word weird has to do with following your unique fate, your path through life. You’re weird if you follow your path and listen to the direction of your inner soul.

So, meditation, in this most basic, ancient sense, helps you be weird. Meditation helps you find your path. Through practice, you discover how to live your true life more fully and more joyfully.

Those are the seven reasons.

Along with ideas on how to move through them.

Because, there’s no reason to let a bit of debris stop you from enjoying a refreshing swim in the deep, clear, refreshing waters of your inner mind.

Ready for the next: step?

Our recommendation is for you to subscribe to the Wisdom Heart newsletter. You’ll receive information and inspiration on how to bring meditation alive in your life. Practical ideas that you can use for peace of mind and the clarity to live with greater fulfillment and purpose.

Go to http://www.wisdomheart.org/subscribe

The Buddha Pill: Can Meditation Change You?

Dr Miguel Farias and Dr Catherine Wikholm

INTRODUCTION

My interest in meditation began at the age of six when my parents did a course on Transcendental Meditation. I didn’t realize it then, but I was effectively being introduced to the idea that meditation can produce all manner of changes in who we are and in what we can achieve. Mind-over-matter stories are both inspiring and bewildering, hard to believe yet compelling. They have stirred me deeply enough to dedicate almost two decades of my life researching what attracts some people to techniques like meditation and yoga and whether, like many claim, they can transform us in a fundamental way.

This book tells the story of the human ambition for personal change, with a primary focus on the techniques of meditation and yoga. Hundreds of millions of people around the world meditate daily. Mindfulness courses, directly inspired by Buddhist meditation, are offered in schools and universities, and mindfulness-based therapies are now available as psychological treatments in the UK’s National Health Service.

Many scientists and teachers claim that this spiritual practice is one of the most efficient and economic tools of personal change. Yoga is no less popular. According to a recent survey by the Yoga Health Foundation, more than 250 million people worldwide practise it regularly. Through yoga we learn to notice thoughts, feelings and sensations while working with physical postures. Often, yoga practice includes a period of lying or sitting meditation.

Psychologists have developed an arsenal of theories and techniques to understand and motivate personal change. But it wasn’t psychology that produced the greatest surge of interest of the twentieth century in this topic, it was meditation. By the 1970s millions of people worldwide were signing up to learn a technique that promised quick and dramatic personal change. Transcendental Meditation was introduced to the West by Maharishi Mahesh Yogi, and quickly spread after the Beatles declared themselves to be followers of this Indian guru. To gain respectability Maharishi sponsored dozens of scientific studies about the effects of Transcendental Meditation, in academic fields ranging from psychophysiology to sociology, showing that its regular practice changed personality traits, improved mood and wellbeing and, not least, reduced criminality rates.

The publicity images for Transcendental Meditation included young people levitating in a cross-legged position and displaying blissful smiles. I recall, as a child, staring at the photographs of the levitating meditators used in the advertising brochures and thinking ‘Can they really do that?’ My parents’ enthusiasm for meditation, though, was short-lived. When I recently asked my mum about it, she just said, ‘It was a seventies thing; most of our friends were trying it out.’

Like my parents’ interest research on meditation waned rapidly. Photos of levitating people didn’t help to persuade the scientific community that this was something worth studying. We had to wait almost thirty years before a new generation of researchers reignited interest in the field, conducting the first neuroimaging studies of Tibetan monks meditating, and the first explorations of the use of mindfulness in the treatment of depression. For yoga, too, there is increasing evidence that its practice can reduce depression?

Meditation and yoga are no longer taboo words in psychology, psychiatry and neuroscience departments. There now are dedicated conferences and journals on the topic and thousands of researchers worldwide using the most advanced scientific tools to study these techniques. Many of the studies are funded by national science agencies; just looking at the US federally funded projects, from 1998 to 2009, the number increased from seven to more than 1205. The idea of personal change is increasingly central to these studies. Recent articles show improvements in cognitive and affective skills after six to eight weeks of mindfulness, including an increase in empathy?

These are exciting findings. Meditation practices seem to have an impact on our thoughts, emotions and behaviours. Yet, these studies report only modest changes. But many who use and teach these techniques make astonishing claims about their powers. At the Patanjali Research Foundation in northern India, the world’s largest yoga research centre, I hear miraculous claims about yoga from the mouth of its director-guru, Swami Ramdev: ‘Yoga can heal anything, whether it’s physical or mental illness.’

Teasing fact from fiction is a major aim of this book.

The first part explores ideas about the effects of meditation and yoga, contrasting them with the current scientific evidence of personal change. The second part puts the theories to the test, we carry out new research and scrutinize both the upsides and downsides of these practices. We have dedicated a full chapter to the darker aspects of meditation, which teachers and researchers seldom or never mention.

Although this isn’t a self-help book, it attempts to answer crucial questions for anyone interested in contemplative techniques: can these practices help me to change? If yes, how much and how do they work? And, if they do change me, is it always for the better?

These questions have shaped a significant part of my own life. In my teenage years I believed that to seek personal growth and transformation was the central goal of human existence; this led me to study psychology. I wanted to learn how to promote change through psychological therapy, although it was only later, while undergoing therapy training, that I considered the subtlety and difficulties of this process. My undergraduate psychology degree turned out to not shed much light on our potential for transformation; it rarely touched on ideas about how to make us more whole, healed, enlightened, or just a better person.

But rather than giving up, I read more about the areas of psychology I wasn’t being taught like consciousness studies and started doing research on the effects of spiritual practices. When I decided it was probably a good idea to do a doctorate, I browsed through hundreds of psychology websites in search of potential supervisors; I found one at Oxford whom I thought was open minded enough to mentor my interests, and I moved to the city in 2000.

This is the pre-history of my motivation to write this book. Its history begins in the early summer of 2009, when Shirley du Boulay, a writer and former journalist with the BBC, invited a number of people to take part in the re-creation of a ceremony that blended Christian and Indian spirituality. Images, readings and songs from both traditions were woven together, following the instructions of Henry le Soux, a French Benedictine monk who went to live in India and founded a number of Christian ashrams that adopted the simplicity of Indian spirituality (think of vegetarian food and a thin orange habit)?

I met Catherine Wikholm, the co-author of this book, at this event. She had studied philosophy and theology at Oxford University before embarking on her psychology training, and was at the time doing research relating to young offenders. Catherine and I were both drawn to an elegant woman in her fifties called Sandy Chubb, who spoke in a gentle but authoritative manner. Sandy showed us a book she had recently published with cartoonish illustrations of yoga postures. I thought it was intended for children and asked her if kids enjoyed yoga. Sandy smiled and told us the book was meant for illiterate prisoners. That was the mission of the Prison Phoenix Trust, a small charity she directed: to teach yoga and meditation in prisons. Trying to escape my feeling of embarrassment, I praised the idea of bringing contemplative techniques to prisoners. ‘It must help them to cope with the lack of freedom,’ I suggested. Sandy frowned slightly.

‘That’s not the main purpose,’ she said. Although going to prison is a punishment, Sandy told us, with the help of meditation and yoga, being locked in a small cell can help prisoners realize their true life mission.

‘Which is?’ Catherine and I both asked at the same time. ‘To be saintly, enlightened beings,’ Sandy answered.

Catherine and I kept silent. We were mildly sceptical. But also intrigued. Sandy seemed to claim that meditation and yoga techniques could radically transform criminals. I went back to my office that same evening to search for studies of meditation and yoga in prisons and found only a handful. The results weren’t dramatic but pointed in the right direction, prisoners reported less aggression and higher self-esteem? Reading closely, I noticed there were serious methodological flaws: most had small sample sizes and none included a control group a standard research practice that ensures results are not owing to chance or some variable the researcher forgot to take into account.

I wanted to know more. If Sandy’s claims were true, if meditation and yoga could transform prisoners, this could have tremendous implications for how psychologists understand and promote personal change in all individuals, not just those who are incarcerated. Having no experience of prisons, I contacted Catherine to ask if she’d be interested in working with me on this topic.

‘l’d love to!’ she said, more enthusiastic than I imagine most would be at the prospect of interviewing numerous convicted criminals and in the process spending weeks behind bars. Having started working for the prison service in her early twenties, Catherine had a strong forensic interest, particularly in the treatment of young offenders. She was passionate about the rehabilitation of prisoners in general and was curious as to whether yoga and meditation might represent an alternative means of facilitating positive, meaningful change for those who were unable or unwilling to engage with traditional rehabilitative efforts, such as offending behaviour programs.

So Catherine and l arranged to meet with Sandy at the Prison Phoenix Trust. Walking through Oxford’s trendy Summertown, where the Trust is based, we wondered what the meeting would bring. On arriving at the offices, we received a warm welcome. Sandy gave us the guided tour of their floor of the building, which comprised four rooms: the office, where she and her colleagues had their desks; a dining room for communal meals; a meditation room with cushions on the floor; and, along a corridor, a room that was wall-to-wall lined with metal filing cabinets. These, Sandy explained, were full of the letters the Prison Phoenix Trust had received from prisoners, estimated at numbering more than ten thousand.

If we were intrigued before, we were now completely hooked. Our minds filled with questions, we sat down with Sandy as she began to reveal the unusual story of how a small charity had persuaded prison governors to let them teach meditation and yoga to a broad range of prisoners, including thieves, murderers and rapists.

This story made quite an impression on us. So much so, in fact, that it inspired us to dedicate much of the following two years to designing and implementing a study of the measurable effects of yoga and meditation on prisoners. The findings of our research (which we’ll reveal later on in the book) not only sparked a flurry of media interest, but inspired us to spend the two years after that writing this book.

Our initial focus on the potential of meditative techniques to transform the ‘worst of the worst’ broadened out, as we became increasingly interested in exploring its full potential. Might Eastern contemplative techniques have the power to change all of us? As we engaged with more and more research literature, the inspiring stories of change we uncovered compounded our broadened view of the potential of yoga and meditation. Our own personal experiences, such as those of my ongoing research and Catherine’s clinical psychology doctoral training and subsequent acquaintance with mindfulness-based therapies and their application within the NHS in turn increased our curiosity.

What began as a perhaps unlikely marriage of my interest in spirituality and Catherine’s in forensic and clinical psychology has evolved into a wider exploration of the science and delusions of personal change. Just as we worked on our research together, so we have written this book together. To reflect the dynamic process of our writing, with the combining of our ideas and to avoid any messy jumping back and forth between us as narrators we have chosen to write this book in first-person narrative, as a singular, joint ‘I’. Although inevitably it may sometimes be apparent which one of us is narrating at a particular point, if simply by virtue of our gender difference, we have sought to write as a shared voice. The personal stories, interviews and accounts depicted in this book are all drawn from our real experiences. However, when discussing any examples relating to therapeutic work, we have anonymized all names and identifying details.

Over the course of the book, we will examine the scientific evidence that actually exists for the claims of change that meditation, mindfulness and yoga practitioners, teachers and enthusiasts propagate.

We also bring together our own experiences as psychologists, one more research-oriented and one more practice oriented, as well as the stories of some of the thought-provoking characters we’ve encountered along our journey. All that is to come. But for now let us begin by letting you in on the unique story that started it all.

The Prison Phoenix Trust

CHAPTER 1

AN ASHRAM IN A CELL

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‘If we forget that in every criminal there is a potential saint, we are dishonouring all of the great spiritual traditions. Saul of Tarsus persecuted and killed Christians before becoming Saint Paul, author of much of the New Testament. Valmiki, the revealer of the Ramayana, was a highwayman, a robber, and a murderer. Milarepa, one of the greatest Tibetan Buddhist gurus, killed 37 people before he became a Saint. We must remember that even the worst of us can change.’ Bo Lozoff (American prison reform activist and founder of the Prison Ashram Project and the Human Kindness Foundation)

Knocking on the door of a house in a quiet street in Oxfordshire, notepad and pen in hand, I stood and waited on the front step. A minute later the door opened. A smartly dressed, elderly lady smiled at me from inside.

‘Tigger?’ I asked. ‘Yes, do come in,’ she replied.

Still full of life at ninety years old, Tigger Ramsey-Brown was a pleasure to interview. I was there to find out from her more about the story of her late younger sister, who had founded the Prison Phoenix Trust. Over cups of tea in her sunny conservatory, Tigger began vividly to recount the story of her sister and how she had started the Trust around thirty years previously.

In the beginning

Tigger pointed out that if we were going to go right to the start, this story actually begins somewhat earlier, with the marine biologist and committed Darwinist Sir Alister Hardy. At one time a Professor of Zoology at Oxford University, Hardy had happened to teach Richard Dawkins, an evolutionary biologist and outspoken atheist. Knighted for his work in biology, Hardy had a strong interest in the evolution of humankind, developing novel theories such as the aquatic ape hypothesis (which proposes that humans went through an aquatic or semi-aquatic stage in our evolution).

But he was also particularly interested in the evolution of religion and religious experience. Hardy viewed humans as spiritual animals, theorizing that spirituality was a natural part of our human consciousness. He mooted that our awareness of something ‘other’ or ‘beyond’ had arisen through exploration of our environment and he wanted to explore this further.

However, aware that fellow scientists and academics were likely to consider his interest in researching spirituality unorthodox, he waited until he retired from Oxford University before he delved deeper and founded the then-called Religious Experience Research Unit (RERU) at Manchester College, Oxford. (It is now the Alister Hardy Religious Experience Research Centre and is based in Wales.)

The goal of Hardy’s research was to discover if people today still had the same kind of mystical experiences they seemed to have had in the past. He began his study by placing adverts in newspapers, asking people to write in with their mystical experiences, in response to what became known as ‘The Hardy Question’: ‘Have you ever been aware of or influenced by a presence or power, whether you call it God or not, which is different from your everyday self?’

‘Thousands of people replied to the adverts, writing about their dreams and spiritual experiences. These responses were compiled into a database to enable researchers to analyze the different natures and functions of people’s religious and spiritual experiences. This is where Ann came in,’ Tigger told me. And so it was that in the mid-1980s in Oxfordshire, a woman named Ann Wetherall spent her days collecting and categorizing people’s dreams, visions and other spiritual experiences.

Looking for a link

Over time, as she examined the letters, Ann began to wonder if there was a common denominator in the accounts.

She noticed that it didn’t seem to matter whether someone was religious or atheist, but, more often than not, it was people who were feeling hopeless or helpless who reported a direct experience of spirituality.

Ann hypothesized that imprisonment might be a context that particularly inspired such despondent feelings and that it therefore might also trigger spiritual experiences. She got in touch with convicted murderer turned sculptor Jimmy Boyle, one of Scotland’s most famous reformed criminals. Boyle helped her to get an advert published in prison newspapers, asking for prisoners to write in about their religious or spiritual episodes. She got quite a response prisoners in their dozens wrote in to her describing their unusual experiences. Many of them had never mentioned these to anyone before and had wondered if they were going mad.

‘Ann wanted to write back and reassure them that they weren’t, and that these were valid spiritual experiences, which could be built on but the Alister Hardy Foundation did not reply to letters,’ Tigger explained. ‘That’s why Ann broke away from the research, so that she could start corresponding with the prisoners who were writing in, and offer support.

Because of their confinement in cells and separation from the outside world, Ann thought that prisoners’ experience was perhaps rather similar to that of monks. While for prisoners this withdrawal from society was not voluntary, she believed that they too could use their cell as a space for spiritual growth.’

‘What was her interpretation of spiritual growth?’ I asked.

‘Not only becoming more in touch with a greater power, but also becoming more aware of inner feelings and thoughts, as well as more connected and sensitive to other people’s needs,’ Tigger explained.

‘And the means of bringing about this kind of change?’ I asked, already pre-empting the answer…

‘Through meditation, of course.’

From spiritual experience to spiritual development

Tigger explained that she and Ann had spent their childhoods in India, growing up among Buddhist monasteries. Because of this upbringing, Ann had had a lifelong involvement with meditation, and believed that prisoners could benefit from learning it. In her letters back and forth to prisoners, she began sharing with them what she knew about meditation, in order to encourage and support their spiritual development.

Over the next couple of years, Ann’s correspondence with convicts came to strengthen her belief that prisoners had real potential for Spiritual development. ‘She thought they had a terrific spirituality, a hunger that wasn’t being met,’ Tigger explained, as our conversation moved onto Ann’s decision to set up a charitable trust, the Prison Ashram Project (now the Prison Phoenix Trust).

