Category Archives: Mental Health

CHILDHOOD TRAUMA AND MENTAL ‘ILLNESS’. Beyond the smoke – Johann Hari.

Depression isn’t a disease; depression is a normal response to abnormal life experiences.

The medical team, and all their friends, expected these people, who had been restored to health to react with joy. Except they didn’t react that way. The people who did best, and lost the most weight were often thrown into a brutal depression, or panic, or rage. Some of them became suicidal.

Was there anything else that happened in your life when you were eleven? Well, Susan replied that was when my grandfather began to rape me.

“Overweight is overlooked, and that’s the way I need to be.”

What we had perceived as the problem, major obesity, was in fact, very frequently, the solution to problems that the rest of us knew nothing about. Obesity, he realized, isn’t the fire. It’s the smoke.

For every category of traumatic experience you go through as a kid, you are radically more likely to become depressed as an adult. The greater the trauma, the greater your risk of depression, anxiety, or suicide.

Emotional abuse especially, is more likely to cause depression than any other kind of trauma, even sexual molestation. Being treated cruelly by your parents is the biggest driver of depression, out of all these categories.

We have failed to see depression as a symptom of something deeper that needs to be dealt with. There’s a house fire inside many of us, and we’ve been concentrating on the smoke.

When the women first came into Dr. Vincent Felitti’s office some of them found it hard to fit through the door. These patients weren’t just a bit overweight: they were eating so much that they were rendering themselves diabetic and destroying their own internal organs. They didn’t seem to be able to stop themselves. They were assigned here, to his clinic, as their last chance.

It was the mid-1980s, and in the California city of San Diego, Vincent had been commissioned by the not-for-profit medical provider Kaiser Permanente to look into the fastest-growing driver of their costs, obesity. Nothing they were trying was working, so he was given a blank sheet of paper. Start from scratch, they said. Total blue-sky thinking. Figure out what we can do to deal with this. And so the patients began to come. But what he was going to learn from them led, in fact, to a major breakthrough in a very different area: how we think about depression and anxiety.

As he tried to scrape away all the assumptions that surround obesity, Vincent learned about a new diet plan based on a maddeningly simple thought. It asked: What if these severely overweight people simply stopped eating, and lived off the fat stores they’d built up in their bodies until they were down to a normal weight? What would happen?

In the news, curiously, there had recently been an experiment in which this was tried, eight thousand miles away, for somewhat strange reasons. For years in Northern Ireland if you were put in jail for being part of the Irish Republican Army’s violent campaign to drive the British out of Northern Ireland, you were classed as a political prisoner. That meant you were treated differently from people who committed (say) bank robberies. You were allowed to wear your own clothes, and you didn’t have to perform the same work as other inmates.

The British government decided to shut down that distinction, and they argued that the prisoners were simply common criminals and shouldn’t get this different treatment anymore. So the prisoners decided to protest by going on a hunger strike. They began, slowly, to waste away.

So the designers of this new diet proposal looked into the medical evidence about these Northern Ireland hunger strikers to find out what killed them. It turns out that the first problem they faced was a lack of potassium and magnesium. Without them, your heart stops beating properly. Okay, the radical dieters thought, what if you give people supplements of potassium and magnesium? Then that doesn’t happen. If you have enough fat on you, you get a few months more to live, until a protein deficiency kills you.

Okay, what if you also give people the supplements that will prevent that? Then, it turns out, you get a year to live, provided there’s enough fat. Then you’ll die from a lack of vitamin C, scurvy, or other deficiencies.

Okay, what if you give people supplements for that, too? Then it looks as though you’ll stay alive, Vincent discovered in the medical literature, and healthy, and you’ll lose three hundred pounds a year. Then you can start eating again, at a healthy level.

All this suggested that in theory, even the most obese person would be down to a normal weight within a manageable time. The patients coming to him had been through everything, every fad diet, every shaming, every prodding and pulling. Nothing had worked. They were ready to try anything. So, under careful monitoring, and with lots of supervision, they began this program. And as the months passed, Vincent noticed something. It worked. The patients were shedding weight. They were not getting sick, in fact, they were returning to health. People who had been rendered disabled by constant eating started to see their bodies transform in front of them.

Their friends and relatives applauded. People who knew them were amazed. Vincent believed he might have found the solution to extreme overweight. “I thought my god, we’ve got this problem licked,” he said.

And then something happened that Vincent never expected.

In the program, there were some stars, people who shed remarkable amounts of weight, remarkably quickly. The medical team, and all their friends, expected these people who had been restored to health to react with joy. Except they didn’t react that way.

The people who did best, and lost the most weight were often thrown into a brutal depression, or panic, or rage. Some of them became suicidal. Without their bulk, they felt they couldn’t cope. They felt unbelievably vulnerable. They often fled the program, gorged on fast food, and put their weight back on very fast.

Vincent was baffled. They were fleeing from a healthy body they now knew they could achieve, toward an unhealthy body they knew would kill them. Why? He didn’t want to be an arrogant, moralistic doctor, standing over his patients, wagging his finger and telling them they were ruining their lives, that’s not his character. He genuinely wanted to help them save themselves. So he felt desperate. That’s why he did something no scientist in this field had done with really obese people before. He stopped telling them what to do, and started listening to them instead. He called in the people who had panicked when they started to shed the pounds, and asked them: What happened when you lost weight? How did you feel?

There was one twenty-eight-year-old woman, who I’ll call Susan to protect her medical confidentiality. In fifty-one weeks, Vincent had taken Susan down from 408 pounds to 132 pounds. It looked like he had saved her life. Then, quite suddenly, for no reason anyone could see, she put on 37 pounds in the space of three weeks. Before long, she was back above 400 pounds. So Vincent asked her gently what had changed when she started to lose weight. It seemed mysterious to both of them. They talked for a long time. There was, she said eventually, one thing. When she was very obese, men never hit on her, but when she got down to a healthy weight, one day she was propositioned by a man, a colleague who she happened to know was married. She fled, and right away began to eat compulsively, and she couldn’t stop.

This was when Vincent thought to ask a question he hadn’t asked his patients before. When did you start to put on weight? If it was (say) when you were thirteen, or when you went to college, why then, and not a year before, or a year after?

Susan thought about the question. She had started to put on weight when she was eleven years old, she said. So he asked: Was there anything else that happened in your life when you were eleven? Well, Susan replied that was when my grandfather began to rape me.