Founded in 1988, the organization was at first very small, comprising just Ann and three other volunteers, who wrote to prisoners, encouraging them to use their spiritual experiences as a springboard for future spiritual development.

‘You are more than you think you are’ was the project’s frequent message.

As the name suggests the Prison Ashram Project had the central premise that a prison cell can be used as an ashram, a Hindi word that refers to a spiritual hermitage, a place to develop deeper spiritual understanding through quiet contemplation or ascetic devotion.

Hermitage is not only an Eastern practice in Western Christian tradition, a monastery is a place of hermitage, too, because it is partially removed from the world. Furthermore, the word ‘cell’ is used in monasteries as well as in prisons, and there are a surprising number of similarities between the living conditions of monks and prisoners. Both live ascetic lives filled with restriction and limitation. Both monks and prisoners are able to meet their basic needs (but little more), both desist from sensual pleasures and the accumulation of wealth, and both follow a strict daily schedule.

Despite these parallels, however, there is undeniably a big difference in how monks and prisoners come to live in their respective cells. For monks living communally in monasteries, as well as hermits who live alone, living ascetically is an intentional choice, aimed at enabling them to better focus on spiritual goals. But for prisoners withdrawing from the world is not their choice; rather, it is imposed upon them as punishment. Which leads to the question: can involuntary confinement really open a door to inner freedom and personal change? Ann Wetherall believed so.

Being confined to a cell for much of the day, even against free will, could be a catalyst for spiritual development. The conditions were conducive; all that anyone needed was a radical shift in thinking. Rather than punishment, incarceration could be reconceived of as an opportunity for positive transformative experience. Prisoners had lost their physical liberty, but they could nevertheless gain spiritual freedom. Ann thought that meditation was the ideal tool with which prisoners could build spiritual growth, requiring only body, mind and breath.

So far, so good. But as Tigger talked something seemed to me to be a distinct obstacle to peaceful meditation behind bars: the undeniable fact that prisons are busy, noisy places. Granted, there might be some similarities between prisons, monasteries and spiritual retreats, I thought, but surely finding peace and quiet in a prison would be a bit of a mission impossible. Wouldn’t that render any attempt to meditate a bit futile?

‘No.’ Tigger smiled. ‘Ann believed this actually increased the importance and worth of meditation practice; the practice would enable prisoners to find a sense of peace despite their surroundings.’

Crossing continents

As it turned out Ann was not the first to think of encouraging prisoners’ spiritual development through in-cell meditation. A couple of years after setting up the Prison Ashram Project, she heard about Bo Lozoff, a spiritual leader and prison reform activist doing similar work in the USA.

Curiously, his organization was also called the Prison Ashram Project. Bo first had the idea that a prison cell could be a kind of ashram when his brother-in-law was sentenced to prison for drug smuggling. At the time Bo and his wife Sita were living at an ashram in North Carolina. There, their daily routine involved waking early, wearing all white, working all day without getting paid, abstaining from sex and eating communally. Visiting his brother-in-law in prison, Bo realized there were remarkable parallels between their day-to-day lives.

Around the same time he came across a book by renowned spiritual teacher Ram Dass, entitled Be Here Now. The combination of these two events inspired Bo and Sita to set up their own Prison Ashram Project in 1973, in cooperation with Ram Dass.

Just like Ann, they had begun corresponding with prisoners, offering encouragement and instruction in meditation and also in yoga. They also sent prisoners copies of Ram Dass’s book, along with the book that Bo himself went on to write: We’re All Doing Time A Guide for Getting Free. The central concept of this book is that it’s not only prisoners who are imprisoned, but that we are all ‘doing time’ because we allow ourselves to be so restricted by hang-ups, blocks and tensions. The message is that through meditation and yoga we can all learn to become free.

The birth of the Prison Phoenix Trust

Not long after meeting Bo, Ann changed her charity’s name to the Prison Phoenix Trust (PPT), in part because she was concerned that the word ‘ashram’ might prove an obstacle for the prison service. She was keen to step things up a notch from written correspondence and start setting up meditation and yoga workshops in prisons themselves. However, even with the new name, prison governors and officers were wary of the charity’s efforts. The Trust tried to get into prisons through the Chaplaincy; however, here too there was a surprising amount of resistance.

It’s worth remembering that in the late 1980s, prison chaplains were almost all Anglican. At that time the Anglican Church was still suspicious of practices such as meditation, which when compared with contemplation or silent prayer seemed ‘unChristian’. Many ministers thought that meditation centred on a spirituality that might be Hindu, Buddhist or even evil (stemming from the notion that to silence the mind also means making it available for the devil).

A 2011 article in the Daily Telegraph highlighted an extreme example of Christian opposition to yoga and meditation, reporting how a Catholic priest named Father Gabriele Amroth, appointed the Vatican’s chief exorcist in 1986, had publicly denounced yoga at a film festival where he had been invited to introduce The Rite (a film about exorcism, starring Anthony Hopkins): ‘Practising yoga is Satanic, it leads to evil just like reading Harry Potter,’ the priest is reported as stating, to an audience of bemused film fans?

Of course, not all devout Christians share such concerns that Christianity and Eastern spiritual practices are incompatible. Offering me another biscuit Tigger revealed the next chapter of her sister’s tale, wherein Ann would join forces with ‘a very forceful and very amazing character’.

A CATHOLIC ZEN MASTER

‘Spirituality is what you do with those fires that burn within you.’ Sister Elaine

Thousands of miles away from Oxford and Ann’s fledgling charity lived a Catholic nun. As well as being a nun, Sister Elaine was a Zen master. She grew up in Canada, where in her youth she became a professional classical musician for the Calgary Symphony Orchestra. At the age of thirty, however, she realized her true calling and joined the convent of Our Lady’s Missionaries in Toronto. In 1961, after several years at the convent, she was sent to Japan for her first assignment as a Catholic missionary. Her mission was to set up a Conservatory and Cultural Centre in Osaka, where she would teach English and music to Japanese people, as well as to baptise as many of them as possible.

In order to get to know the Japanese people better, she began to practise Zen Buddhism. She started zazen (sitting meditation) and koan study, under the guidance of Yamada Koun Roshi, a well-known Zen master from the Japanese Sanbo Kyodan order. Perhaps surprisingly, it did not matter to him that Sister Elaine was a Catholic nun with no intention of becoming a Buddhist. Yamada Koun Roshi did not draw a division between different people or religions, and similarly neither does Sister Elaine, who maintains, ‘There is no separation. We make separation?

Devoted to her new discipline, Sister Elaine went on to spend some time living with Buddhist nuns in Kyoto, where the daily regime involved ten hours a day of sitting in silence.

To call the koan study lengthy would be an understatement; it took her nearly two decades of studying with her Zen teacher before she was made a roshi. This title, which translates literally as ‘old teacher’, marks the top echelon of Zen teachers. There are an estimated only 100 roshis worldwide. Very few of them are Westerners, but in 1980 Sister Elaine finally became one of them, an accredited Zen teacher of the Sanbo Kyodan order. Her achievement made her the first Canadian, and certainly the first Catholic nun, to be recognized as one of the world’s highest-ranking teachers of Zen.

In 1976, after 15 years in Japan, Our Lady’s Missionaries back in Toronto transferred Sister Elaine to the Philippines. This was during the worst years of the Marcos regime, and Sister Elaine was to be involved with animal husbandry. However, she did more than merely raise livestock. Once in the Philippines she set up a zendo (Zen meditation centre), for the Catholic Church in Manila. Word spread about her work and a leading dissident, Horacio ‘Boy’ Morales, who had headed the New People’s Army against the Marcos dictatorship, came to hear of her. Held as a political prisoner at the Bago Bantay detention centre, Morales asked Sister Elaine to come to prison to teach meditation to him and a group of fellow prisoners, each of whom had, like him, been tortured. His hope was that the practice could help them to cope with the stress of imprisonment and find inner peace.

Despite the hostility of the authorities and worrying reports of other prison visitors ‘vanishing’, Sister Elaine spent four-and-a-half years teaching meditation to those prisoners every week. During that time she witnessed a remarkable change: the prisoners transformed from being angry, tense men, trembling from torture, to being calm. This convinced her both of the therapeutic power of silent meditation and of the potential for prisoners to develop spiritually while incarcerated.

Sister Elaine’s life makes for quite an unusual story, and her work in the Philippines caught the attention of the media and subsequently of Ann Wetherall. Leaning forward in her seat, Ann’s sister, Tigger, told me of the unexpected events that would subsequently unfold.

Ann’s legacy

In 1992, four years after founding the Prison Phoenix Trust, Ann discovered she had terminal cancer. Coming to terms with this news, Ann felt fearful for the prisoners she was involved with; what would happen to her charity after she was gone? She had heard of Sister Elaine and wrote to her, asking if she would consider taking over as director after she died. Sister Elaine flew over from the Philippines to spend a week with Arm to try to come to a decision. Shortly after returning home, she phoned Ann to accept her offer, telling her ‘don’t die until I get there’.

Sadly, Ann passed away while Sister Elaine was on her way back to England. Over the six years Sister Elaine was director, the idea that yoga and meditation are beneficial for prisoners became increasingly accepted among prison governors and officers. They might not have been as interested in the potential spiritual development of prisoners, but many acknowledged the range of other, more down-to-earth benefits: prisoners doing yoga and meditation were reportedly calmer, slept better and felt less stressed and so were easier to work with.

While, like Ann, Sister Elaine believed that meditation was the key to stilling the mind, incorporating yoga into the classes was important: when the body can be still, the mind can be still.

Aged 75, Sister Elaine left the Trust not to retire, but to return to her native Canada to found a similar organization called Freeing the Human Spirit, based in Toronto.

In the years since Sister Elaine’s departure, the Prison Phoenix Trust (PPT) has continued to develop its work, with classes now running in the majority of UK prisons. Reflecting on the Trust’s progress, Sandy Chubb, the PPT’s subsequent director, remarked to me with a smile, ‘Yes, gone are the days when yoga teachers were branded yoghurt pots.’

Hearing the stories about Ann and Sister Elaine, so vividly recounted to me by Tigger and others, including the Trust’s current director Sam Settle, it made sense to me that yoga and meditation could lead to personal change in prisoners. Certainly the PPT had a whole lot of anecdotal evidence attesting to its benefits. Over the course of 25 years, PPT letter-writers have received more than 10,000 replies from prisoners reporting the positive effects of these techniques. The benefits range from increased self-esteem, better sleep and reduced dependence on drugs, medication or cigarettes, to improved emotional management and reduced stress.

Anecdote or evidence

I was invited to come and have a look through the filing cabinets that contained these letters, the amount of correspondence astounded me. Yet despite all those positive responses, as a psychologist I couldn’t help but be a little sceptical, testimonials are all very well, but what was the empirical evidence that yoga and meditation can help incarcerated criminals change for the better? Searching scientific databases I discovered there was very little rigorous research out there into the measurable psychological effects of these practices on prison populations.

The majority of studies that did exist focused specifically on meditation with some interesting results. Research into the effects of Transcendental Meditation on criminals had been taking place since the 1970s. For example, a study by US researchers Abrams and Siegel found that those prisoners who received a 14-week course of TM training showed a significant reduction in anxiety, neuroticism, hostility and insomnia compared with the control group. This would seemingly constitute early evidence for the rehabilitative effects of TM. However, the study was criticized on the grounds that it had inadequate controls, limiting the conclusions we can draw from the findings and calling into question the authors’ somewhat liberal interpretation of their statistical results.

More recent studies using other meditation techniques also yielded some promising evidence. In these studies, researchers concluded that meditation led to such positive results as improved psychosocial functioning”, a reduction in substance abuse, and decreased recidivism rates?

However, while all that sounds really promising, most of this research also had serious shortcomings. For example, sample sizes were usually very small, there was not a control group, or the research drew evidence only from questionnaire measures.

I realized that if we were to draw any realistic conclusions about whether or not yoga and meditation are effective in bringing about measureable psychological changes in incarcerated criminals, we needed better research evidence. And so the seeds were sown for our Oxford Study, the journey and findings of which we reveal in Chapter 8. While this was in the planning, I wanted to gain a deeper understanding about the PPT’s rationale for encouraging prisoners to practise yoga and meditation, and their conceptualizations of personal change.

PERFECT PRISONERS

While the PPT does believe that yoga and meditation can lead to beneficial psychological effects in prisoners, what they’re really interested in is the possibility of a radical ‘self-change’. This involves a significant shift in perspective. Sandy Chubb told me that in her experience (of teaching yoga in prisons), prisoners are lovely to work with. This didn’t surprise me all that much we all tend to be co-operative when we’re getting to do something we want to do.

What did surprise me was the comment that followed: Sandy told me that ‘prisoners are all perfect’.

Perfect is certainly not the adjective most of us would choose to describe murderers, rapists and paedophiles; for many it’s perhaps even the antonym of the word they would use. I needed Sandy to clarify. ‘What’s perfect about them?’ I asked.

The answer appears to lie in Sandy’s spiritual worldview. Like many others who believe in a universal spirituality, Sandy recognizes the divine nature of each of us including criminals and is convinced of the interconnectedness of all things. She smiles serenely when she tells me what to her is a simple, obvious truth: ‘We are a whole creation that works dynamically.’

The concept of unity or non-duality is a central premise in some Eastern spiritual belief systems, and one that effectively eliminates the ‘us’ and ‘them’ mentality that most of us have in relation to convicted criminals. Early into my interview with Sam Settle, the current director of the PPT and a former Buddhist monk, I encountered the same belief: ‘lf prisoners realized that we are all connected,’ Sam told me, ‘then they would not commit crimes.’

So while reducing re-offending is not an asserted aim of the PPT, it is considered likely to occur as a side-effect of spiritual growth. The hypothesis is that it is criminals’ mistaken idea of separateness that allows them to act in a harmful way towards others. From Sandy and Sam’s perspective, there is no ‘other’, and there are no ‘bad’ people; we are all part of the same perfect whole and meditation and yoga can help people to realize this.

Later in the book I will discuss how many people share this perspective, people who believe that not just individual but worldwide change is possible, if only there are enough people meditating.

SILENT REHABILITATION

While we could dismiss some of these ideas about the transformative potential of meditation and yoga for prisoners as utopian, Romantic, or LaLa-Land spirituality, we can also consider them in a purely secular sense, in terms of psychological and behavioural changes.

But, even if we cast aside, for now, the spiritual dimension, the notion that yoga and meditation can produce meaningful change in prisoners might still be considered somewhat ‘out there’. The very idea of the possibility of personal change is itself a loaded topic, especially in the context of prisons. Young repeat offenders are often labelled hopeless cases, written off by the time they have barely left their teens, undermining the ethos of rehabilitation that should be central to the prison system. However, for many offenders there are myriad factors that may obstruct attempts to rehabilitate not only in terms of overcoming backgrounds of adversity, but also in terms of their perceived (lack of) prospects for the future.

The institution of home

For many who have lived in prisons from an early age, the prospect of going outside is daunting.

I once worked with a prisoner, ‘John’, who was serving his tenth prison sentence at the age of only 21 years old. He attended every session of the offending behaviour program I was facilitating, only to in the final session suddenly become aggressive and disruptive to the point where he had to be removed from the group. Talking to him afterwards, trying to understand why he had sabotaged something that could have helped him towards securing an earlier release date, he admitted he was scared of being released. ‘There is nothing for me outside,’ he said, visibly upset.

When John was a young child, one of his parents murdered the other; he went on to spend the rest of his childhood in numerous short-term foster care placements. Angry and distrusting of people, he would repeatedly run away from them. He committed his first offence aged ten and received his first custodial sentence aged 15. The frequency of his impulsive crimes meant that he had spent the majority of the past six years behind bars. There were no family or friends waiting for him on the outside. The uncertainty of how to build a meaningful life, alone, in the ‘real world’ was overwhelming. Prison was all he felt he knew.

Self-belief

All staff members working in prisons from officers, to psychologists, to governors are acutely aware that changing prisoners can be extraordinarily difficult but it’s not impossible. In my own work with young male offenders, I lost count of the number of times I heard ‘he’ll never change’ from prison officers, who generally would have little idea of that individual’s backstory and the factors that contributed to his offending behaviour. Often the prisoners in question were boys still in their teens, some of them coming from such difficult backgrounds that it would have been a miracle if they hadn’t ended up in prison.

The desire to reform is often unsupported, sometimes owing to budget restrictions, but other times owing to a lack of belief. Changing is hard. And it’s even harder without a helping hand.

The support of others, whether friend, therapist or institution can be fundamental in whether or not we succeed in bringing about a desired change. Feeling that others believe in us can significantly boost our sense of self-efficacy. Feeling that others don’t believe in us at all undermines our self-belief so that we may start to feel a dramatic waning of our own confidence and motivation to try to change.

Changing attitudes

It was a Thursday afternoon and I was on my lunch break, in between research interviews at a West Midlands prison. I was accompanied by an officer in his late fifties, who had been assigned to facilitate the interviews; escorting prisoners from the wings to the interview room. As our break drew to a close, the officer suddenly deviated from his impromptu monologue on the joys of pigeon fancying, my knowledge of which had substantially increased over the hour, to ask whether I really thought that yoga and meditation would do anything at all for prisoners.

‘Well,’ I replied, ‘we think it might. There’s evidence that it works outside of prisons to reduce stress and increase positive emotions. So it may help prisoners to manage their emotions better and improve their self control, which might also reduce their aggression.’

‘Ha!’ said the officer. ‘I doubt it.’

‘Why?’ I asked.

‘I don’t think any of these can change,’ he told me. ‘I’m a firm believer that leopards never change their spots.’

It wasn’t just yoga and meditation the officer was dismissing as futile. He went on to say that he thought nothing could be done to change prisoners for the better; each and every one of them was a hopeless cause. ‘No matter what,’ he told me, ‘they will always revert back to what they are. It’s like a man who used to be a philanderer; he could get married to a woman and be faithful for, let’s say, ten years, but in the end, he’ll always cheat again.’

My attempts to debate failed miserably. When I maintained that I did think we could rehabilitate prisoners, he delivered his closing argument: ‘Well I’m older than you and I’ve met quite a lot of different people, so I think I know.’

Fortunately, this old-style officer is not representative of the majority of prison staff I have encountered. Over the last twenty years, a number of accredited offending behaviour programs (psychological group interventions that aim to reduce re-offending) have been developed that have been shown to be effective in bringing about improvements in prisoner behaviour, such as reducing aggression?

Despite this positive progress, with the reduction-rate for recidivism being generally around 10 per cent for program-completers, there is still clearly room for new and additional approaches particularly as many prisoners are reluctant or unable to engage with psychological treatment at all.

Arriving at a recent meeting at HMP Shrewsbury, l was escorted by a female officer who gave me a quick overview of the prison. She told me that the population was mostly sex offenders and that it was the most overcrowded prison in the country, adding, ‘We’re full of bed blockers.’

‘Bed blockers?’ I asked.

She explained that these are prisoners who had been through the sex offenders treatment program, but for one reason or another hadn’t been moved on to a different prison. The result was that they were taking up spaces that other, as yet untreated, offenders could use.

However, the main problem at Shrewsbury was not the ‘bed blockers’, who had accepted their offences and received treatment, but the many sex offenders who were in denial, and so could not be treated. Owing to the nature of their offences, such prisoners may be limited in what activities they can undertake during their sentences. Typically, for their own protection, sex offenders are segregated from ‘mainstream’ prisoners and even with good behaviour are not deemed suitable for outside work.

HMP Shrewsbury was one of the prisons that participated in our own research study. This prison had by far the biggest number of prisoners keen to do yoga and meditation, many more than we could actually manage to interview during the time we had allocated there.

As I interviewed prisoner after prisoner, all expressing a desire to do the yoga classes, it seemed to me that it could be possible that these techniques if effective could represent an alternative way to encourage positive personal change in prisoners whom the system might otherwise not be able to reach. Why? Because practising meditation and yoga doesn’t involve asking probing questions about offences of which prisoners may be deeply ashamed, feel in denial of, or simply not yet ready to address.

Sandy confirmed the particular utility of yoga and meditation for this demographic: ‘Not only is silence therapeutic and inclusive, it’s also safe for people with addiction and sex-offending histories.’ On the surface yoga is a physical activity, with desirable physiological benefits; it’s unthreatening, non-blaming and doesn’t require the admission of guilt. In this way it is possible that prisoners who would otherwise avoid explicit attempts to ‘change’ their behaviour, may nevertheless engage with a technique that could anyway bring about deep, personal transformation.

FROM MONSTER TO BUDDHA

The concept of a prison cell as an ashram is an idea that captures the imagination, and the paradox of finding spiritual freedom through the loss of physical freedom is intriguing. Might there actually be truth in this unusual idea, can daily yogic sun salutations and deep breathing really make convicted rapists and murderers less violent and impulsive?

While it’s unlikely that yoga and meditation could replace traditional rehabilitative approaches, it seems possible that they may have a unique ability to reach prisoners on a different level: to make them feel more at peace, and more valued and connected. Bo Lozoff summarizes the aim of organizations that teach contemplative techniques to prisoners worldwide when he says that we should ‘allow for transformation, not merely rehabilitation’.

In other words the change that charities such as his and the PPT seek to encourage goes far beyond the cessation of offending behaviour; we are talking about a radical change in worldview. The PPT’s current director Sam Settle describes this transformation as ‘the forgetting of one’s self as one lives the forgetting of me’. In essence moving from focusing on oneself as a separate individual to seeing oneself as part of a larger whole.

Whether or not we share these ideas about the possibility of the transformation of convicted criminals from sinner to saint, from ‘monster’ to Buddha on a theoretical and anecdotal level, there does seem to be reason to think that yoga and meditation can bring about positive personal change in prisoners.

In Chaoter 8 we reveal how we put that theory to the test, but first let’s take a look at what science can tell us about the potential of Eastern techniques for bringing about meaningful change not just for prisoners, but for any of us.

CHAPTER 2

SET LIKE PLASTER

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‘Change is an odd process, almost contradictory: you want it, but don’t want it,’ said my clinical supervisor, playing with his curled beard and looking at me. What was he talking about? I had started my training in cognitive behavioural therapy (CBT) eight weeks earlier and was discussing my first client, ‘Mary’, a woman in her thirties, whose husband had died while on a family holiday. He had killed himself jumping off a cliff, right in front of his wife and their young child. Six months after the incident, Mary found herself depressed and sleepless.

‘I felt shock and disbelief,’ she told me, remembering. ‘I felt like I had been disembowelled and bricks sewn inside. I had to register his death the next day and felt terrible anger at having to describe myself as a widow, 24 hours after I had been a wife. Bureaucracy shouldn’t require that, you know?’ I nodded but felt tense, eager to show empathy. For the past eight weeks, l’d spent most . . .

*

from

The Buddha Pill: Can Meditation Change You?

by Dr Miguel Farias and Dr Catherine Wikholm

get it at Amazon.com

Dr Miguel Farias writes about the psychology of belief and spiritual practices, including meditation. He was a lecturer at the University of Oxford and is now the leader of the Brain, Belief and Behaviour group at Coventry University.

.
Dr Catherine Wikholm is a Clinical Psychologist registered with the Health Care and Professions Council (HCPC) and a Chartered Psychologist with the British Psychological Society (BPS). She completed her undergraduate degree in Philosophy and Theology at Oxford University, before embarking on her psychology training and gaining a Postgraduate Diploma in Psychology, Masters in Forensic Psychology and a Doctorate in Clinical Psychology. Catherine was previously employed by HM Prison Service where she worked with young offenders. She went on to work alongside Dr Miguel Farias at the Department of Experimental Psychology, Oxford University, on a randomised controlled trial that looked at the psychological effects of yoga and meditation in prisoners. The findings of this research study sparked the idea for ‘The Buddha Pill’, which she co-wrote while completing her doctorate. Catherine currently works in a NHS child and adolescent mental health service (CAMHS) in London, UK.

What happened when the US last introduced tariffs? – Dominic Rushe.

Anyone?

Willis Hawley and Reed Smoot were reviled for a bill blamed for triggering the Great Depression. Will Trump follow their lead?

America inches towards a potential trade war over steel prices, can Donald Trump hear whispering voices?

Alone in the Oval Office in the wee dark hours, illuminated by the glow of his Twitter app, does he feel the sudden chill flowing from those freshly hung gold drapes? It is the shades of Smoot and Hawley.

Willis Hawley and Reed Smoot have haunted Congress since the 1930s when they were the architects of the Smoot Hawley tariff bill, among the most decried pieces of legislation in US history and a bill blamed by some for not only for triggering the Great Depression but also contributing to the start of the second world war.

Pilloried even in their own time, their bloodied names have been brought out like Jacob Marley’s ghost every time America has taken a protectionist turn on trade policy. And America has certainly taken a protectionist turn.

Successful presidents including Barack Obama and Bill Clinton have campaigned on the perils of free trade only to drop the rhetoric once installed in the White House. Trump called Mexicans “rapists” on the campaign trail. And China? “There are people who wish I wouldn’t refer to China as our enemy. But that’s exactly what they are,” Trump said.

As commander in chief he has shown no signs of softening and this week took major action announcing steel imports would face a 25% tariff and aluminium 10%.

Canada and the EU said they would bring forward their own countermeasures. Mexico, China and Brazil have also said they are considering retaliatory steps.

Trump doesn’t seem worried. “Trade wars are good,” he tweeted even as the usually friendly Wall Street Journal thundered that “Trump’s tariff folly ”is the “biggest policy blunder of his Presidency”.

It is not his first protectionist move. In his first days in office the president has vetoed the Trans Pacific Partnership (TPP), the biggest trade deal in a generation, said he will review the North American Free Trade Agreement (Nafta), a deal he has called “the worst in history”, and had his visit with Mexico’s president cancelled over his plans to make them pay for a border wall.

Free traders may have become complacent after hearing tough talk on trade from so many presidential candidates on the campaign trail only to watch them furiously back pedal when they get into ofhce, said Dartmouth professor and trade expert Douglas Irwin. “Unfortunately that pattern may have been broken,” he says. “It looks like we have to take Trump literally and seriously about his threats on trade.”

Not since Herbert Hoover has a US president been so down on free trade. And Hoover was the man who signed off on Smoot and Hawley’s bill.

Hawley, an Oregon congressman and a professor a history and economics, became a stock figure in the textbooks of his successors thanks to his partnership with the lean, patrician figure of Senator Reed Smoot, a Mormon apostle known as the “sugar senator” for his protectionist stance towards Utah’s sugar beet industry.

Before he was shackled to Hawley for eternity Smoot was more famous for his Mormonism and his abhorrence of bawdy books, a disgust that inspired the immortal headline “Smoot Smites Smut” after he attacked the importation of Lady’s Chatterley’s Lover, Robert Burns’ more risque poems and similar texts as “worse than opium I would rather have a child of mine use opium than read these books.”

But it was imports of another kind that secured Smoot and Hawley’s place in infamy.

The US economy was doing well in the 1920s as the consumer society was being born to the sound of jazz. The Tariff Act began life largely as a politically motivated response to appease the agricultural lobby that had fallen behind as American workers, and money, consolidated in the cities.

Foreign demand for US produce had soared during the first world war, and farm prices doubled between 1915 and 1918. A wave of land speculation followed and farmers took on debt as they looked to expand production. By the early 1920s farmers had found themselves heavily in debt and squeezed by tightening monetary policy and an unexpected collapse in commodity prices.

Nearly a quarter of the American labor force was then employed on the land, and Congress could not ignore heartland America. Cheap foreign imports and their toll on the domestic market became a hot issue in the 1928 election. Even bananas weren’t safe. Irwin quotes one critic in his book Peddling Protectionism: Smoot Hawley and the Great Depression: “The enormous imports of cheap bananas into the United States tend to curtail the domestic consumption of fresh fruits produced in the United States.”

Hoover won in a landslide against Albert E Smith, an out of touch New Yorker who didn’t appeal to middle America, and soon after promised to pass “limited” tariff reforms.

Hawley started the bill but with Smoot behind him it metastasized as lobby groups shoehorned their products into the bill, eventually proposing higher tariffs on more than 20,000 imported goods.

Siren voices warned of dire consequences. Henry Ford reportedly told Hoover the bill was “an economic stupidity”.

Critics of the tariffs were being aided and abetted by “internationalists” willing to “betray American interests”, said Smoot. Reports claiming the bill would harm the US economy were decried as fake news. Republican Frank Crowther, dismissed press criticism as “demagoguery and untruth, scandalous untruth”.

In October 1929 as the Senate debated the tariff bill the stock market crashed. When the bill finally made it to Hoover’s desk in June 1930 it had morphed from his original “limited” plan to the “highest rates ever known”, according to a New York Times editorial.

The extent to which Smoot and Hawley were to blame for the coming Great Depression is still a matter of debate. “Ask a thousand economists and you will get a thousand and five answers,” said Charles Geisst, professor of economics at Manhattan College and author of Wall Street: A History.

What is apparent is that the bill sparked international outrage and a backlash. Canada and Europe reacted with a wave of protectionist tariffs that deepened a global depression that presaged the rise of Hitler and the second world war. A myriad other factors contributed to the Depression, and to the second world war, but inarguably one consequence of Smoot Hawley in the US was that never again would a sitting US president be so avowedly anti trade. Until today.

Franklin D Roosevelt swept into power in 1933 and for the first time the president was granted the authority to undertake trade negotiations to reduce foreign barriers on US exports in exchange for lower US tariffs.

The backlash against Smoot and Hawley continued to the present day. The average tariff on dutiable imports was 45% in 1930; by 2010 it was 5%.

The lessons of Smoot Hawley used to be taught in high schools. Presidents from Lyndon Johnson to Ronald Reagan have enlisted the unhappy duo when facing off with free trade critics. “I have been around long enough to remember that when we did that once before in this century, something called Smoot Hawley, we lived through a nightmare,” Reagan, who came of age during the Great Depression, said in 1984.

They even got a mention in Ferris Bueller’s Day Off when actor Ben Stein’s teacher bores his class with it. “I don’t think the current generation are taught it. It’s in the past and we are more interested in the future.”

But that might be about to change. “The main lesson is that you have to worry about what other countries do. Countries will retaliate,” said Irwin. “When Congress was considering Smoot Hawley in the 1930s they didn’t consider what other countries might do in reaction. They thought other countries would remain passive. But other countries don’t remain passive.”

The consequences of a trade war today are far worse than in the 1930s. Exports of goods and services account for about 13% of US gross domestic product (GDP) the broadest measure of an economy. It was roughly 5% back in 1920.

“The US is much more engaged in trade, it’s much more a part of the fabric of the country, than it was in the 1920s and 1930s. That means the ripple effects are widespread. Many more industries will be hit by it and the scope for foreign retaliation, which in the case of Smoot Hawley was quite limited, is going to be much more widespread if a trade war was to start.”

“When you start talking about withdrawing from trade agreements or imposing tariffs of 35%, if you are doing that as a protectionist measure, that would be blowing up the system.”

That the promise of “blowing up the system” got Trump elected may be why the ghosts of Smoot and Hawley are once again walking the halls of Congress.

The Guardian

CFT: Focusing on Compassion In Next Generation CBT Dennis Tirch Ph.D * Compassion Focused Therapy For Dummies – Mary Welford * Compassion Focused Therapy – Paul Gilbert.

Compassion Focused Therapy offers therapists new options.

Dennis Tirch Ph.D

Compassion is currently being studied and used as an evidence based ingredient in effective psychotherapy more than ever before. This might not seem surprising, given that practicing compassion has been at the center of emotional healing in global wisdom traditions for at least 2,600 years. Empathy and emotional validation have been identified as some of the most important components of psychotherapy effectiveness for decades. However, compassion, as a process in itself, has only recently come to be seen as a core focus of psychotherapeutic work. A growing body of research continues to demonstrate how cultivating our compassionate minds can help us to alleviate and prevent a range of psychological problems, including anxiety and shame (Tirch and Gilbert, 2014). Rather than being a soft option, the deliberate activation of our compassion system can generate the courage and psychological flexibility we need to face life’s challenges, and step forward into lives of meaning, purpose and vitality.