Vincent began to ask all his patients these three simple questions. How did you feel when you lost weight? When in your life did you start to put on weight? What else happened around that time? As he spoke to the 183 people on the program, he started to notice some patterns. One woman started to rapidly put on weight when she was twenty-three. What happened then? She was raped. She looked at the ground after she confessed this, and said softly: “Overweight is overlooked, and that’s the way I need to be.”

“I was incredulous,” he told me when I sat with him in San Diego. “It seemed every other person I was asking was acknowledging such a history. I kept thinking, it can’t be. People would know if this was true. Somebody would’ve told me. Isn’t that what medical school is for?” When five of his colleagues came in to conduct further interviews, it turned out some 55 percent of the patients in the program had been sexually abused, far more than people in the wider population. And even more, including most of the men, had had severely traumatic childhoods.

Many of these women had been making themselves obese for an unconscious reason: to protect themselves from the attention of men, who they believed would hurt them. Being very fat stops most men from looking at you that way. It works. It was when he was listening to another grueling account of sexual abuse that it hit Vincent. He told me later:

“What we had perceived as the problem, major obesity, was in fact, very frequently, the solution to problems that the rest of us knew nothing about.”

Vincent began to wonder if the anti-obesity programs, including his own, had been doing it all wrong, by (for example) giving out nutritional advice. Obese people didn’t need to be told what to eat; they knew the nutritional advice better than he did. They needed someone to understand why they ate. After meeting a person who had been raped, he told me, “I thought with a tremendously clear insight that sending this woman to see a dietitian to learn how to eat right would be grotesque.”

Far from teaching the obese people, he realized they were the people who could teach him what was really going on. So he gathered the patients in groups of around fifteen, and asked them: “Why do you think people get fat? Not how. How is obvious. I’m asking why. What are the benefits?” Encouraged to think about it for the first time, they told him. The answers came in three different categories. The first was that it is sexually protective: men are less interested in you, so you are safer. The second was that it is physically protective: for example, in the program there were two prison guards, who lost between 100 and 150 pounds each. Suddenly, as they shed their bulk, they felt much more vulnerable among the prisoners, they could be more easily beaten up. To walk through those cell blocks with confidence, they explained, they needed to be the size of a refrigerator.

And the third category was that it reduced people’s expectations of them. “You apply for a job weighing four hundred pounds, people assume you’re stupid, lazy,” Vincent said. If you’ve been badly hurt by the world, and sexual abuse is not the only way this can happen, you often want to retreat. Putting on a lot of weight is, paradoxically, a way of becoming invisible to a lot of humanity.

“When you look at a house burning down, the most obvious manifestation is the huge smoke billowing out,” he told me. It would be easy, then, to think that the smoke is the problem, and if you deal with the smoke, you’ve solved it. But “thank God that fire departments understand that the piece that you treat is the piece you don’t see, the flames inside, not the smoke billowing out. Otherwise, house fires would be treated by bringing big fans to blow the smoke away. [And that would] make the house burn down faster.”

Obesity, he realized, isn’t the fire. It’s the smoke.

One day, Vincent went to a medical conference dedicated to obesity to present his findings. After he had spoken, a doctor stood up in the audience and explained: “People who are more familiar with these matters recognize that these statements by patients describing their sexual abuse, are basically fabrications, to provide a cover for their failed lives. It turned out people treating obesity had noticed before that a disproportionate number of obese people described being abused. They just assumed that they were making excuses.

Vincent was horrified. He had in fact verified the abuse claims of many of his patients, by talking to their relatives, or to law enforcement officials who had investigated them. But he knew he didn’t have hard scientific proof yet to rebut people like this. His impressions from talking to individual patients, even gathering the figures from within his group, didn’t prove much. He wanted to gather proper scientific data. So he teamed up with a scientist named Dr. Robert Anda, who had specialized for years in the study of why people do self-destructive things like smoking. Together, funded by the Center for Disease Control, a major US. agency funding medical research, they drew up a way of testing all this, to see if it was true beyond the small sample of people in Vincent’s program.

They called it the Adverse Childhood Experiences (ACE) Study, and it’s quite simple. It’s a questionnaire. You are asked about ten different categories of terrible things that can happen to you when you’re a kid, from being sexually abused, to being emotionally abused, to being neglected. And then there’s a detailed medical questionnaire, to test for all sorts of things that could be going wrong with you, like obesity, or addiction. One of the things they added to the list, almost as an afterthought, was the question: Are you suffering from depression?

This survey was then given to seventeen thousand people who were seeking health care, for a whole range of reasons, from Kaiser Permanente in San Diego. The people who filled in the form were somewhat wealthier and a little older than the general population, but otherwise fairly representative of the city’s population.

When the results came in, they added them up, at first, to see if there were any correlations.

It turned out that for every category of traumatic experience you went through as a kid, you were radically more likely to become depressed as an adult. If you had six categories of traumatic events in your childhood, you were five times more likely to become depressed as an adult than somebody who didn’t have any. If you had seven categories of traumatic events as a child, you were 3,100 percent more likely to attempt to commit suicide as an adult.

“When the results came out, I was in a state of disbelief,” Dr. Anda told me. “I looked at it and I said, really? This can’t be true.” You just don’t get figures like this in medicine very often. Crucially, they hadn’t just stumbled on proof that there is a correlation, that these two things happen at the same time. They seemed to have found evidence that these traumas help cause these problems. How do we know? The greater the trauma, the greater your risk of depression, anxiety, or suicide. The technical term for this is “dose-response effect.” The more cigarettes you smoke, the more your risk of lung cancer goes up, that’s one reason we know smoking causes cancer. In the same way, the more you were traumatized as a child, the more your risk of depression rises.

Curiously, it turned out emotional abuse was more likely to cause depression than any other kind of trauma, even sexual molestation. Being treated cruelly by your parents was the biggest driver of depression, out of all these categories.

When they showed the results to other scientists, including the Centers for Disease Control (CDC), who cofunded the research, they too were incredulous. “The study shocked people,” Dr. Anda told me. “People didn’t want to believe it. People at the CDC didn’t want to believe it. There was resistance within the CDC when I brought the data around, and the medical journals, initially, didn’t want to believe it, because it was so astonishing that they had to doubt it. Because it made them challenge the way they thought about childhood. It challenged so many things, all at one time.” In the years that followed, the study has been replicated many times, and it always finds similar results. But we have barely begun, Vincent told me, to think through its implications.