Paul Gilbert (2009) has drawn upon developmental psychology, affective neuroscience, Buddhist practical philosophy, and evolutionary theory to develop a comprehensive form of experiential behavior therapy known as Compassion Focused Therapy (CFT). Gilbert describes compassion as a multifaceted process that has evolved from the caregiver mentality found in human parental care and child rearing. As such, compassion includes a number of emotional, cognitive, and motivational elements involved in the ability to create opportunities for growth and change with warmth and care. CFT involves training and enhancing this evolved capacity for compassion.

Gilbert defines the essence of compassion as “a basic kindness, with deep awareness of the suffering of oneself and of other living things, coupled with the wish and effort to relieve it” (2009, p. xiii). This definition involves two central dimensions of compassion. The first is known as the psychology of engagement and involves sensitivity to and awareness of the presence of suffering and its causes. The second dimension is known as the psychology of alleviation and constitutes both the motivation and the commitment to take actual steps to alleviate the suffering we encounter (Gilbert and Choden, 2013).

Over the last few years, the research base for compassion psychology generally and CFT specifically has been growing at a remarkable rate, with a rapid increase in the number of research and clinical publications addressing compassion. For example, the last ten years have seen a major upsurge in exploration into the benefits of cultivating compassion, especially through imagery practice (Fehr, Sprecher, and Underwood, 2008). Neuroscience and imaging research has demonstrated that practices of imagining compassion for others produce changes in the frontal cortex, the immune system, and overall well-being (Lutz et al., 2008). Notably, one study (Hutcherson, Seppala, and Gross, 2008) found that even just a brief loving-kindness meditation increased feelings of social connectedness and affiliation toward strangers.

Several compassion-focused intervention components have been found to enhance psychotherapy outcomes, and to serve as mediator variables in outcomes. For example, one study (Schanche, Stiles, McCullough, Svartberg, and Nielsen, 2011) found that self-compassion was an important mediator of reduction in negative emotions associated with personality disorders. In a study of the effectiveness of mindfulness-based cognitive therapy for depression (Kuyken et al., 2010), researchers found that self-compassion was a significant mediator between mindfulness and recovery. In fact, in a meta-analysis of research concerning both clinical and nonclinical settings, compassion-focused interventions were found to be significantly effective (Hofmann et al., 2011).

CFT is also seeing increasing empirical supported through outcome research. An early clinical trial involving a group of people with chronic mental health problems who were attending a day hospital (Gilbert and Procter, 2006) found that CFT significantly reduced self-criticism, shame, sense of inferiority, depression, and anxiety. In other outcome research, CFT has been found to be significantly effective for the treatment of personality disorders (Lucre and Corten, 2012), eating disorders (Gale, Gilbert, Read, and Goss, 2012), psychosis (Braehler, Harper, and Gilbert, 2012) and in people presenting to community mental health teams (Judge, Cleghorn, McEwan, and Gilbert, 2012). As CFT continues to become more widely disseminated and growing numbers of clinicians and researchers acquire understanding and skill in its methods and philosophy, increasing outcome research will further test the model, leading to innovation and improvement.

The following brief tips can help psychotherapists begin to appreciate how useful a compassion focus can be in practicing ACT, CBT or, in fact, any form of psychotherapy. Furthermore, we can see how remembering to practice compassion for ourselves might help to restore the energy and attention we bring to our work, of sharing compassion with our clients. Feel free to experiement with the following:

1. “It is not your fault…”

From a perspective of compassion, we remember how much of the pain and suffering in life is not of our choosing, and couldn’t really be our fault. In CFT we practice the “wisdom of no-blame” which means that taking responsibility for the direction you choose in life is essential, while languishing in shame, social fears and self-blame seldom leads to effective action. We know we didn’t choose our place in the genetic lottery. We didn’t choose to have a tricky human brain that is set up with a hair-trigger threat detection system and confusing loops of thoughts and actions. We didn’t choose our parents, our childhood or the myriad of social circumstances of life. By realizing that much of what we suffer with is simply not our fault, we can begin to activate compassion for ourselves and others, as we contact and engage with the tragedies of life.

2. Holding ourselves and others in warmth and kindness

When humans are in the presence of warmth, acceptance and affiliative emotions, we are likely to be at our most flexible, empathic, responsive and healthiest mode of operation. From the day we are born and throughout our lives the presence of kindess, support and emotional strength will have powerful impacts on every aspect of our health and behavior. In CFT, we use methods drawn from ancient visualization practices, and also modern techniques drawn from method acting to create the conditions and context that can allow for the experience of compassion. So, when we practice compassion for ourselves and others, we remember to slow down, to have a warm and caring expression on our face, and to use open and centered body language. Adopting a slow pace of our breathing and a warm tone of voice, we do all that we can to invite an experience of compassion. Images that evoke compassion are also used to bring us into contact with our compassionate mind. Can you imagine the most elegant cognitive reframe shouted at you with a cruel voice, such as a depressed client telling themselves, “The evidence doesn’t add up that you are a loser, so stop being so stupid about everything and suck it up and deal with life!” Perhaps even worse, can you imagine the condeming inner monologue of a mindfulness practitioner saying something like, “You’re not supposed to be judgemental about judging your thoughts! My God, you are terrible at this!” No matter how clever the content of our minds may seem to be, an emotional tone of acceptance, kindess and compasion is an essential ingredient to our experience of well-being.

3. Practicing compassion as a flow

We all can feel distressed in our work as psychotherapists, when we repeatedly encounter the suffering of others, which activates sympathetic emotional pain that we experience within our own minds, hearts and brains. Practicing deliberate, consistent compassion for ourselves and for others can help us to prevent empathic distress fatigue, and can build our inner architecture of compassionate strength. When you find yourself feeling that your reservoir of empathy, wisdom and warmth is slightly drained, deliberately breathe in compassionate intentions for yourself. As you exhale, direct compassionate intentions towards your client. This can be done silently, secretly, and consistently. As we breathe in, we wish for our suffering to cease and for ourselves to find peace and happiness. As we breathe out, we wish for our clients suffering to cease also, and we wish them happiness, wellness and an end to needless struggles. When this simple gesture becomes a therapist’s habit, they can quickly activate affiliative emotions to help them work towards their own compassionate mission of alleviating and preventing the suffering that they find in themselves and in others.

*

Dennis Tirch, Ph.D., is a compassion-focused psychologist, the author of The Compassionate Mind Guide to Overcoming Anxiety, and a faculty member at Weill Cornell Medical College.

Paul Gilbert, Ph.D., is currently a professor of clinical psychology at the University of Derby in the United Kingdom, and director of the Mental Health Research Unit at Derbyshire Mental Health Trust.

***

Compassion Focused Therapy For Dummies
Mary Welford.

Introduction

You can work through a never-ending list of things you could do to improve your wellbeing. Getting more sleep, taking regular exercise, eating a healthier diet, developing a positive mental attitude and drinking less alcohol are just some of the things you may benefit from. Advice comes from the TV, newspapers, self-help books, friends, relatives, colleagues, healthcare professionals and even the chats we have with ourselves! But it’s hard to motivate ourselves to make helpful changes. It’s even harder to maintain them.

Compassion Focused Therapy (CFT) is here to help. This approach offers life-changing insights into our amazing capacities and also the challenges we face in our everyday lives. By understanding ourselves, we become motivated to act out of true care for our wellbeing. This changes the relationship we have with ourselves and others. Practicing CFT won’t mean you suddenly turn into a ‘perfect’version of yourself. It does however mean that you become more aware of the choices you have and you’re motivated to make ones that are more helpful to you. And yes, you find plenty of advice in here to guide you on your way too!

About This Book

Compassion Focused Therapy For Dummies contains a wealth of important information that can help you to understand yourself, and others, better. It also introduces you to practices that you can integrate into your everyday life, minute by minute, hour by hour, day by day…. I’ve used as little jargon and off-putting technical terms as possible, and so you don’t need to approach this book with a background knowledge of psychology. Simply put, if you’re in possession of a human brain and you’d like to discover more about CFT, this book is written for you.

That said, two factors may motivate you to continue developing your understanding of CFT once you finish this book: CFT is rooted in a scientific understanding of what it is to be human. As such, the approach constantly evolves to reflect the science. In the same way as it’s helpful to keep up with advancing technology, it’s also good to keep up with advancing our understanding of ourselves. We humans are highly complex.

This book simply doesn’t have the room to do CFT complete justice –not if you want to be able to lift it up! When you finish reading, you may want to move on to explore the comprehensive work of Paul Gilbert (the originator of the CFT approach), his colleagues and collaborators.

Foolish Assumptions In writing this book

I’ve had to make a few assumptions about you. I’ve assumed that: You’re interested in improving your wellbeing. You appreciate that CFT is based on an incredible amount of research –but you don’t necessarily want to plough through it all! You realise that I’ve had to make some tough decisions about what to include and what to leave out. Hopefully most of the choices I’ve made are right (but thankfully I won’t criticise myself if I’ve made a mistake; I hope you don’t either!). You recognise that I’m not trying to pass CFT off as my own creation. Instead, I set out to describe the work of Paul Gilbert and colleagues (of whom I am privileged to be one).

You may be selective about which parts of the book you read. As such, I’ve written this book in a way that allows each chapter to ‘stand alone’ so that you can pick and choose the content you want to read, and when you want to read it. You’re prepared to give new things a go! If you’re a therapist or studying CFT, I also assume that you recognise the importance of learning the approach ‘from the inside out’, and as such that you’ll work through the book with this in mind.

Beyond the Book

In addition to the material in this book, I also provide a free access-anywhere Cheat Sheet that offers some helpful reminders about the many benefits of CFT. To get this Cheat Sheet, simply go to http://www.dummies.com and search for ‘Compassion Focused Therapy For Dummies Cheat Sheet’ in the Search box.

Where to Go from Here

If you’re new to CFT, you may find it helpful to start with Chapter 1 before you decide how to tackle the rest of the chapters (you may even decide that you want to read the book from start to finish –but you don’t have to take that approach, as you find plenty of helpful cross-references to other useful chapters as you work through each chapter).

However you decide to begin, do this at a pace to suit both your understanding and emotional experience. If you have some experience of CFT, you may choose to skip to a particular topic due to a need or question you may have. If this is the case, use the table of contents and the index to help you find your way to the required information. Regardless of how you find your way around this book, I hope you appreciate the journey.

Finally, CFT aims to assist you to develop a compassionate understanding and relationship with yourself and others. If you find the approach helpful, it’s likely to become a way of life. To support your journey, you can access a number of courses to assist you. These course can also connect you with a wider group of people. You can find suitable courses advertised on a range of websites, including http://www.compassionatemind.co.uk, http://www.compassioninmind.co.uk and http://www.compassionatewellbeing.co.uk.

Part 1

Getting Started with Compassion Focused Therapy

IN THIS PART Discover what CFT is all about and how it can be helpful. Explore what compassion is, including the skills and attributes of compassion. Find out about the challenges we face and how our minds are organised.

Chapter 1
Introducing Compassion Focused Therapy

IN THIS CHAPTER
– Understanding how Compassion Focused Therapy works
– Discovering the benefits of compassion
– Exploring the effects of shame and self-criticism
– Beginning your journey
– Reaching out to others with compassion

People are more similar than different. We’re all born into a set of circumstances that we don’t choose, and in possession of a phenomenal yet very tricky brain. We’re all trying to get by, doing the best we can. The sooner we wake up to this reality the better.

Compassion Focused Therapy (CFT) is here to help. This approach aims to liberate you from shame and self-criticism, replacing these feelings with more helpful ways of relating to yourself. It helps you to choose the type of person you want to be and to develop ways to make this choice a reality. In this chapter, I introduce you to CFT, offering you an understanding of how it works and helping you to understand the benefits. I also point out the steps you may take along the way as you work with the information in this book. Finally, I take a moment to help you connect to the wider community around you as you begin this journey.

CFT advocates that you don’t rush to ‘learn’ about the approach but instead allow space to experience and ‘feel’ it. So take your time with this book as you apply it to your life, and really discover the benefits.

Getting to Grips with Compassion Focused Therapy

CFT was founded by UK clinical psychologist Paul Gilbert, OBE.

The name of the approach was chosen to represent three important aspects:

Compassion, in its simplest yet potentially most powerful definition, involves a sensitivity to our own, and other people’s, distress, plus a motivation to prevent or alleviate this distress. As such, it has two vital components. One involves engaging with suffering while the other involves doing something about it. Chapter 2 delves into the ins and outs of compassion in more detail.

Focused means that we actively develop and apply compassion to ourselves. It also involves accepting and experiencing compassion from and for others.

Therapy is a term to describe the processes and techniques used to address an issue or difficulty.

CFT looks to social, developmental and evolutionary psychology and neuroscience to help us understand how our minds develop and work, and the problems we encounter. This scientific understanding (of ourselves and others) calls into question our experiences of shame and self-criticism and helps us to develop the motivation to make helpful changes in our lives.

CFT utilises a range of Eastern and Western methods to enhance our wellbeing. Attention training, mindfulness and imagery combine with techniques used in Cognitive Behavioural Therapy (CBT), and Person Centred, Gestalt and Narrative therapies (to name but a few), resulting in a powerful mix of strategies that can help you become the version of yourself you wish to be.

CFT is often referred to as part of a ‘third-wave’ of cognitive behavioural therapy because it incorporates a number of CBT techniques. However, CFT derives from an evolutionary model (which you find out more about in Chapters 3, 4 and 5) and it uses techniques from many other therapies that have been found to be of benefit. As such, CFT builds upon and integrates with other therapies. As therapies become more rooted in science, we may see increasing overlap rather than diversification.

Compassion can involve kindness and warmth, but it also takes strength and courage to engage with suffering and to do something about it. CFT is by no means the easy or ‘fluffy’ option. Head to Chapter 6 to address some of the myths associated with compassion.

You may be reading this book because you want to find out more about this form of therapy. Alternatively, you may want to develop your compassionate mind and compassionate self out of care for your own wellbeing. The why or your motivation for reading this book has a big effect on the experience and, potentially, the outcome. Personally, I hope that whatever your motivation, you consider applying the approach to yourself in order that you can learn it ‘from the inside out’.

Defining common terms

You may find that some of the terms used in CFT are new to you. Here are a few common terms that I use throughout this book, along with an explanation of what they mean:

Common humanity: This refers to the fact that, as human beings, we all face difficulties and struggles. We’re more alike than different, and this realisation brings with it a sense of belonging to the human family.

Tricky brain: Our highly complex brains can cause us problems. For example, our capacity to think about the future and the past makes us prone to worry and rumination, while our inbuilt tendency to work out our place in a hierarchy can have a huge impact on our mood and self-esteem. In CFT, we use the term tricky brain to recognise our brain’s complexity and the problems this complexity can lead to. We consider our tricky brain in more detail in Chapter 3.

Compassionate mind: This is simply an aspect of our mind. It comes with a set of attributes and skills that are useful for us to cultivate (I introduce these attributes and skills in Chapter 2). This frame of mind is highly important for our wellbeing, relationships and communities. But just as we have a compassionate mind, we also have a competitive and threat-focused mind –which is highly useful, if not a necessity, at certain times (Chapter 4 takes a look at our threat-focused mind).

Compassionate mind training: This describes specific activities designed to develop compassionate attributes and skills, particularly those that influence and help us to regulate emotions. Attention training and mindfulness are used as a means to prepare us for this work, and we look at these practices in Part 3.

Compassionate self: This is the embodiment of your compassionate mind. It’s a whole mind and body experience. Your compassionate self incorporates your compassionate mind but also moves and interacts with the world.

Compassionate self cultivation: Your compassionate self is an identity that you can embody, cultivate and enhance. Compassionate self cultivation describes the range of activities that help you develop your compassionate self. Head to Chapter 10 for more on the cultivation of your compassionate self.

Engagement in the compassionate mind training and compassionate self cultivation activities provided in this book is often referred to as ‘physiotherapy for the brain’, as their use has been found to literally change the brain! Compassionate mind training and compassionate self cultivation are integral to CFT, but there’s so much more to CFT.

For many, getting to a point at which you can see the relevance and benefits of compassionate mind training and compassionate self cultivation, and overcome blocks and barriers to compassion, is the most significant aspect of your compassionate journey.