So Vincent, as he absorbed all this, came to believe that we have been making the same mistake with depression that he had been making before with obesity. We have failed to see it as a symptom of something deeper that needs to be dealt with. There’s a house fire inside many of us, Vincent had come to believe, and we’ve been concentrating on the smoke.

Many scientists and psychologists had been presenting depression as an irrational malfunction in your brain or in your genes, but he learned that Allen Barbour, an internist at Stanford University, had said that depression isn’t a disease; depression is a normal response to abnormal life experiences. “I think that’s a very important idea,” Vincent told me. “It takes you beyond the comforting, limited idea that the reason I’m depressed is I have a serotonin imbalance, or a dopamine imbalance, or what have you.” It is true that something is happening in your brain when you become depressed, he says, but that “is not a causal explanation”; it is “a necessary intermediary mechanism.”

Some people don’t want to see this because, at least at first, “it’s more comforting,” Vincent said, to think it’s all happening simply because of changes in the brain. “It takes away an experiential process and substitutes a mechanistic process.” It turns your pain into a trick of the light that can be banished with drugs. But they don’t ultimately solve the problem, he says, any more than just getting the obese patients to stop eating solved their problems. “Medications have a role,” he told me. “Are they the ultimate be and end-all? No. Do they sometimes short-change people? Absolutely.”

To solve the problem for his obese patients, Vincent said, they had all realized, together, that they had to solve the problems that were leading them to eat obsessively in the first place. So he set up support groups where they could discuss the real reasons why they ate and talk about what they had been through. Once that was in place, far more people became able to keep going through the fasting program and stay at a safe weight. He was going to start exploring a way to do this with depression, with startling results.

More than anyone else I spoke to about the hidden causes of depression, Vincent made me angry. After I met with him, I went to the beach in San Diego and raged against what he had said. I was looking hard for reasons to dismiss it. Then I asked myself. Why are you so angry about this? It seemed peculiar, and I didn’t really understand it. Then, as I discussed it with some people I trust, I began to understand.

If you believe that your depression is due solely to a broken brain, you don’t have to think about your life, or about what anyone might have done to you. The belief that it all comes down to biology protects you, in a way, for a while. If you absorb this different story, though, you have to think about those things. And that hurts.

I asked Vincent why he thinks traumatic childhoods so often produce depressed and anxious adults, and he said that he honestly doesn’t know. He’s a good scientist. He didn’t want to speculate. But I think I might know, although it goes beyond anything I can prove scientifically.

When you are a child and you experience something really traumatic, you almost always think it is your fault. There’s a reason for this, and it’s not irrational; like obesity, it is, in fact, a solution to a problem most people can’t see. When I was young, my mother was ill a lot, and my father was mostly gone, usually in a different country. In the chaos of that, I experienced some extreme acts of violence from an adult in my life. For example, I was strangled with an electrical cord on one occasion. By the time I was sixteen, I left to go and live in another city, away from any adults I knew, and when I was there, I found myself, like many people who have been treated this way at a formative age, seeking out dangerous situations where I was again treated in ways I should not have been treated.

Even now, as a thirty-seven-year-old adult, I feel like writing this down, and saying it to you, is an act of betrayal of the adult who carried out these acts of violence, and the other adults who behaved in ways they shouldn’t have.

I know you can’t figure out who these people are from what I’ve written. I know that if I saw an adult strangling a child with an electrical cord, it would not even occur to me to blame the child, and that if I heard somebody try to suggest such a thing, I would assume they were insane. I know rationally where the real betrayal lies in this situation. But still, I feel it. It’s there, and that feeling almost stopped me from saying this.

Why do so many people who experience violence in childhood feel the same way? Why does it lead many of them to self-destructive behavior, like obesity, or hard core addiction, or suicide? I have spent a lot of time thinking about this. When you’re a child, you have very little power to change your environment. You can’t move away, or force somebody to stop hurting you. So you have two choices. You can admit to yourself that you are powerless, that at any moment, you could be badly hurt, and there’s simply nothing you can do about it. Or you can tell yourself it’s your fault. If you do that, you actually gain some power, at least in your own mind. If it’s your fault, then there’s something you can do that might make it different. You aren’t a pinball being smacked around a pinball machine. You’re the person controlling the machine. You have your hands on the dangerous levers.

In this way, just like obesity protected those women from the men they feared would rape them, blaming yourself for your childhood traumas protects you from seeing how vulnerable you were and are. You can become the powerful one. If it’s your fault, it’s under your control.

But that comes at a cost. If you were responsible for being hurt, then at some level, you have to think you deserved it. A person who thinks they deserved to be injured as a child isn’t going to think they deserve much as an adult, either.

This is no way to live. But it’s a misfiring of the thing that made it possible for you to survive at an earlier point in your life.

You might have noticed that this cause of depression and anxiety is a little different from the ones I have discussed up to now, and it’s different from the ones I’m going to discuss next.

As I mentioned before, most people who have studied the scientific evidence accept that there are three different kinds of causes of depression and anxiety, biological, psychological, and social. The causes I’ve discussed up to now, and will come back to in a moment, are environmental. I’ll come to biological factors soon.

But childhood trauma belongs in a different category. It’s a psychological cause. By discussing it here, I’m hoping childhood trauma can indicate toward the many other psychological causes of depression that are too specific to be discussed in a big, broad way. The ways our psyches can be damaged are almost infinite. I know somebody whose wife cheated on him for years with his best friend and who became deeply depressed when he found out. I know somebody who survived a terror attack and was almost constantly anxious for a decade after. I know someone whose mother was perfectly competent and never cruel to her but was relentlessly negative and taught her always to see the worst in people and to keep them at a distance. You can’t squeeze these experiences into neat categories, it wouldn’t make sense to list “adultery,” “terror attacks,” or “cold parents” as causes of depression and anxiety.

But here’s what we know.

Psychological damage doesn’t have to be as extreme as childhood violence to affect you profoundly. Your wife cheating on you with your best friend isn’t a malfunction in your brain. But it is a cause of deep psychological distress, and it can cause depression and anxiety. If you are ever told a story about these problems that doesn’t talk about your personal psychology, don’t take it seriously.

Dr. Anda, one of the pioneers of this research, told me it had forced him to turn his thinking about depression and other problems inside out.

“When people have these kind of problems, it’s time to stop asking what’s wrong with them,” he said, “and time to start asking what happened to them.”

from

Lost Connections. Uncovering the Real Causes of Depression and the Unexpected Solutions

by Johann Hari

get it at Amazon.com

JUNK VALUES. CONSUMERISM LITERALLY IS DEPRESSING – Johann Hari.

Just as we have shifted en masse from eating food to eating junk food, we have also shifted from having meaningful values to having junk values.

All this mass-produced fried chicken looks like food, and it appeals to the part of us that evolved to need food; yet it doesn’t give us what we need from food, nutrition. Instead, it fills us with toxins.

In the same way, all these materialistic values, telling us to spend our way to happiness, look like real values; they appeal to the part of us that has evolved to need some basic principles to guide us through life; yet they don’t give us what we need from values, a path to a satisfying life.

Studies show that materialistic people are having a worse time, day by day, on all sorts of fronts. They feel sicker, and they are angrier. Something about a strong desire for materialistic pursuits actually affects their day-to-day lives, and decreases the quality of their daily experience. They experienced less joy, and more despair.

For thousands of years, philosophers have been suggesting that if you overvalue money and possessions, or if you think about life mainly in terms of how you look to other people, you will be unhappy.

Modern research indicates that materialistic people, who think happiness comes from accumulating stuff and a superior status, have much higher levels of depression and anxiety. The more our kids value getting things and being seen to have things, the more likely they are to be suffering from depression and anxiety.

The pressure, in our culture, runs overwhelmingly one way, spend more; work more. We live under a system that constantly distracts us from what’s really good about life. We are being propagandized to live in a way that doesn’t meet our basic psychological needs, so we are left with a permanent, puzzling sense of dissatisfaction.

The more materialistic and extrinsically motivated you become, the more depressed you will be.

When I was in my late twenties, I got really fat. It was partly a side effect of antidepressants, and partly a side effect of fried chicken. I could still, from memory, talk you through the relative merits of all the fried chicken shops in East London that were the staples of my diet, from Chicken Cottage to Tennessee Fried Chicken (with its logo of a smiling cartoon chicken holding a bucket of fried chicken legs: who knew cannibalism could be an effective marketing tool?). My own favorite was the brilliantly named Chicken Chicken Chicken. Their hot wings were, to me, the Mona Lisa of grease.

One Christmas Eve, I went to my local branch of Kentucky Fried Chicken, and one of the staff behind the counter saw me approaching and beamed. “Johann!” he said. “We have something for you!” The other staff turned and looked at me expectantly. From somewhere behind the grill and the grizzle, he took out a Christmas card. I was forced, by their expectant smiles, to open it in front of them. “To our best customer,” it said, next to personal messages from every member of the staff.

I never ate at KFC again.

Most of us know there is something wrong with our physical diets. We aren’t all gold medalists in the consumption of lard like I was, but more and more of us are eating the wrong things, and it is making us physically sick. As I investigated depression and anxiety, I began to learn something similar is happening to our values, and it is making many of us emotionally sick.

This was discovered by an American psychologist named Tim Kasser, so I went to see him, to learn his story.

As a little boy, Tim arrived in the middle of a long stretch of swampland and open beaches. His dad worked as a manager at an insurance company, and in the early 1970s, he was posted to a place called Pinellas County, on the west coast of Florida. The area was mostly undeveloped and had plenty of big, broad outdoor spaces for a kid to play, but this county soon became the fastest growing in the entire United States, and it was about to be transformed in front of Tim’s eyes. “By the time I left Florida,” he told me, “it was a completely different physical environment. You couldn’t drive along the beach roads anymore and see the water, because it was all condos and high-rises. Areas that had been open land with alligators and rattlesnakes became subdivision after subdivision after shopping mall.”

Tim was drawn to the shopping malls that replaced the beaches and marshes, like all the other kids he knew. There, he would play Asteroids and Space Invaders for hours. He soon found himself longing for stuff, the toys he saw in ads.

It sounds like Edgware, where I am from. I was eight or nine when its shopping mall, the Broadwalk Centre, opened, and I remember wandering around its bright storefronts and gazing at the things I wanted to buy in a thrilled trance. I obsessively coveted the green plastic toy of Castle Grayskull, the fortress where the cartoon character He-Man lived, and Care-a-Lot, the home in the clouds of some animated creatures called the Care Bears. One Christmas, my mother missed my hints and failed to buy me Care-a-Lot, and I was crestfallen for months. I ached and pined for that lump of plastic.

Like most kids at the time, I spent at least three hours a day watching TV, usually more, and whole days would pass in the summer when my only break from television would be to go to the Broadwalk Centre and back again. I don’t remember anyone ever telling me this explicitly, but it seemed to me then that happiness meant being able to buy lots of the things on display there. I think my nine-year-old self, if you had asked him what it meant to be happy, would have said: somebody who could walk through the Broadwalk Centre and buy whatever he wanted. I would ask my dad how much each famous person I saw on television earned, and he would guess, and we would both marvel at what we would do with the money. It was a little bonding ritual, over a fantasy of spending.

I asked Tim if, in Pinellas County where he grew up, he ever heard anyone talking about a different way of valuing things, beyond the idea that happiness came from getting and possessing stuff. “Well, I think, not growing up. No,” he said. In Edgware, there must have been people who acted on different values, but I don’t think I ever saw them.

When Tim was a teenager, his swim coach moved away one summer and gave him a small record collection, and it included albums by John Lennon and Bob Dylan. As he listened to them, he realized they seemed to be expressing something he didn’t really hear anywhere else. He began to wonder if there were hints of a different way to live lying in their lyrics, but he couldn’t find anyone to discuss it with.

It was only when Tim went to study at Vanderbilt University, a very conservative college in the South, at the height of the Reagan years, that it occurred to him, slowly, to think more deeply about this. In 1984, he voted for Ronald Reagan, but he was starting to think a lot about the question of authenticity. “I was stumbling around,” he told me. “I think I was questioning just about everything. I wasn’t just questioning these values. I was questioning lots about myself, I was questioning lots about the nature of reality and the values of society.” He feels like there were pinatas all around him and he was hitting chaotically at them all. He added: “I think I went through that phase for a long time, to be honest.”