Exercises: These are activities for you to try. Sometimes they help to illustrate a point or provide a useful insight. Other exercises can give you an idea of what helps you to develop and maintain your compassionate mind.

Practice: Once you’re aware of which exercises are helpful to you, you can then incorporate these into your everyday life. Regular use of these exercises becomes your practice.

Observing the origins of CFT

CFT is closely tied to advances in our understanding of the mind and, because scientific advances never stop, the therapy continues to adapt and change based upon it. Much of this book focuses on sharing the science to help develop a compassionate understanding of yourself and a sense of connection with fellow travellers on this mortal coil.

CFT is also born out of a number of clinical observations:

– People demonstrating high levels of shame and self-criticism often struggle with standard psychological therapies. For example, using CBT, many find that they’re not reassured by the generation or discovery of alternative beliefs and views and that this doesn’t result in changes to the way they feel. Individuals may say ‘Logically, I know I’m not bad/not to blame, but I still feel it’ and ‘I know it’s unlikely that things will go wrong, but I still feel terrible’.

– What we say to ourselves is important, but how we say it is even more important.

Ever called yourself ‘idiot’ in a light-hearted and jovial manner? You probably did so without feeling any negative effects. But, have you ever called yourself an idiot in a harsh and judgemental manner? You probably felt much worse on that occasion, perhaps resulting in an urge to withdraw or isolate yourself.

Consider phrases such as, ‘look on the bright side’ or ‘count your blessings’.

Sometimes these phrases can be said in a life-affirming way, but using a condescending, frustrated or angry tone represents a whole different ball game. This helps illustrate that your emotional tone is important. Therapy can result in improvement in mood, self-esteem, sense of control and achievement, alongside a reduction in difficulties.

However, life events can trigger relapse. How we relate to ourselves, especially when life doesn’t go the way we hope, is pivotal to our ongoing wellbeing. Post therapy, many people report that they never disclosed to their therapist the things that caused them the most distress. This resulted from their sense of shame and the way they believed others (the therapist) would feel about them.

In addition to this, consider how many people simply don’t seek help at all because they fear what others think. People struggle to feel loved, valued, safe or content if they’ve never experienced these feelings. For some people, these feelings are alien concepts and, most of all, alien experiences, difficult to generate by discussion alone. As such, it’s important to develop the emotional resources and skills to deal with difficult emotions without turning to alcohol, food, drugs, work, excessive exercise or particular fixations.

– Most of us struggle with emotions such as anger, anxiety and vulnerability, but many also find positive emotions extremely difficult, even frightening. For some people, care, kindness, love and intimacy are terrifying, and to be avoided.

– People experiencing depression often worry that something bad will happen when their mood lifts.

– Likewise, feelings of connection and trust often stir up feelings of isolation and rejection, and a fear of loss.

These difficulties can interfere with the goals we set ourselves unless we address them.

CFT is an accumulation of years of research, clinical insights and teachings drawn from a broad range of areas. Much of this research and study is summarised and published in scientific papers, textbooks and self-help books by Paul Gilbert and colleagues. A number of websites also provide additional resources. You can find details of these in the Appendix. This book provides you with a starting point for your CFT journey and offers a framework upon which you can hang your future CFT practice –use these resources to develop your practice further.

TAKING A COMPASSIONATELY THERAPEUTIC APPROACH

It has long been established that compassionate, respectful and supportive relationships are key to our wellbeing and integral to effective psychotherapies. A key goal of many therapies is the development of a better relationship with yourself. However, different therapies place emphasis on different methods to account for and produce change, for example: CBT focuses primarily (but not exclusively) on the link between thoughts, feelings and behaviours and helps you generate new thoughts and behaviours in order to change your feelings. Interpersonal therapy focuses on your relationships and how they affect you. Psychodynamic therapy aims to bring the unconscious mind into consciousness, helping you to experience and understand your true feelings in order to resolve them.

In contrast, CFT begins with your experience of compassion from your therapist (in person or through books like this one). This relationship with your therapist is pivotal. It then focuses on the personal development and cultivation of compassion to help you to make beneficial choices for yourself and for others.

With this in mind, this book contains quite a bit of me –as an author, as a psychologist and, most of all, as a human being who struggles too. I hope that the bits of me enhance your experience of reading the words I have chosen to write for you.

Making the Case for Compassion

If we view compassion as ‘a sensitivity to our own and other people’s distress plus a motivation to prevent or alleviate it’, we can easily appreciate the many individual, group and societal benefits to developing and maintaining compassion in our lives. It makes intuitive sense and it’s the reason why compassion has been a central component of many religious and spiritual traditions across the centuries.

Research studies support the benefits of bringing compassion into your life. Higher levels of compassion are associated with fewer psychological difficulties. Compassion enhances our social relationships and emotional wellbeing: it alters our neurophysiology in a positive way and can even strengthen our immune systems. Research also suggests that CFT can be successfully used to address difficulties associated with eating, trauma, mood and psychosis.

However, for me, you can observe the power of the CFT approach in training clinicians. As they discover this approach to help their clients, they often report that the application of CFT in their personal lives can be transformative, leading many clinicians to develop and maintain their own personal practice. I believe that personal practice is vital for any clinician. I attribute much of my wellbeing and my ability to engage with other people’s suffering to the application of this approach in my life.

SO I’LL NEVER FEEL BAD AGAIN?

CFT won’t rid you of life’s difficulties. You won’t find yourself day after day serenely swanning around, impervious to life’s difficulties. We practise compassion because life is hard. Compassion can assist us to make helpful choices and, when ready, create a space in which we can work through strong emotions, and grieve for things we’ve lost and wish had been different. With compassion, we relate to our anger, anxiety and sadness with kindness, warmth and non-judgement. This allows us to consider the reasons such emotions are there, work through them and face the issues they are alerting us to. The development and cultivation of compassion isn’t a quick fix. It’s a way of living our lives.

Understanding the Effects of Shame and Self-Criticism

Shame and self-criticism are common blocks to wellbeing, and CFT is designed to overcome them. The following sections help you consider how shame and self-criticism can affect you and what you can do to address and overcome these issues.

The isolating nature of shame

Shame is an excruciatingly difficult psychological state. The term comes from the Indo-European word ‘sham’meaning ‘to hide’, and, as such, the experience of shame is isolating. When we feel shame, we feel bad about ourselves. We believe others judge us as inadequate, inferior or incompetent.

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The next exercise helps you to explore the nature of shame and how it may affect you.

Begin by finding a place you can sit for a short time that is free of distractions. Allow yourself to settle for a few moments. It may help to lower your gaze or close your eyes during the exercise. Bring to mind a time when you felt ashamed (nothing too distressing, but something you feel okay to revisit briefly). Allow the experience to occupy your mind for a few moments.
Slowly ask yourself the following questions, allowing time after each question to properly explore your experience:
– How (and where) does shame feel as a sensation in your body?
– What thoughts go through your mind about yourself?
– What do you think other people thought/would think or make of you if they knew this about you?
– What emotions do you feel? What does it make you want to do?

Allow the experience to fade from your mind’s eye. Recall a time you’ve felt content or happy, perhaps on your own or with someone else, and let this memory fill your mind and body.

Depending upon the situation you brought to mind, a sense of anxiety, disgust or anger may have come to the fore. You may feel exposed, flawed, inadequate, disconnected or bad. Maybe you experience the urge to curl up, hide or run away, or perhaps feelings of anger and injustice leave you with the urge to defend yourself or confront someone.

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Often, shame results in a feeling of disconnection. We don’t like ourselves (or a part of ourselves) and we don’t want to experience closeness to others because this may result in rejection. Our head goes down and we want to creep away. In addition, shame can affect our bodily sensations, maybe leading to tension, nausea or hotness. When you combine these negative views of yourself with predicted negative views from others, you create a very difficult concoction of experiences.

Shame brings with it a range of difficult experiences. Strong physical sensations, thoughts and images are just some of them. Emotions such as anxiety, sadness and anger can race through you as you feel the urge to withdraw, isolate or defend yourself.

Some of the things we feel shame about include:
– Our body (for example, its shape, or our facial features, hair or skin)
– Our body in action (for example, when sweating, urinating, defecating, burping, shaking, walking or running)
– Our health (for example, illnesses, infections, diseases or genetic conditions)
– Our mind (for example, our thoughts, including any intrusive images in our heads, our impulses, forgetfulness and our psychological health)
– Our emotions (for example, anxiety, anger, disgust, sadness, jealousy or envy)
– Our behaviour (for example, things we’ve said and the way we’ve said them, our use of alcohol and drugs, our compulsions, our eating patterns, or our tendency to avoid other people)
– Our environment (for example, our house, neighbourhood, car or bedroom)
– Other people (for example, our friends, family, cultural or religious group, or community)

Exploring why we feel shame

Human beings are social animals and need the protection, kindness and caring of others. Our brains are social organs. We like to feel valued, accepted and wanted by those around us in order to feel safe. There’s no shame in this. These needs represent a deep-rooted part of us that’s been highly significant in our evolution and survival. Shame begins in how you feel you live in the mind of another –and it is a social regulator. In other words, we’re programmed to try to work out, ‘What are they thinking about or feeling toward me?’, ‘Do they like me?’ and ‘Who can I trust?’

Just to add a further layer of complexity, we also try to work out, ‘Do I like myself or this aspect of me?’ and ‘Can I trust myself?’ If we perceive rejection from our social group or reject an aspect of ourselves, shame can be the result.

Although difficult to experience, shame can trigger us to make helpful changes and others to come to our aid in order to soothe the difficulties we experience. But what happens if we feel shame about things we are unable to change (such as our appearance, an aspect of our personality or our culture)? What happens if shame is attached to historical events that we blame ourselves for and can do nothing about? What happens when nobody comes to our assistance or we’re unable to accept the help offered to us?

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Dr. Mary Welford, Consultant Clinical Psychologist, lives and works in the South West of England. She is a founding member of the Compassionate Mind Foundation, Chair to the charity from 2009-2015 and authored the Compassionate Mind Guide to Building Self Confidence.

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from

Compassion Focused Therapy For Dummies

by Mary Welford

get it at Amazon.com

***

COMPASSION FOCUSED THERAPY

Paul Gilbert

Research into the beneficial effect of developing compassion has advanced enormously in the last ten years, with the development of inner compassion being an important therapeutic focus and goal.

This book explains how Compassion Focused Therapy (CFT)—a process of developing compassion for the self and others to increase well-being and aid recovery—varies from other forms of Cognitive Behaviour Therapy.

Comprising 30 key points this book explores the founding principles of CFT and outlines the detailed aspects of compassion in the CFT approach. Divided into two parts—Theory and Compassion Practice—this concise book provides a clear guide to the distinctive characteristics of CFT. Compassion Focused Therapy will be a valuable source for students and professionals in training as well as practising therapists who want to learn more about the distinctive features of CFT.

Paul Gilbert is Professor of Clinical Psychology, University of Derby and has been actively involved in research and treating people with shame-based and mood disorders for over 30 years. He is a past President of the British Association for Cognitive and Behavioural Psychotherapy and a fellow of the British Psychological Society and has been developing CFT for twenty years.

Part 1

THEORY: UNDERSTANDING THE MODEL

1 Some basics

All psychotherapies believe that therapy should be conducted in a compassionate way that is respectful, supportive and generally kind to people (Gilbert, 2007a; Glasser, 2005). Rogers (1957) articulated core aspects of the therapeutic relationship involving positive regard, genuineness and empathy—which can be seen as “compassionate”. More recently, helping people develop self-compassion has received research attention (Gilbert & Procter, 2006; Leary, Tate, Adams, Allen, & Hancock, 2007; Neff, 2003a, 2003b) and become a focus for self-help (Germer, 2009; Gilbert, 2009a, 2009b; Rubin, 1975/ 1998; Salzberg, 1995).

Developing compassion for self and others, as a way to enhance well-being, has also been central to Buddhist practice for the enhancement of well-being for thousands of years (Dalai Lama, 1995; Leighton, 2003; Vessantara, 1993).

After exploring the background principles for developing Compassion Focused Therapy (CFT), Point 16 outlines the detailed aspects of compassion in the CFT approach. We can make a preliminary note, however, that different models of compassion are emerging based on different theories, traditions and research (Fehr, Sprecher, & Underwood, 2009).

The word “compassion” comes from the Latin word compati, which means “to suffer with”. Probably the best-known definition is that of the Dalai Lama who defined compassion as “a sensitivity to the suffering of self and others, with a deep commitment to try to relieve it”, i.e., sensitive attention-awareness plus motivation. In the Buddhist model true compassion arises from insight into the illusory nature of a separate self and the grasping to maintain its boundaries—from what is called an enlightened or awake mind.

Kristin Neff (2003a, 2003b; see http://www.self-compassion.org), a pioneer in the research on self-compassion, derived her model and self-report measures from Theravada Buddhism. Her approach to self-compassion involves three main components:
– 1 being mindful and open to one’s own suffering;
– 2 being kind, and non self-condemning; and
– 3 an awareness of sharing experiences of suffering with others rather than feeling ashamed and alone—an openness to our common humanity.

In contrast, CFT was developed with and for people who have chronic and complex mental-health problems linked to shame and self-criticism, and who often come from difficult (e.g., neglectful or abusive) backgrounds.

The CFT approach to compassion borrows from many Buddhist teachings (especially the roles of sensitivity to and motivation to relieve suffering) but its roots are derived from an evolutionary, neuroscience and social psychology approach, linked to the psychology and neurophysiology of caring—both giving and receiving (Gilbert, 1989, 2000a, 2005a, 2009a). Feeling cared for, accepted and having a sense of belonging and affiliation with others is fundamental to our physiological maturation and well-being (Cozolino, 2007; Siegel, 2001, 2007). These are linked to particular types of positive affect that are associated with well-being (Depue & Morrone-Strupinsky, 2005; Mikulincer & Shaver, 2007; Panksepp, 1998), and a neuro-hormonal profile of increased endorphins and oxytocin (Carter, 1998; Panksepp, 1998).

These calm, peaceful types of positive feelings can be distinguished from those psychomotor activating emotions associated with achievement, excitement and resource seeking (Depue & Morrone-Strupinsky, 2005). Feeling a positive sense of well-being, contentment and safeness, in contrast to feeling excited or achievement focused, can now be distinguished on self-report (Gilbert et al., 2008). In that study, we found that emotions of contentment and safeness were more strongly associated with lower depression, anxiety and stress, than were positive emotions of excitement or feeling energized. So, if there are different types of positive emotions—and there are different brain systems underpinning these positive emotions—then it makes sense that psychotherapists could focus on how to stimulate capacities for the positive emotions associated with calming and well-being.

As we will see, this involves helping clients (become motivated to) develop compassion for themselves, compassion for others and the ability to be sensitive to the compassion from others. There are compassionate (and non-compassionate) ways to engage with painful experiences, frightening feelings or traumatic memories.

CFT is not about avoidance of the painful, or trying to “soothe it away”, but rather is a way of engaging with the painful. In Point 29 we’ll note that many clients are fearful of compassionate feelings from others, and for the self, and it is working with that fear that can constitute the major focus of the work.

A second aspect of the CFT evolutionary approach suggests that self-evaluative systems operate through the same processing systems that we use when evaluating social and interpersonal processes (Gilbert, 1989, 2000a).

So, for example, as behaviourists have long noted, whether we see something sexual or fantasise about something sexual, the sexual arousal system is the same—there aren’t different systems for internal and external stimuli. Similarly, self-criticism and self-compassion can operate through similar brain processes that are stimulated when other people are critical of or compassionate to us. Increasing evidence for this view has come from the study of empathy and mirror neurons (Decety & Jackson, 2004) and our own recent fMRI study on self-criticism and self-compassion (Longe et al., 2010).

Interventions

CFT is a multimodal therapy that builds on a range of cognitive-behavioural (CBT) and other therapies and interventions.

Hence, it focuses on attention, reasoning and rumination, behaviour, emotions, motives and imagery.