When he went to graduate school, he started to read a lot about psychology. It was around this time that Tim realized something odd.

For thousands of years, philosophers had been suggesting that if you overvalue money and possessions, or if you think about life mainly in terms of how you look to other people, you will be unhappy, that the values of Pinellas County and Edgware were, in some deep sense, mistaken. It had been talked about a lot, by some of the finest minds who ever lived, and Tim thought it might be true. But nobody had ever conducted a scientific investigation to see whether all these philosophers were right.

This realization is what launched him on a project that he was going to pursue for the next twenty-five years. It led him to discover subtle evidence about why we feel the way we do, and why it is getting worse.

It all started in grad school, with a simple survey.

Tim came up with a way of measuring how much a person really values getting things and having money compared to other values, like spending time with their family or trying to make the world a better place. He called it the Aspiration Index, and it is pretty straightforward. You ask people how much they agree with statements such as “It is important to have expensive possessions” and how much they agree with very different statements such as “It is important to make the world a better place for others.” You can then calculate their values.

At the same time, you can ask people lots of other questions, and one of them is whether they are unhappy or if they are suffering (or have suffered) from depression or anxiety. Then, as a first step, you see if they match.

Tim’s first tentative piece of research was to give this survey to 316 students. When the results came back and were all calculated out, Tim was struck by the results: materialistic people, who think happiness comes from accumulating stuff and a superior status, had much higher levels of depression and anxiety.

This was, he knew, just a primitive first shot in the dark. So Tim’s next step was, as part of a larger study, to get a clinical psychologist to assess 140 eighteen-year-olds in depth, calculating where they were on the Aspiration Index and if they were depressed or anxious. When the results were added up, they were the same: the more the kids valued getting things and being seen to have things, the more likely they were to be suffering from depression and anxiety.

Was this something that happened only with young people? To find out, Tim measured one hundred citizens of Rochester in upstate New York, who came from a range of age groups and economic backgrounds. The result was the same.

But how could he figure out what was really happening, and why?

Tim’s next step was to conduct a more detailed study, to track how these values affect you over time. He got 192 students to keep a detailed mood diary in which, twice a day, they had to record how much they were feeling nine different emotions, such as happiness or anger, and how much they were experiencing any of nine physical symptoms, such as backache. When he calculated out the results, he found, again, higher depression among the materialistic students; but there was a result more important than that. It really did seem that materialistic people were having a worse time, day by day, on all sorts of fronts. They felt sicker, and they were angrier. “Something about a strong desire for materialistic pursuits,” he was starting to believe, “actually affected the participants’ day-to-day lives, and decreased the quality of their daily experience.” They experienced less joy, and more despair.

Why would this be? What could be happening here? Ever since the 1960s, psychologists have known that there are two different ways you can motivate yourself to get out of bed in the morning. The first are called intrinsic motives, they are the things you do purely because you value them in and of themselves, not because of anything you get out of them. When a kid plays, she’s acting totally on intrinsic motives, she’s doing it because it gives her joy. The other day, I asked my friend’s five-year-old son why he was playing. “Because I love it,” he said. Then he scrunched up his face and said “You’re silly!” and ran off, pretending to be Batman. These intrinsic motivations persist all through our lives, long after childhood.

At the same time, there’s a rival set of values, which are called extrinsic motives. They’re the things you do not because you actually want to do them, but because you’ll get something in return, whether it’s money, or admiration, or sex, or superior status. Joe, who you met two chapters ago, went to work every day in the paint shop for purely extrinsic reasons, he hated the job, but he needed to be able to pay the rent, buy the Oxy that would numb his way through the day, and have the car and clothes that he thought made people respect him. We all have some motives like that.

Imagine you play the piano. If you play it for yourself because you love it, then you are being driven to do it by intrinsic values. If you play in a dive bar you hate, just to make enough cash to ensure you don’t get thrown out of your apartment, then you are being driven to do it by extrinsic values.

These rival sets of values exist in all of us. Nobody is driven totally by one or the other.

Tim began to wonder if looking into this conflict more deeply could reveal something important. So he started to study a group of two hundred people in detail over time. He got them to lay out their goals for the future. He then figured out with them if these were extrinsic goals, like getting a promotion, or a bigger apartment, or intrinsic goals, like being a better friend or a more loving son or a better piano player. And then he got them to keep a detailed mood diary.

What he wanted to know was, Does achieving extrinsic goals make you happy? And how does that compare to achieving intrinsic goals?

The results, when he calculated them out were quite startling. People who achieved their extrinsic goals didn’t experience any increase in day-to-day happiness, none. They spent a huge amount of energy chasing these goals, but when they fulfilled them, they felt the same as they had at the start, Your promotion? Your fancy car? The new iPhone? The expensive necklace? They won’t improve your happiness even one inch.

But people who achieved their intrinsic goals did become significantly happier, and less depressed and anxious. You could track the movement. As they worked at it and felt they became (for example) a better friend, not because they wanted anything out of it but because they felt it was a good thing to do, they became more satisfied with life. Being a better dad? Dancing for the sheer joy of it? Helping another person, just because it’s the right thing to do? They do significantly boost your happiness.

Yet most of us, most of the time, spend our time chasing extrinsic goals, the very thing that will give us nothing. Our whole culture is set up to get us to think this way. Get the right grades. Get the best-paying job. Rise through the ranks. Display your earnings through clothes and cars. That’s how to make yourself feel good.

What Tim had discovered is that the message our culture is telling us about how to have a decent and satisfying life, virtually all the time, is not true. The more this was studied, the clearer it became! Twenty-two different studies have in the years since, found that the more materialistic and extrinsically motivated you become, the more depressed you will be. Twelve different studies found that the more materialistic and extrinsically motivated you become, the more anxious you will be. Similar studies, inspired by Tim’s work and using similar techniques, have now been carried out in Britain, Denmark, Germany, India, South Korea, Russia, Romania, Australia, and Canada-and the results, all over the world, keep coming back the same.

Just as we have shifted en masse from eating food to eating junk food, Tim has discovered, in effect, that we have shifted from having meaningful values to having junk values. All this mass-produced fried chicken looks like food, and it appeals to the part of us that evolved to need food; yet it doesn’t give us what we need from food, nutrition. Instead, it fills us with toxins.

In the same way, all these materialistic values, telling us to spend our way to happiness, look like real values; they appeal to the part of us that has evolved to need some basic principles to guide us through life; yet they don’t give us what we need from values, a path to a satisfying life. Instead, they fill us with psychological toxins. Junk food is distorting our bodies. Junk values are distorting our minds.

Materialism is KFC for the soul.

When Tim studied this in greater depth, he was able to identify at least four key reasons why junk values are making us feel so bad.

The first is that thinking extrinsically poisons your relationships with other people. He teamed up again with another professor, Richard Ryan, who had been an ally from the start, to study two hundred people in depth, and they found that the more materialistic you become, the shorter your relationships will be, and the worse their quality will be. If you value people for how they look, or how they impress other people, it’s easy to see that you’ll be happy to dump them if someone hotter or more impressive comes along. And at the same time, if all you’re interested in is the surface of another person, it’s easy to see why you’ll be less rewarding to be around, and they’ll be more likely to dump you, too. You will have fewer friends and connections, and they won’t last as long.

Their second finding relates to another change that happens as you become more driven by junk values. Let’s go back to the example of playing the piano. Every day, Tim spends at least half an hour playing the piano and singing, often with his kids. He does it for no reason except that he loves it, it makes him, on a good day, feel satisfied, and joyful. He feels his ego dissolve, and he is purely present in the moment. There’s strong scientific evidence that we all get most pleasure from what are called “flow states” like this, moments when we simply lose ourselves doing something we love and are carried along in the moment. They’re proof we can maintain the pure intrinsic motivation that a child feels when she is playing.

But when Tim studied highly materialistic people, he discovered they experience significantly fewer flow states than the rest of us. Why would that be?

He seems to have found an explanation. Imagine if, when Tim was playing the piano every day, he kept thinking: Am I the best piano player in Illinois? Are people going to applaud this performance? Am l going to get paid for this? How much? Suddenly his joy would shrivel up like a salted snail. Instead of his ego dissolving, his ego would be aggravated and jabbed and poked.

That is what your head starts to look like when you become more materialistic. If you are doing something not for itself but to achieve an effect, you can’t relax into the pleasure of a moment. You are constantly monitoring yourself. Your ego will shriek like an alarm you can’t shut off.

This leads to a third reason why junk values make you feel so bad. When you are extremely materialistic, Tim said to me, “you’ve always kind of got to be wondering about yourself, how are people judging you?” It forces you to “focus on other people’s opinions of you, and their praise of you, and then you’re kind of locked into having to worry what other people think about you, and if other people are going to give you those rewards that you want. That’s a heavy load to bear, instead of walking around doing what it is you’re interested in doing, or being around people who love you just for who you are.”

If “your self-esteem, your sense of self-worth, is contingent upon how much money you’ve got, or what your clothes are like, or how big your house is,” you are forced into constant external comparisons, Tim says. “There’s always somebody who’s got a nicer house or better clothes or more money.” Even if you’re the richest person in the world, how long will that last? Materialism leaves you constantly vulnerable to a world beyond your control.

And then, he says, there is a crucial fourth reason. It’s worth pausing on this one, because I think it’s the most important.

All of us have certain innate needs, to feel connected, to feel valued, to feel secure, to feel we make a difference in the world, to have autonomy, to feel we’re good at something. Materialistic people, he believes, are less happy, because they are chasing a way of life that does a bad job of meeting these needs.

What you really need are connections. But what you are told you need, in our culture, is stuff and a superior status, and in the gap between those two signals, from yourself and from society, depression and anxiety will grow as your real needs go unmet.

You have to picture all the values that guide why you do things in your life, Tim said, as being like a pie. “Each value” you have, he explained, “is like a slice of that pie. So you’ve got your spirituality slice, and your family slice, and your money slice, and your hedonism slice. We’ve all got all the slices.” When you become obsessed with materialism and status, that slice gets bigger. And “the bigger one slice gets, the smaller other slices have to get.” So if you become fixated on getting stuff and a superior status, the parts of the pie that care about tending to your relationships, or finding meaning, or making the world better have to shrink, to make way.

“On Friday at four, I can stay [in my office] and work more, or I can go home and play with my kids,” he told me. “I can’t do both. It’s one or the other. If my materialistic values are bigger, I’m going to stay and work. If my family values are bigger, I’m going to go home and play with my kids.” It’s not that materialistic people don’t care about their kids, but “as the materialistic values get bigger, other values are necessarily going to be crowded out,” he says, even if you tell yourself they won’t.

And the pressure, in our culture, runs overwhelmingly one way, spend more; work more. We live under a system, Tim says, that constantly “distracts us from what’s really good about life.” We are being propagandized to live in a way that doesn’t meet our basic psychological needs, so we are left with a permanent, puzzling sense of dissatisfaction.

For millennia, humans have talked about something called the Golden Rule. It’s the idea that you should do unto others as you would have them do unto you. Tim, I think, has discovered something we should call the I-Want-Golden-Things Rule. The more you think life is about having stuff and superiority and showing it off, the more unhappy, and the more depressed and anxious, you will be.

But why would human beings turn, so dramatically, to something that made us less happy and more depressed? Isn’t it implausible that we would do something so irrational? In the later phase of his research, Tim began to dig into the question.

Nobody’s values are totally fixed. Your level of junk values, Tim discovered by following people in his studies, can change over your lifetime. You can become more materialistic, and more unhappy; or you can become less materialistic, and less unhappy. So we shouldn’t be asking, Tim believes, “Who is materialistic?” We should be asking: “When are people materialistic?” Tim wanted to know: What causes the variation?

There’s an experiment, by a different group of social scientists, that gives us one early clue. In 1978, two Canadian social scientists got a bunch of four and five year old kids and divided them into two groups. The first group was shown no commercials. The second group was shown two commercials for a particular toy. Then they offered these four or five year old kids a choice. They told them: You have to choose, now, to play with one of these two boys here. You can play with this little boy who has the toy from the commercials, but we have to warn you, he’s not a nice boy. He’s mean. Or you can play with a boy who doesn’t have the toy, but who is really nice.

If they had seen the commercial for the toy, the kids mostly chose to play with the mean boy with the toy. If they hadn’t seen the commercial, they mostly chose to play with the nice boy who had no toys.

In other words, the advertisements led them to choose an inferior human connection over a superior human connection, because they’d been primed to think that a lump of plastic is what really matters.