It utilizes: the therapeutic relationship (see below); Socratic dialogues, guided discovery, psycho-education (of the CFT model); structured formulations; thought, emotion, behaviour and “body” monitoring; inference chaining; functional analysis; behavioural experiments; exposure, graded tasks; compassion focused imagery; chair work; enactment of different selves; mindfulness; learning emotional tolerance, learning to understand and cope with emotional complexities and conflicts, making commitments for effort and practice, illuminating safety strategies; mentalizing; expressive (letter) writing, forgiveness, distinguishing shame-criticizing from compassionate self-correction and out-of-session work and guided practice—to name a few! Feeling the change CFT adds distinctive features in its compassion focus and use of compassion imagery to traditional CBT-type approaches.

As with many of the recent developments in therapy, special attention is given to mindfulness in both client and therapist (Siegel, 2010). In the formulation CFT is focused on the affect-regulation model outlined in Point 6, and interventions are used to develop specific patterns of affect regulation, brain states and self-experiences that underpin change processes.

This is particularly important when it comes to working with self-criticism and shame in people from harsh backgrounds. Such individuals may not have experienced much in the way of caring or affiliative behaviour from others and therefore the (soothing) emotion-regulation system is less accessible to them. These are individuals who are likely to say, “I understand the logic of [say] CBT, but I can’t feel any different”. To feel different requires the ability to access affect systems (a specific neurophysiology) that give rise to our feelings of reassurance and safeness. This is a well-known issue in CBT (Leahy, 2001; Stott, 2007; Wills, 2009, p. 57).

Over twenty years ago I explored why “alternative thoughts” were not “experienced” as helpful. This revealed that the emotional tone, and the way that such clients “heard” alternative thoughts in their head, was often analytical, cold, detached or even aggressive. Alternative thoughts to feeling a failure, like: “Come on, the evidence does not support this negative view; remember how much you achieved last week!” will have a very different impact if said to oneself (experienced) aggressively and with irritation than if said slowly and with kindness and warmth. It was the same with exposures or home-works—the way they are done (bullying and forcing oneself verses encouraging and being kind to oneself) can be as important as what is done.

So, it seemed clear that we needed to focus far more on the feelings of alternatives not just the content—indeed, an over focus on content often was not helpful.

So, my first steps into CFT simply tried to encourage clients to imagine a warm, kind voice offering them the alternatives; or working with them in their behavioural tasks. By the time of the second edition of Counselling for Depression (Gilbert, 2000b) a whole focus had become concentrated on “developing inner warmth”(see also Gilbert, 2000a).

So, CFT progressed from doing CBT and emotion work with a compassion (kindness) focus and, then, as the evidence for the model developed and more specific exercises proved helpful, on to CFT.

The therapeutic relationship

The therapeutic relationship plays a key role in CFT (Gilbert, 2007c; Gilbert & Leahy, 2007), paying particular attention to the micro-skills of therapeutic engagement (Ivey & Ivey, 2003), issues of transference/countertransference (Miranda & Andersen, 2007), expression, amplification, inhibition and/or fear of emotion (Elliott, Watson, Goldman, & Greenberg, 2003; Leahy, 2001), shame (Gilbert, 2007c), validation (Leahy, 2005), and mindfulness of the therapist (Siegel, 2010).

When training people from other approaches, particularly CBT, we find that we have to slow them down; to allow spaces, and silences for reflection, and experiencing within the therapy rather than a series of Socratic questions or “target setting”. We teach how to use one’s voice speed and tone, nonverbal communication, the pacing of the therapy, being mindful (Katzow & Safran, 2007; Siegel, 2010) and the reflective process in the service of creating “safeness” to explore, discover, experiment and develop.

Key is to provide emotional contexts where the client can experience (and internalize) therapists as “compassionately alongside them”—no easy task because as we will discuss below (see Point 10) shame often involves clients having emotional experiences (transference) of being misunderstood, getting things wrong, trying to work out what the other person wants them to do and intense aloneness.

The emotional tone in the therapy is created partly by the whole manner and pacing of the therapist and is important in this process of experiencing “togetherness”. CF therapists are sensitive to how clients can actually find it hard to experience “togetherness” or “being cared about”, and wrap themselves in safety strategies of sealing the self off from “the feelings of togetherness and connectedness” (see Point 29; Gilbert, 1997, 2007a, especially Chapters 5 and 6, 2007c). CBT focuses on collaboration, where the therapist and client focus on the problem together—as a team.

CFT also focuses on (mind) “sharing”.

The evolution of sharing (and motives to share), e.g., not only objects but also our thoughts, ideas and feelings, is one of humans’ most important adaptations and we excel at wanting to share. As an especially social species, humans have an innate desire to share—not only material things but also their knowledge, values and the content of their minds—to be known, understood and validated. Thus, issues of motivation to share versus fear of sharing (shame), empathy and theory of mind are important evolved motives and competencies. It is the felt barriers to this “flow of minds” that can be problematic for some people and the way that the therapist “unblocks” this flow that can be therapeutic.

Dialectical Behaviour Therapy (DBT; Linehan, 1993) addresses the key issue of therapy-interfering behaviours. CFT, like any other therapy, needs to be able to set clear boundaries, and use authority as a containing process. Some clients can be “emotional bullies”, threatening the therapist (e.g., with litigation or suicide) and are demanding. Frightened therapists may submit or back off. The client, at some level, is frightened of their own capacity to force others away from them.

For other clients, during painful moments, therapists might try to rescue rather than be silent. So, clarification of the therapeutic relationship is very important. This is why DBT wisely recommends a support group for therapists working with these kinds of clients. Research has shown that compassion can become a genuine part of self-identity but it can also be linked to self-image goals where people are compassionate in order to be liked (Crocker & Canevello, 2008). Compassion focused self-image goals are problematic in many ways.

Researchers are also beginning to explore attachment style and therapeutic relationships with evidence that securely attached therapists develop therapeutic alliances easier and with less problems than therapists with an insecure attachment style (Black, Hardy, Turpin, & Parry, 2005; see also Liotti, 2007). Leahy (2007) has also outlined how the personality and schema organization of the therapist can play a huge role in the therapeutic relationship—for example, autocratic therapists with dependent patients, or dependent therapists with autocratic patients. So, compassion is not about submissive “niceness”—it can be tough, setting boundaries, being honest and not giving clients what they want but what they need. An alcoholic wants another drink—that is not what they need; many people want to avoid pain and may try to do so in a variety of ways—but (kind) clarity, exposure and acceptance may be what actually facilitates change and growth (Siegel, 2010).

Evidence for the benefits of compassion

Although CFT is rooted in an evolutionary, neuro- and psychological science model, it is important to recognize its heavy borrowing from Buddhist influences. For over 2500 years Buddhism has focused on compassion and mindfulness as central to enlightenment and “healing our mind”. While Theravada Buddhism focuses on mindfulness and loving-( friendly)-kindness, Mahayana practices are specifically compassion focused (Leighton, 2003; Vessantara, 1993).

At the end of his life the Buddha said that his main teachings were mindfulness and compassion—to do no harm to self or others. The Buddha outlined an eight-fold path for practice and training one’s mind to avoid harming and promote compassion. This includes: compassionate meditations and imagery, compassionate behaviour, compassionate thinking, compassionate attention, compassionate feeling, compassion speech and compassionate livelihood.

It is these multimodal components that lead to a compassionate mind. We now know that the practice of various aspects of compassion increases well-being and affects brain functioning, especially in areas of emotional regulation (Begley, 2007; Davidson et al., 2003).

The last 10 years have seen a major upsurge in exploring the benefits of cultivating compassion (Fehr et al., 2009). In an early study Rein, Atkinson and McCraty (1995) found that directing people in compassion imagery had positive effects on an indictor of immune functioning (S-IgA) while anger imagery had negative effects. Practices of imagining compassion for others, produce changes in the frontal cortex, immune system and wellbeing (Lutz, Brefczynski-Lewis, Johnstone, & Davidson, 2008). Hutcherson, Seppala and Gross (2008) found that a brief loving-kindness meditation increased feelings of social connectedness and affiliation towards strangers. Fredrickson, Cohn, Coffey, Pek and Finkel (2008) allocated 67 Compuware employees to a loving-kindness meditation group and 72 to waiting-list control.

They found that six 60-minute weekly group sessions with home practice based on a CD of loving kindness meditations (compassion directed to self, then others, then strangers) increased positive emotions, mindfulness, feelings of purpose in life and social support, and decreased illness symptoms. Pace, Negi and Adame (2008) found that compassion meditation (for six weeks) improved immune function and neuroendocrine and behavioural responses to stress. Rockliff, Gilbert, McEwan, Lightman and Glover (2008) found that compassionate imagery increased heart rate variability and reduced cortisol in low self-critics, but not in high self-critics.

In our recent fMRI study we found that self-criticism and self-reassurance to imagined threatening events (e.g., a job rejection) stimulated different brain areas, with self-compassion but not self-criticism stimulating the insula—a brain area associated with empathy (Longe et al., 2010). Viewing sad faces, neutrally or with a compassionate attitude, influences neurophysiological responses to faces (Ji-Woong et al., 2009). In a small uncontrolled study of people with chronic mentalhealth problems, compassion training significantly reduced shame, self-criticism, depression and anxiety (Gilbert & Procter, 2006). Compassion training has also been found to be helpful for psychotic voice hearers (Mayhew & Gilbert, 2008). In a study of group-based CFT for 19 clients in a high-security psychiatric setting, Laithwaite et al. (2009) found “…a large magnitude of change for levels of depression and self-esteem…. A moderate magnitude of change was found for the social comparison scale and general psychopathology, with a small magnitude of change for shame,…. These changes were maintained at 6-week follow-up”(p. 521).

In the field of relationships and well-being, there is now good evidence that caring for others, showing appreciation and gratitude, having empathic and mentalizing skills, does much to build positive relationships, which significantly influence well-being and mental and physical health (Cacioppo, Berston, Sheridan, & McClintock, 2000; Cozolino, 2007, 2008).

There is increasing evidence that the kind of “self” we try to become will influence our well-being and social relationships, and compassionate rather than self-focused self-identities are associated with the better outcomes (Crocker & Canevello, 2008).

Taken together there are good grounds for the further development of and research into CFT.

Neff (2003a, 2003b) has been a pioneer in studies of self-compassion (see pages 3–4). She has shown that self-compassion can be distinguished from self-esteem and predicts some aspects of well-being better than self-esteem (Neff & Vonk, 2009), and that self-compassion aids in coping with academic failure (Neff, Hsieh, & Dejitterat, 2005; Neely, Schallert, Mohammed, Roberts, & Chen, 2009). Compassionate letter writing to oneself, improves coping with life events and reduces depression (Leary et al., 2007).

As noted, however, Neff’s concepts of compassion are different from the evolutionary and attachment-rooted model outlined here and, as yet, there is no agreed definition of compassion—indeed, the word compassion can have slightly (but important) different meanings in different languages. So, here compassion will be defined as a “mind set”, a basic mentality, and explored in detail in Point 16.

2 A personal journey

My interest in developing people’s capacities for compassion and self-compassion was fuelled by a number of issues:
• First, was a long interest in evolutionary approaches to human behaviour, suffering and growth (Gilbert, 1984, 1989, 1995, 2001a, 2001b, 2005a, 2005b, 2007a, 2007b, 2009a). The idea that cognitive systems tap underlying evolved motivation and emotional mechanisms has also been central to Beck’s cognitive approach (Beck, 1987, 1996; Beck, Emery, & Greenberg, 1985), with a special edition dedicated to exploring the evolutionary-cognitive interface (Gilbert, 2002, 2004).
• Second, evolutionary psychology has focused significantly on the issue of altruism and caring (Gilbert, 2005a) with increasing recognition of just how important these have been in our evolution (Bowlby, 1969; Hrdy, 2009) and now are to our physical and psychological development (Cozolino, 2007) and well-being (Cozolino, 2008; Gilbert, 2009a; Siegel, 2007).
• Third, people with chronic mental-health problems often come from backgrounds of high stress and/ or low altruism and caring (Bifulco & Moran, 1998), backgrounds that significantly affect physical and psychological development (Cozolino, 2007; Gerhardt, 2004; Teicher, 2002).
• Fourth, partly as a consequence of these life experiences, people with chronic and complex problems can be especially, deeply troubled by shame and self-criticism and/ or self-hatred and find it enormously difficult to be open to the kindness of others or to be kind to themselves (Gilbert, 1992, 2000a, 2007a, 2007c; Gilbert & Procter, 2006).
• Fifth, as noted on page 6, when using CBT they would typically say, “I can see the logic of alternative thoughts but I still feel X, or Y. I can understand why I wasn’t to blame for my abuse but I still feel I’m to blame”, or, “I still feel there is something bad about me”.
• Sixth, there is increasing awareness that the way clients are able to think about and reflect on the contents of their own minds (e.g., competencies to mentalize in contrast to being alexithymic) has major implications for the process and focus of therapy (Bateman & Fonagy, 2006; Choi-Kain & Gunderson, 2008; Liotti & Gilbert, in press; Liotti & Prunetti, 2010).
• Last, but not least, is a long personal interest in the philosophies and practices of Buddhism—although I do not regard myself as a Buddhist as such. Compassion practices, such as becoming the compassionate self (see Part 2), may create a sense of safeness that aides the development of mindfulness and mentalizing.

In Buddhist psychology compassion “transforms” the mind.

Logic and emotion

It has been known for a long time that logic and emotion can be in conflict. Indeed, since the 1980s research has shown that we have quite different processing systems in our minds.

One is linked to what is called implicit (automatic) processing, which is non-conscious, fast, emotional, requires little effort, is subject to classical conditioning and self-identify functions, and may generate feelings and fantasies even against conscious desires. This is the system which gives that “felt sense of something”.

This can be contrasted with an explicit (controlled) processing system, which is slower, consciously focused, reflective, verbal and effortful (Haidt, 2001; Hassin, Uleman, & Bargh, 2005).

These findings have been usefully formulated for clinical work (e.g., Power & Dalgleish, 1997) with more complex models being offered by Teasdale and Barnard (1993).

But the basic point is that there is no simple connection of cognition to emotion, and there are different neurophysiological systems underpinning them (Panksepp, 1998).

So, one of the problems linking thinking and feeling (“I know it but I don’t feel it”) can be attributed to (different) implicit and explicit systems coming up with different processing strategies and conclusions.

Cognitive, and many other, therapists and psychologists have not helped matters by using the concept of cognition and information processing interchangeably as if they are the same thing. They are not.

Your computer and DNA—indeed every cell in your body—are information processing mechanisms but I don’t think that they have “cognitions”.

This failure to define what is and is not “a cognition” or “cognitive” in contrast to a motive or an emotion has caused difficulties in this area of research.

Various solutions have been offered to work with the problems of feelings not following cognitions or logical reasoning, such as: needing more time to practise; most change is slow and hard work; more exposure to problematic emotions; identifying “roadblocks” and their functions (Leahy, 2001); a need for a particular therapeutic relationship (Wallin, 2007); or developing mindfulness and acceptance (Hayes, Follette, & Linehan, 2004; Liotti & Prunetti, 2010).

CFT offers an additional position

CFT suggests that there can be a fundamental problem in an implicit emotional system that evolved with mammalian and human caring systems and which gives rise to feelings of reassurance, safeness and connectedness (see Point 6).

The inability to access that affect system is what underpins this problem. Indeed, as noted (page 6), some people can cognitively (logically) generate “alternative thoughts” but hear them in their head as cold, detached or aggressive. There is no warmth or encouragement in their alternative thoughts—the emotional tone is more like cold instruction.

I have found that the idea of feeling (inner) kindness and supportiveness as part of generating alternative “thoughts” is an anathema to them. So, they just cannot “feel” their alternative thoughts and images.

*

Paul Gilbert, Ph.D., is currently a professor of clinical psychology at the University of Derby in the United Kingdom, and director of the Mental Health Research Unit at Derbyshire Mental Health Trust.