Two commercials, just two, did that. Today, every person sees way more advertising messages than that in an average morning. More eighteen-month-olds can recognize the McDonald’s M than know their own surname. By the time an average child is thirty-six months old she aIready knows a hundred brand logos.

Tim suspected that advertising plays a key role in why we are, every day, choosing a value system that makes us feel worse. So with another social scientist named Jean Twenge he tracked the percentage of total US. national wealth that’s spent on advertising, from 1976 to 2003, and he discovered that the more money is spent on ads, the more materialistic teenagers become.

A few years ago, an advertising agency head named Nancy Shalek explained approvingly: “Advertising at its best is making peopie feel that without their product, you’re a loser. Kids are very sensitive to that. You open up emotionaI vulnerabilities, and it’s very easy to do with kids because they’re the most emotionally vulnerable.”

This sounds harsh, until you think through the logic. Imagine if I watched an ad and it told me, Johann, you’re fine how you are. You look good. You smell good. You’re likable. People want to be around you. You’ve got enough stuff now. You don’t need any more. Enjoy life.

That would, from the perspective of the advertising industry, be the worst ad in human history, because I wouldn’t want to go out shopping, or lunge at my laptop to spend, or do any of the other things that feed my junk values. It would make me want to pursue my intrinsic values, which involve a whole lot less spending, and a whole lot more happiness.

When they talk among themselves, advertising people have been admitting since the 1920s that their job is to make people feel inadequate, and then offer their product as the solution to the sense of inadequacy they have created. Ads are the ultimate frenemy, they’re always saying: Oh babe, I want you to look/smell/feel great; it makes me so sad that at the moment you’re ugly/ stinking/miserable; here’s this thing that will make you into the person you and I really want you to be. Oh, did I mention you have to pay a few bucks? I just want you to be the person you deserve to be. Isn’t that worth a few dollars? You’re worth it.

This logic radiates out through the culture, and we start to impose it on each other, even when ads aren’t there. Why did I, as a child, crave Nike air-pumps, even though I was as likely to play basketball as I was to go to the moon? It was partly because of the ads, but mostly because the ads created a group dynamic among everyone I knew. It created a marker of status, that we then policed. As adults, we do the same, only in slightly more subtle ways.

This system trains us, Tim says, to feel “there’s never enough. When you’re focused on money and status and possessions, consumer society is always telling you more, more, more, more. Capitalism is always telling you more, more, more. Your boss is telling you work more, work more, work more. You internalize that and you think: Oh, I’ve got to work more, because my self depends on my status and my achievement. You internalize that. It’s a kind of form of internalized oppression.”

He believes it also explains why junk values lead to such an increase in anxiety. “You’re always thinking: Are they going to reward me? Does the person love me for who I am, or for my handbag? Am I going to be able to climb the ladder of success?” he said. You are hollow, and exist only in other people’s reflections. “That’s going to be anxiety-provoking.”

We are all vulnerable to this, he believes. “The way I understand the intrinsic values,” Tim told me, is that they “are a fundamental part of what we are as humans, but they’re fragile. It’s easy to distract us from them. You give people social models of consumerism and they move in an extrinsic way.” The desire to find meaningful intrinsic values is “there, it’s a powerful part of who we are, but it’s not hard to distract us.” And we have an economic system built around doing precisely that.

As I sat with Tim, discussing all this for hours, I kept thinking of a middle-class married couple who live in a nice semidetached house in the suburbs in Edgware, where we grew up. They are close to me; I have known them all my life; I love them.

If you peeked through their window, you’d think they have everything you need for happiness, each other, two kids, a good home, all the consumer goods we’re told to buy. Both of them work really hard at jobs they have little interest in, so that they can earn money, and with the money they earn, they buy the things that we have learned from television will make us happy, clothes and cars, gadgets and status symbols. They display these things to people they know on social media, and they get lots of likes and comments like “OMG, so jealous!” After the brief buzz that comes from displaying their goods, they usually find they become dissatisfied and down again. They are puzzled by this, and they often assume it’s because they didn’t buy the right thing. So they work harder, and they buy more goods, display them through their devices, feel the buzz, and then slump back to where they started.

They both seem to me to be depressed. They alternate between being blank, or angry, or engaging in compulsive behaviors. She had a drug problem for a long time, although not anymore; he gambles online at least two hours a day. They are furious a lot of the time, at each other, at their children, at their colleagues, and, diffusely, at the world, at anyone else on the road when they are driving, for example, who they scream and swear at. They have a sense of anxiety they can’t shake off, and they often attach it to things outside them, she obsessively monitors where her teenage son is at any moment, and is afraid all the time that he will be a victim of crime or terrorism.

This couple has no vocabulary to understand why they feel so bad. They are doing what the culture has been priming them to do since we were infants, they are working hard and buying the right things, the expensive things. They are every advertising slogan made flesh.

Like the kids in the sandbox, they have been primed to lunge for objects and ignore the prospect of interaction with the people around them.

I see now they aren’t just suffering from the absence of something, such as meaningful work, or community. They are also suffering from the presence of something, an incorrect set of values telling them to seek happiness in all the wrong places, and to ignore the potential human connections that are right in front of them.

When Tim discovered all these facts, it didn’t just guide his scientific work. He began to move toward a life that made it possible for him to live consistent with his own findings, to go back, in a sense, to something more like the beach he had discovered joyfully in Florida as a kid. “You’ve got to pull yourself out of the materialistic environments, the environments that are reinforcing the materialistic values,” he says, because they cripple your internal satisfactions. And then, he says, to make that sustainable, you have to “replace them with actions that are going to provide those intrinsic satisfactions, and encourage those intrinsic goals.”

So, with his wife and his two sons, he moved to a farmhouse on ten acres of land in Illinois, where they live with a donkey and a herd of goats. They have a small TV in the basement, but it isn’t connected to any stations or to cable, it’s just to watch old movies on sometimes. They only recently got the Internet (against his protestations), and they don’t use it much. He works part time, and so does his wife, “so we could spend more time with our kids, and be in the garden more and do volunteer work and do activism work and I could write more”, all the things that give them intrinsic satisfaction. “We play a lot of games. We play a lot of music. We have a lot of family conversations.” They sing together.