*

from

Compassion Focused Therapy

by Paul Gilbert

get it at Amazon.com

***

Authoritative Websites on CFT

Centre for Mindful Self Compassion

Mindful Self Compassion for Teens

Chris Germer

Mindful.org

The Mindfulness

The Compassion

Center For Healthy Minds

Mindfulness Research

Mindfulness Exercises

Compassionate Living

Foundation For Active Compassion

Mindsight Institute

Center For Nonviolent Communication

Awareness In Action

Center for Compassion and Altruism Research and Education

Greater Good: The Science of a Meaningful Life

Charter For Compassion

Compassionate Mind Foundation

Christopher Germer, PhD, Author of The Mindful Path to Self-Compassion

Mindful Awareness Research Center at University of California Los Angeles

University of Massachusetts Center for Mindfulness

Institute for Meditation and Psychotherapy

University of California at San Diego Center for Mindfulness

Mind And Life Institute

Centre for Mindfulness Research and Practice

Mindfulness page maintained by David Fresco

Mindfulness page maintained by Christopher Walsh

Center for Contemplative Mind in Society

Wellspring Institute for Neuroscience and Contemplative Wisdom

Centre for Mindfulness Studies

Recommended Reading:

  • Highly Recommended: Germer, C. K. (2009). The mindful path to self-compassion: Freeing yourself from destructive thoughts and emotions.New York: Guilford Press.
  • Bennett-Goleman, T. (2001). Emotional alchemy: How the mind can heal the heart.New York: Three Rivers Press.
  • Brach, T. (2003) Radical Acceptance: Embracing your life with the heart of a Buddha. New York: Bantam.
  • Brown, B. (1999). Soul without shame: A guide to liberating yourself from the judge within. Boston: Shambala.
  • Brown, B. (2010). The Gifts of Imperfection. Center City, MN: Hazelden.
  • Feldman, C. (2005). Compassion: Listening to the cries of the world.Berkeley: Rodmell Press.
  • Gilbert, P. (2009). The compassionate mind. London: Constable.
  • Goldstein, E. (2015). Uncovering Happiness: Overcoming Depression with Mindfulness and Self-Compassion. New York: Simon & Schuster.
  • Goldstein, J., & Kornfield, J. (1987). Seeking the heart of wisdom: The path of insight meditation. Boston: Shambhala.
  • Hanh, T. N. (1997). Teachings on love.Berkeley, CA: Parallax Press.
  • Kornfield, J. (1993). A path with heart.New York: Bantam Books.
  • Marlowe, S. (2016). My new best friend. Summerville, MA: Wisdom Publications.
  • Rosenberg, M. (2003). Nonviolent Communication: A Language of Life.Encinitas, CA: Puddledancer Press.
  • Salzberg, S. (1997). Lovingkindness: The revolutionary art of happiness.Boston: Shambala.
  • Salzberg, S. (2005). The force of kindness: change your life with love and compassion. Boulder, CO: Sounds True.

Out Of The Woods. Sir Arthur Williams. A hidden life of Depression and Abuse – Cherie Howie.

In the high-powered, ­influential world he spent much of his adult life, Sir ­Arthur Williams was charming and generous.

Another Sir – Robert Muldoon – was among those the married entrepreneur brought home to his family of five children. The then Finance Minister watched across the dinner table as Sir Arthur, smiling and laughing, told stories.

Also at the table was Sir Arthur’s middle child, Brent Williams.

The scene, repeated whenever the property developer philanthropist brought colleagues, church leaders, businessmen – and future Prime Ministers – to the family home in Karori was confusing and intriguing for those close to him.

“I would just sit in awe. I would just sit there thinking: ‘Who is this other man?’ He was so different, he was animated, he was fun,” ­Williams tells the Herald on Sunday.

When his father, who died at 73 in 2001, came home without guests, things were very different.

“We were physically prepared, we were verbally prepared, before he arrived. We sort of ran around like headless chickens, trying to make sure everything was perfect.”

A light left on was enough to spark his father’s rage. He would scream and shout about the waste of electricity. If all the lights were off, he’d find something else. Williams learned to hide in corners and hide under the bed from a young age.

Sir Arthur went into the ­construction business after emigrating from the United Kingdom in the late 1940s. He was later responsible for building dozens of commercial buildings in Wellington, used Valium to get through the day and tranquilisers to get through the night, Williams says.

He took all the stress in his life out on his family. “From as early as I can remember it wasn’t a case of ‘Yay, Dad’s home.’ You’d go into a state of anxiety. What was going to happen?

“There was every form of abuse, in different ways, in different forms, in different levels, but every form of violence was carried out.”

It took decades for Williams to understand the awful toll his ­childhood took.

Despite a successful career and becoming the proud dad of four children, he broke down in his late 40s.

Now he has written an ­innovative graphic novel-style memoir to help others chart their way back from depression. He hopes it will help others struggling to find their way back to health, and also lay his own ghosts to rest.

Arthur imposed his will on everything his family did – from the partners they chose, to the subjects they took at school. He even took ownership of their dreams.

“My father wanted me to be a lawyer. He told me, since the age of 5: ‘Brent’s going to be a lawyer.’ And I believed that.”

Williams went to law school, but another man with a large presence and a powerful voice lit the spark that would become his life’s work – helping the vulnerable.

“This wonderful big man came and gave a guest lecture one day and told me what he was doing with his practice in Mangere and it ­totally inspired me.

“That man was David Lange.”

The community law movement was gaining traction overseas and Williams realised he wanted to work not in a traditional legal way, but by offering people legal ­resources.

His father didn’t approve but, with law student friends, ­Williams set up a community law centre in Wellington in 1981.

They helped street kids, tenants’ groups and victims of domestic abuse and child abuse.

Later, he took his skills to the Legal ­Resources Trust and the Family Court.

But although he walked among the vulnerable, he did not count himself among their ranks.

“My work was totally my life ­experience. There was a lot of ­anger there that I was able to vent in a very constructive way by being an advocate for people who were ­vulnerable.

“But in a way it totally hid the fact that I was actually vulnerable and I’d experienced this. It was really weird to think that I was making videos that were very much based on my personal story, but I was ­totally unaware of it.”

His work revealed to him the truth he had been fighting to hide.

Williams was stressed and ­exhausted and being hard on the photographers trying to capture an image he was obsessed with – a child hiding under a bed as his ­parents screamed and shouted at each other.

“I had no awareness that it was me. Then I was getting the publication reviewed and … the woman, she just stopped and looked at me and said, ‘Now, Brent, what has brought you to this?’

“I just started crying, and that was the start of my journey.”

The first decade of the 21st ­century was coming to a close and ­Williams was about to crash. He’d been fighting it for a while – refusing to accept he was depressed. Eventually, he had to give up work.

His journey back to health would be long.

Almost a decade on, ­Williams holds firm to routines that keep him well.

But in those dark ­early days, putting his thoughts in writing was a first step, which ­eventually turned into his book.

“As time went on and I got a bit stronger, when I was partly ­acknowledging that I had this illness called depression and ­anxiety, I started doing some ­research and I started writing more, my writing had shifted from being more personal to trying to ­understand the illness.

Because of Williams’ job producing ­material to help people, it felt ­natural to get into writing a book.

“I didn’t start off writing a book. I was literally just writing to help ­myself.”

The result – Out of the Woods, out on September 19 – is as honest as it is simply told.

Williams tells his story ­entirely through 700 watercolour ­illustrations by Turkish ­artist ­Korkut Oztekin – from his ­realisation something was wrong to finding his way back to health, and the setbacks along the way.

Williams says he always knew his book had to be in pictures.

“When I was depressed I couldn’t take on board information or advice from people. I certainly couldn’t read good advice – and I think there’s a lot of good advice out there.”

Each illustration chronicles his battle to accept his illness and how he became well – neither one a neatly linear experience.

Some events are condensed – a panic ­attack over a baked beans purchase came from several events, one of which did involve buying beans.

“It’s faithful to the feelings I had. The brain is struggling so much that a simple decision becomes overwhelming and then something else can spark it – a noise, a bump, an ­unfriendly interaction.”

Other experiences are more ­palpably dark.

In one scene ­Williams, in his mid-teens, is the victim of sexual abuse – which he didn’t report to police, and didn’t plan to.

“I felt the guilt of it for so many years and here I am writing about it and still protecting him to some extent … I feel comfortable with how I’ve dealt with it.

“I don’t want to stir his reaction and I don’t really want to hurt ­anybody that doesn’t need to be hurt. It’s what happened and I’ve forgiven him.”

The book helped him forgive both the man, and his own father, Williams says.

Intially, Sir Arthur did not feature in the book. A question from his therapist changed Williams’ mind.

“She just quietly posed the question: ‘Why isn’t he in there and why won’t you talk about that event that had such a big impact on your life?’

“I went home and picked up my pen and it all came out. Draft two was a very different story.”

It was the right decision, he says.

“Without my father it wouldn’t have been a personal book. It would’ve been a story of a person pretending to be well and trying to tell other people what they should do. A pretty, clean, self-help book.

“From then on I knew it had to be very faithful to my journey, my ­inner emotional journey, my ­history, my experiences and it had to really be honest about what got me well.”

The unusual style is winning plaudits from mental health ­experts at home as well as at Stanford University in the US and ­Oxford University in the UK.

Dr Ben Beaglehole, from ­Otago University’s Department of ­Psychological Medicine, wrote the book could provide an “invaluable lifeline to those experiencing ­depression”.

For Williams, though, the ­backing of those closest to him is the most powerful validation.

“My mum, she said: ‘Write what you need to say – it needs to be said.’

“My younger sister just said, ‘Let the crows fly.’ When my mum read it, it was very emotional. She just gave me a big hug and said, ‘I love you. Thank you for writing.”

Williams still dreams about his dad, and it’s frightening, he says.

But he also thinks his dad would be proud of him for doing something that gave him back his life.

It was something Sir Arthur ­never achieved. Late in life, he struggled to get off prescription drugs and, in a single, unexpected conversation with his son, he expressed regret.

“He said, ‘I’ve filled my life with a whole lot of useless things.’ Even though he’d achieved so much building, he realised his life was not what he really wanted. In a way, I can say he would be proud of me doing something that got me well.”

Like all of us, Williams is still a work in progress.

He is well, but he has to work at it. Routine is his best friend.

“I go to the pool most mornings. I eat well, I sleep well. I’m careful about who I’m around and I go to therapy and if I do all that I’m really well and I can really see so much joy in life.”

His dad might still come to him in the night, but the rest of his life feels like when you wake from a bad dream, pull back the curtains and let sunlight flood the room.

“It’s really wonderful. Sometimes I’m sort of bursting in what I see in life – the colours, the people, smiles, little children.

“It’s just fantastic and it’s so different to a life that I was hiding from.”

NZ Herald

Out Of The Woods website. 

get it from Amazon.com

***

WHERE TO GET HELP

The following free helplines operate 24/7:

DEPRESSION HELPLINE: 0800 111 757

LIFELINE: 0800 543 354

NEED TO TALK? Call or text 1737

SAMARITANS: 0800 726 666

YOUTHLINE: 0800 376 633 or text 234

* If you need immediate help contact the police on 111.

FAMILY VIOLENCE – WHERE TO GET HELP

If you’re in danger now:

• Phone the police on 111 or ask neighbours of friends to ring for you.

• Run outside and head for where there are other people.

• Scream for help so your neighbours can hear you.

• Take the children with you.

• Don’t stop to get anything else.

• If you are being abused, remember it’s not your fault. Violence is never okay

Where to go for help or more information:

• Women’s Refuge: Free national crisis line operates 24/7 – 0800 refuge or 0800 733 843 www.womensrefuge.org.nz

• Shine, free national helpline 9am- 11pm every day – 0508 744 633 www.2shine.org.nz

• It’s Not Ok: Information line 0800 456 450 www.areyouok.org.nz

• Shakti: Providing specialist cultural services for African, Asian and middle eastern women and their children. Crisis line 24/7 0800 742 584 • Ministry of Justice: www.justice.govt.nz/family-justice/domestic-violence

• National Network of Stopping Violence: www.nnsvs.org.nz

• White Ribbon: Aiming to eliminate men’s violence towards women, focusing this year on sexual violence and the issue of consent. www.whiteribbon.org.nz

 

A Chance Discovery May Lead to a Vaccine for Depression and PTSD – Robby Berman. 

“Fortune favors the prepared mind.” Louis Pasteur. 

“It is possible that 20, 50, 100 years from now, we will look back at depression and PTSD the way we look back at tuberculosis sanatoriums as a thing of the past. This could be the beginning of the end of the mental health epidemic.” Rebecca Brachman.

Calypsol: it seems it had somehow inoculated the laboratory mice against the effects of stress.

For the over 16 million people in the U.S. each year with severe depression and the 8 million sufferers yearly of post-traumatic stress disorder (PTSD), Brachman’s accidental discovery may result in medicine that can prevent the debilitating responses to trauma or severe stress. It’s at the very least likely to change the way many think of and talk about mental illness.

BigThink

What the 21st century can learn from the 1929 crash – Larry Elliott. 

As the summer of 1929 drew to a close, the celebrated Yale university economist Irving Fisher took to the pages of the New York Times to opine about Wall Street. Share prices had been rising all year; investors had been speculating with borrowed money on the assumption that the good times would continue. It was the bull market of all time, and those taking a punt wanted reassurance that their money was safe.

Fisher provided it for them, predicting confidently: “Stock markets have reached what looks like a permanently high plateau.” On that day, the Wall Street Crash of October 1929 was less than two months away. It was the worst share tip in history. Nothing else comes close.

The crisis broke on Thursday 24 October, when the market dropped by 11%. Black Thursday was followed by a 13% fall on Black Monday and a further 12% tumble on Black Tuesday. By early November, Fisher was ruined and the stock market was in a downward spiral that would only bottom out in June 1932, at which point companies quoted on the New York stock exchange had lost 90% of their value and the world had changed utterly.

The Great Crash was followed by the Great Depression, the biggest setback to the global economy since the dawn of the modern industrial age in the middle of the 18th century. Within three years of Fisher’s ill-judged prediction, a quarter of America’s working population was unemployed and desperate. As the economist JK Galbraith put it: “Some people were hungry in 1930, 31 and 32. Others were tortured by the fear that they might go hungry.”

Banks that weren’t failing were foreclosing on debtors. There was no welfare state to cushion the fall for those such as John Steinbeck’s Okies – farmers caught between rising debts and crashing commodity prices. One estimate suggests 34 million Americans had no income at all. By mid-1932, the do-nothing approach of Herbert Hoover was discredited and the Democrat Franklin Roosevelt was on course to become US president.

Across the Atlantic, Germany was suffering its second economic calamity in less than a decade. In 1923, the vindictive peace terms imposed by the Treaty of Versailles had helped to create the conditions for hyperinflation, when one dollar could be exchanged for 4.2 trillion marks, people carted wheelbarrows full of useless notes through the streets, and cigarettes were used as money. In 1932, a savage austerity programme left 6 million unemployed.

Germany suffered as the pound fell and rival British exports became cheaper. More than 40% of Germany’s industrial workers were idle and Nazi brownshirts were fighting communists for control of the streets. By 1932, the austerity policies of the German chancellor Heinrich Brüning were discredited and Adolf Hitler was on course to replace him.

Timeline of turmoil

It would be wrong to think nobody saw the crisis coming. Fisher’s prediction may well have been a riposte to a quite different (and remarkably accurate) prediction made by the investment adviser Roger Babson in early September 1929. Babson to the US National Business Conference that a crash was coming and that it would be a bad one. “Factories will shut down,” Babson predicted, “men will be thrown out of work.” Anticipating how the slump would feed on itself, he warned: “The vicious cycle will get in and the result will be a serious business depression.”

Cassandras are ignored until it is too late. And Babson, who had form as a pessimist, was duly ignored. The Dr Doom of the 2008 crisis, New York University Nouriel Roubini, suffered the same fate.

F Scott Fitzgerald described the Great Crash as the moment the jazz age dived to its death. It marked the passing of a first age of globalisation that had flourished in the decades before the first world war with free movements of capital, freedom and – to a lesser extent – goods. In the decade or so after the guns fell silent in 1918, policymakers had been trying to re-create what they saw as a golden period of liberalism. The Great Depression put paid to those plans, ushering in, instead, an era of isolationism, protectionism, aggressive nationalism and totalitarianism. There was no meaningful recovery until nations took up arms again in 1939.

In Britain, recovery was concentrated in the south of England and too weak to dent ingrained unemployment in the old industrial areas. The Jarrow march for jobs took place in 1936, seven years after the start of the crisis. It was a similar story in the US, where a recovery during Roosevelt’s first presidential term ended in a second mini-slump in 1937. Sir Winston Churchill, who lost a packet in the Crash, described the period 1914 to 1945 as the second 30 years’ war.

Only one other financial meltdown can compare to the Wall Street Crash for the length of its impact: the one that hit a climax with the bankruptcy of Lehman Brothers in September 2008. Without the Great Depression, there would have been no New Deal and no Keynesian revolution in economics. Roosevelt might never have progressed beyond the New York governor’s mansion in Albany. Hitler, whose political star was on the wane by the late 1920s, would have been a historical footnote .

Similarly, without the long-lingering effects of the 2008 crash, there would have been no Brexit, Donald Trump would still be a New York City builder and Europe would not be quaking at the possibility of Marine Le Pen replacing François Hollande as French president.

Not since the 1930s have there been such acute fears of a populist backlash against the prevailing orthodoxy. As then, a prolonged period of poor economic performance has led to a political reaction that looks like feeding back into a desire for a different economic approach. The early 30s share with the mid-2010s a sense that the political establishment has lost the confidence of large numbers of voters, who have rejected “business as usual” and backed politicians they see as challenging the status quo.

Trump is not the first president to urge an America-first policy: Roosevelt was of a similar mind after he replaced Herbert Hoover in 1933. Nor is this the first time there has been such a wide gulf between Wall Street and the rest of the country. The loathing of the bankers in the 20s hardened into a desire for retribution in the 30s.
According to Lord Robert Skidelsky, biographer of John Maynard Keynes: “We got into the Great Depression for the same reason as in 2008: there was a great pile of debt, there was gambling on margin on the stock market, there was over-inflation of assets, and interest rates were too high to support a full employment level of investment.”

There are other similarities. The 20s had been good for owners of assets but not for workers. There had been a sharp increase in unemployment at the start of the decade and labour markets had not fully recovered by the time an even bigger slump began in 1929. But while employees saw their slice of the economic cake get smaller, for the rich and powerful, the Roaring Twenties were the best of times. In the US, the halving of the top rate of income tax to 32% meant more money for speculation in the stock and property markets. Share prices rose sixfold on Wall Street in the decade leading up to the Wall Street Crash.

Inequality was high and rising, and demand only maintained through a credit bubble. Unemployment between 1921 and 1929 averaged 8% in the US, 9% in Germany and 12% in Britain. Labour markets had never really recovered from a severe recession at the start of the 20s designed to stamp out a post-war inflationary boom.

Above all, in both periods global politics were in flux. From around 1890, the balance of power between the great European nations that had kept the peace for three quarters of a century after the battle of Waterloo in 1815 started to break down. The Ottoman and Austro-Hungarian empires were in decline before the first world war; the US, Germany and Russia were on the rise.

More importantly, Britain, which had been the linchpin of late 19th-century globalisation had been weakened by the first world war and was no longer able to provide the leadership role. America was not yet ready to take up the mantle.

Stephen King, senior economic adviser to HSBC and author of a forthcoming book on the crisis of globalisation, Grave New World, says: “There are similarities between now and the 1920 and 1930s in the sense that you had a declining superpower. Britain was declining then and the US is potentially declining now.”

King says that in the 20s, the idea of a world ruled by empires was crumbling. Eventually, the US did take on Britain’s role as the defender of western values, but not until the 40s, when it was pivotal in both defeating totalitarianism and in creating the economic and political institutions – the United Nations, the International Monetary Fund, the World Bank – that were designed to ensure the calamitous events of the 30s never happened again.

“There are severe doubts about whether the US is able or willing to play the role it played in the second half of the 20th century, and that’s worrisome because if the US is not playing it, who does? If nobody is prepared to play that role, the question is whether we are moving towards a more chaotic era.”

Deflationary Disaster
There are, of course, differences as well as similarities between the two epochs. At this year’s meeting of the World Economic Forum in Davos, Switzerland, held in the week of Trump’s inauguration, members of the global business elite found reasons to be cheerful.

Some took comfort from technology: the idea that Facebook, Snapchat and Google have shrunk the world. Others said slapping tariffs on imported goods in an era of complex international supply chains would push up the cost of exports and make it unthinkable even for a country as big as the US to adopt a go-it-alone economic strategy. Roberto Azevêdo, managing director of the World Trade Organisation said: “The big difference between the financial crisis of 2008 and the early 1930s is that today we have multilateral trade rules, and in the 30s we didn’t.”

The biggest difference between the two crises, however, is that in the early 1930s blunders by central banks and finance ministries made matters a lot worse than they need have been. Not all stock market crashes morph into slumps, and one was avoided – just about – in the period after the collapse of Lehman Brothers.

Early signs from data for industrial production and world trade in late 2008 showed declines akin to those during the first months of the Great Depression. Policymakers have been rightly castigated for being asleep at the wheel while the sub-prime mortgage crisis was gestating, but knowing some economic history helped when Lehman Brothers went bust. In the early 30s, central banks waited too long to cut interest rates and allowed deflation to set in. There was a policy of malign neglect towards the banks, which were allowed to go bust in droves. Faced with higher budget deficits caused by higher unemployment and slower growth, finance ministers made matters worse by raising taxes and cutting spending.

The response to the Crash, according to Adam Tooze in his book The Deluge, was deflationary policies were pursued everywhere. “The question that critics have asked ever since is why the world was so eager to commit to this collective austerity. If Keynesian and monetarist economists can agree on one thing, it is the disastrous consequences of this deflationary consensus.”

At the heart of this consensus was the gold standard, the strongly held belief that it should be possible to exchange pounds, dollars, marks or francs for gold at a fixed exchange rate. The system had its own automatic regulatory process: if a country lived beyond its means and ran a current account surplus, gold would flow out and would only return once policy had been tightened to reduce imports.

After concerted efforts by the Bank of England and the Treasury, Britain returned to the gold standard in 1925 at its pre-war parity of $4.86. This involved a rise in the exchange rate that made life more difficult for exporters.

What the policymakers failed to realise was that the world had moved on since the pre-1914 era. Despite being on the winning side, Britain’s economy was much weaker. Germany’s economy had also suffered between 1914 and 1918, and was further hobbled by reparations. America, by contrast, was in a much stronger position.

This changing balance of power meant that restoring the pre-war regime was a long and painful process, and by the late 20s the strains of attempting to do so were starting to become unbearable in just the same way as the strains on the euro – the closest modern equivalent to the gold standard – have become evident since 2008.

Instead of easing off, policymakers in the early stages of the Great Depression thought the answer was to redouble their efforts. Peter Temin, an economic historian, compares central banks and finance ministries to the 18th-century doctors who treated Mozart with mercury: “Not only were they singularly ineffective in curing the economic disease; they also killed the patient.”

Skidelsky explains that in Britain, the so-called “automatic stabilisers” kicked in during the early stages of the crisis. Tax revenues fell because growth was weaker while spending on unemployment benefits rose. The public finances fell into the red.

Instead of welcoming the extra borrowing as a cushion against a deeper recession, the authorities took steps to balance the budget. Ramsay MacDonald’s government set up the May committee to see what could be done about the deficit. Given the membership, heavily weighted in favour of businessmen, the outcome was never in doubt: sterling was under pressure and in order to maintain Britain’s gold standard parity, the May committee recommended cuts of £97m from the state’s £885m budget. Unemployment pay was to be cut by 30% in order to balance the budget within a year.
The severity of the cuts split the Labour government and prompted the formation of a national government led by MacDonald. Philip Snowden, the chancellor, said the alternative to the status quo was “the Deluge”. Financial editors were invited to the Treasury to be briefed on measures being taken to protect the pound, and when one asked whether Britain should or could stay on the gold standard, the Treasury mandarin Sir Warren Hastings rose to his feet and thundered: “To suggest we should leave the gold standard is an affront not only to the national honour, but to the personal honour of every man or woman in the country.”

The show of fiscal masochism failed to prevent fresh selling of the pound, and eventually the pressure became unbearable. In September 1931, Britain provided as big a shock to the rest of the world as it did on 23 June 2016, by coming off the gold standard.

The pound fell and the boost to UK exports was reinforced six months later when the coalition government announced a policy of imperial preference, the erection of tariff barriers around colonies and former colonies such as Australia and New Zealand.

Britain was not the first country to resort to protectionism. The now infamous Smoot-Hawley tariff had been announced in the US in 1930. But America had a recent history of protectionism – it had built up its manufacturing strength behind a 40% tariff in the second half of the 19th century. Britain, as Tooze explains, had been in favour of free trade since the repeal of the corn laws in 1846. 

“Now it was responsible for initiating the death spiral of protectionism and beggar-thy-neighbour currency wars that would tear the global economy apart.”

Britain’s 1931 exit from the gold standard meant it secured first-mover advantage over its main rivals. For Germany, the pain was especially severe, since the country’s mountain of foreign debt ruled out devaluation and left Chancellor Brüning’s government with the choice between default and deflation. Brüning settled for another round of austerity, not realising that for voters there was a third choice: a party that insisted that national solutions were the answer to a broken international system.
The reason borrowing costs were slashed in 2008 is that central bankers knew their history. Ben Bernanke, then chairman of America’s Federal Reserve, was a student of the Great Depression and fully acknowledged that his institution could not afford to make the same mistake twice. Interest rates were cut to barely above zero; money was created through the process known as quantitative easing; the banks were bailed out; Barack Obama pushed a fiscal stimulus programme through Congress.

But the policy was only a partial success. Low interest rates and quantitative easing have averted Great Depression 2.0 by flooding economies with cheap money. This has driven up the prices of assets – shares, bonds and houses – to the benefit of those who are rich or comfortably off.

For those not doing so well, it has been a different story. Wage increases have been hard to come by, and the strong desire of governments to reduce budget deficits has resulted in unpopular austerity measures. Not all the lessons of the 1930s have been well learned , and the over-hasty tightening of fiscal policy has slowed growth and caused political alienation among those who feel they are being punished for a crisis they did not create, while the real villains get away scot-free . A familiar refrain in both the referendum on Brexit and the 2016 US presidential election was: there might be a recovery going on, but it’s not happening around here.

Authoritarian solutions

Internationalism died in the early 30s because it came to be associated with discredited policies: rampant speculation, mass unemployment, permanent austerity and falling living standards.

Totalitarian states promoted themselves as alternatives to failed and decrepit liberal democracies. Hitler’s Germany was one, Stalin’s Soviet Union another. While the first era of globalisation was breaking up, Moscow was pushing ahead with the collectivisation of agriculture and rapid industrialisation.

What’s more, the economic record of the totalitarian countries in the 30s was far superior to that of the liberal democracies. Growth averaged 0.3% a year in Britain, the US and France, compared with 3.1% a year in Germany, Italy, Japan and the Soviet Union.

Erik Britton, founder of the consultancy Fathom , says: “The 1920s saw the failure of liberal free-trade, free-market policies to deliver stability and growth. Alternative people came along with a populist stance that really worked, for a while.”

There is, Britton says, a reason mainstream parties are currently being rejected: “It is not safe to assume you can deliver unsatisfactory economic outcomes for a decade without a political reaction that feeds back into the economics.”

Economic devastation caused by the Great Depression did eventually force western democracies into rethinking policy. The key period was the 18 months between Britain coming off the gold standard in September 1931 and Roosevelt’s arrival in the White House in March 1933.

Under Hoover, US economic policy had been relentlessly deflationary. As in Germany – the other country to suffer most grievously from the Depression – there was a dogged insistence on protecting the currency and on balancing the budget.

The Great Depression ushered in isolationism, protectionism, aggressive nationalism and totalitarianism

That changed under FDR. Policy became both more interventionist and more isolationist. If London could adopt a Britain-first policy, then so could Washington. Roosevelt swiftly took the dollar off the gold standard and scuppered attempts to prevent currency wars. Wall Street was reined in; fiscal policy was loosened. But it was too late. By then, Hitler was chancellor and tightening his grip on power. Ultimately, the Depression was brought to an end not by the New Deal, but by war.

King says the world is already starting to become more protectionist in terms of movement of capital and labour. Trump has been naming and shaming US companies seeking to take advantage of cheaper labour in the emerging countries, while Brexit is an example of the idea that migration needs to be controlled.

The US supported the post-war global instutional framework: the UN, IMF and European Union, through the Marshall Plan. “It tried to create a framework in which individual countries could flourish,” King adds. “But I don’t see that [happening again] in the future, which creates difficulties for the rest of the world.”

So far, financial markets have taken a positive view of Trump. They have concentrated on the growth potential of his plans for tax cuts and higher infrastructure spending, rather than his threat to build a wall along the Rio Grande and to slap tariffs on Mexican and Chinese imports.

There is, though, a darker vision of the future, where every country tries to do what Trump is doing. In this scenario, a shrinking global economy leads to shrinking global trade, and deflation means personal debts become more onerous. “It becomes a vicious, self-fulfilling cycle,” Britton says. “People seek answers and find it in authoritarianism, populism and protectionism. If one country can show it works, there is a strong temptation for others to follow suit.”

This may prove too pessimistic. The global economy is growing by around 3% a year; Britain and the US (if not the eurozone) have seen unemployment halve since the 2008-09 crisis; low oil prices have kept inflation low and led to rising living standards.

Even so, it is not hard to see why support for the policy ideas that have driven the second era of globalisation – free movement of capital, goods and people – has started to fracture. The winners from the liberal economic system that emerged at the end of the cold war have, like their forebears in the 20s, failed to look out for the losers. A rising tide has not lifted all boats, and those who do not consider themselves the beneficiaries of globalisation have grown weary of hearing how marvellous it is.

The 30s are proof that nothing in economics is inevitable. There was eventually a backlash against the economic orthodoxies and Skidelsky can see why there is another backlash happening today. “Globalisation enables capital to escape national and union control. I am much more sympathetic since the start of the crisis to the Marxist way of analysing things.

“Trump will be impeached, assassinated or frustrated by Congress,” Skidelsky suggests. “Or he will remain popular enough to overcome the liberal consensus that he is a shit of the first order. After all, a lot of people agree with what he is doing.”

The Guardian

Depression is. . . 

A series of behaviours, motivated by strong emotions, that result in a person being stuck in a deeply painful, hopeless mood state. This leads to withdrawal, isolation, and an overwhelming sense of hopelessness.

People experiencing depression generally believe themselves to be worthless, and the future to be a long, never-ending continuation of the misery they now feel. It results in an inability to feel pleasure, or enjoyment.

Kyle MacDonald, Psychotherapist. 

How to identify signs of depression. 

Despite all the attention depression receives these days, it’s really hard to spot sometimes. Depression is not “having a bad day”, and it’s also not an emotion: It’s no more possible to be a “little bit depressed” than it is to be a little bit pregnant.

And it’s not uncommon for people feeling depressed to hide it from others, often with a high level of success. People often talk of putting on a “mask”, and how painful and excruciating that can be.

That can make it really hard for friends and family to know what’s going on. Don’t worry, it’s not personal, the nature of depression means the person suffering feels they have to hide how they feel.

Depression also isn’t an “illness”, in the same sense as the flu, or diabetes. At the risk of being really picky, I’m not even comfortable with the phrase “having depression”, I think “experiencing depression” is more helpful.

Why? It’s important from the point of view of expectations: studies have shown that when people are told their depression is due to a “chemical imbalance in their brain” they report less hope and faith in any treatment being able to help them.

Nz Herald

My Fight to Speak with the Enemy

Hi Everyone,

My name is Rob Ah Chong. I am a New Zealand born Samoan. On Dec 10, I have challenged myself to take part for the first time in a corporate boxing fight. My Purpose for this challenge is to raise the awareness on mental illness and encourage People, Family and Friends especially within our culture to speak about it. Everyday Hero

James Reardon: Let’s talk about suicide

Why is New Zealand’s most serious, persistent health problem banished to the coroner’s files?

It prevents nothing, but promotes the myth that suicide is a mysterious, fatal disease that is never talked about, even after death. NZ Herald 

‘Today I’m going back on my antidepressants’

I weaned myself off anti-depressants about 18 months ago. After six years, I wanted to see if I was able to manage my depression naturally. I was in a safe and happy place in my life and trusted that I would have all of the support I needed to help me on that journey.

 I feel like I know myself really well now and that’s really important to me. And that’s also why I have chosen to go back on my medication.

For the most part, life has been really good. Day to day, I can’t really complain outside the usual stresses of family life. I’m mostly happy.

But man, I’m tired. The Spinoff