Where they live in western Illinois is “not the most exciting place in the world,” Tim says, “but I have ten acres of land, I have a twelve-minute commute with one flashing light and three stop signs on my way to my office, and we afford that on one [combined full-time] salary.”

I ask him if he had withdrawal symptoms from the materialistic world we were both immersed in for so long. “Never,” he says right away. “People ask me that: “Don’t you miss this? Don’t you wish you had that?” No, I don’t, because I am never exposed to the messages telling me that I should want it. I don’t expose myself to those things, so no, I don’t have that.”

One of his proudest moments was when one of his sons came home one day and said: “Dad, some kids at school are making fun of my sneakers.” They were not a brand name, or shiny-new. “Oh, what’d you say to them?” Tim asked. His son explained he looked at them and said: “Why do you care?” He was nonplussed, he could see that what they valued was empty, and absurd.

By living without these polluting values, Tim has, he says, discovered a secret. This way of life is more pleasurable than materialism. “It’s more fun to play these games with your kids,” he told me. “It’s more fun to do the intrinsically motivated stuff than to go to work and do stuff you don’t necessarily want to do. It’s more fun to feel like people love you for who you are, instead of loving you because you gave them a big diamond ring.”

Most people know all this in their hearts, he believes. “At some level I really believe that most people know that intrinsic values are what’s going to give them a good life,” he told me. When you do surveys and ask people what’s most important in life, they almost always name personal growth and relationships as the top two. “But I think part of why people are depressed is that our society is not set up in order to help people live lifestyles, have jobs, participate in the economy, or participate in their neighborhoods” in ways that support their intrinsic values. The change Tim saw happening in Florida as a kid, when the beachfronts were transformed into shopping malls and people shifted their attention there, has happened to the whole culture.

Tim told me people can apply these insights to their own life, on their own, to some extent. “The first thing is for people to ask themselves, Am I setting up my life so I can have a chance of succeeding at my intrinsic values? Am I hanging out with the right people, who are going to make me feel loved, as opposed to making me feel like I made it? Those are hard choices sometimes.” But often, he says, you will hit up against a limit in our culture. You can make improvements, but often “the solutions to the problems that I’m interested in can’t be easily solved at the individual person level, or in the therapeutic consulting room, or by a pill.” They require something more, as I was going to explore later.

When I interviewed Tim, I felt he solved a mystery for me. I had been puzzled back in Philadelphia about why Joe didn’t leave the job he hated at the paint company and go become a fisherman in Florida, when he knew life in the Sunshine State would make him so much happier. It seemed like a metaphor for why so many of us stay in situations we know make us miserable.

I think I see why now. Joe is constantly bombarded with messages that he shouldn’t do the thing that his heart is telling him would make him feel calm and satisfied. The whole logic of our culture tells him to stay on the consumerist treadmill, to go shopping when he feels lousy, to chase junk values. He has been immersed in those messages since the day he was born. So he has been trained to distrust his own wisest instincts.

When I yelled after him “Go to Florida!” I was yelling into a hurricane of messages, and a whole value system, that is saying the exact opposite.

from

Lost Connections. Uncovering the Real Causes of Depression and the Unexpected Solutions

by Johann Hari

get it at Amazon.com

DEPRESSION, THE CHEMICAL IMBALANCE MYTH – Johann Hari * THE EMPEROR’S NEW DRUGS – Irving Kirsch.

There is a problem with what everyone knows about antidepressant drugs. It isn’t true. The whole idea of mental distress being caused simply by a chemical imbalance is “a myth,”, sold to us by the drug companies.

In the United States, 40 percent of the regulators’ wages are paid by the drug companies, and in Britain, it’s 100 percent. The rules they have written are designed to make it extraordinarily easy to get a drug approved.

“There was never any basis for it, ever. It was just marketing copy. At the time the drugs came out in the early 1990s, you couldn’t have got any decent expert to go on a platform and say, ‘Look, there’s a lowering of serotonin in the brains of people who are depressed’ There wasn’t ever any evidence for it.” It hasn’t been discredited, because “it didn’t ever get ‘credited.” We don’t know what a “chemically balanced” brain would look like. The effects of these drugs on depression itself are in reality tiny. No matter what chemical you tinker with, you get the same outcome. Antidepressants are little more than active placebos, drugs with very little specific therapeutic benefit, but with serious side effects.

What do the people taking these different drugs actually have in common? Only one thing: the belief that the drugs work, because you believe you are being looked after and offered a solution. Clever marketing over solid empirical evidence.

The serotonin theory “is a lie. I don’t think we should dress it up and say, ‘Oh, well, maybe there’s evidence to support that.’ There isn’t.” Most people on these drugs, after an initial kick, remain depressed or anxious. The belief that antidepressants can cure depression chemically is simply wrong.

The year after I swallowed my first antidepressant, Tipper Gore, the wife of Vice President Al Gore, explained to the newspaper USA Today why she had recently become depressed. “It was definitely a clinical depression, one that I was going to have to have help to overcome,” she said. “What I learned about is your brain needs a certain amount of serotonin and when you run out of that, it’s like running out of gas.” Tens of millions of people, including me, were being told the same thing.

When Irving Kirsch discovered that these serotonin boosting drugs were not having the effects that everyone was being sold, complete/nonfiltered FDA drug company study/research records show that the effects of these drugs on depression itself are in reality tiny, he began, to his surprise, to ask an even more basic question.

What’s the evidence, he began to wonder, that depression is caused primarily by an imbalance of serotonin, or any other chemical, in the brain? Where did it come from?

The serotonin story began, Irving learned, quite by accident in a tuberculosis ward in New York City in the clammy summer of 1952, when some patients began to dance uncontrollably down a hospital corridor. A new drug named Marsilid had come along that doctors thought might help TB patients. It turned out it didn’t have much effect on TB, but the doctors noticed it did something else entirely. They could hardly miss it. It made the patients gleefully, joyfully euphoric, some began to dance frenetically.

So it wasn’t long before somebody decided, perfectly logically, to try to give it to depressed people, and it seemed to have a similar effect on them, for a short time. Not long after that, other drugs came along that seemed to have similar effects (also for short periods), ones named Ipronid and Imipramine. So what, people started to ask, could these new drugs have in common? And whatever it was, could it hold the key to unlocking depression?

Nobody really knew where to look, and so for a decade the question hung in the air, tantalizing researchers. And then in 1965, a British doctor called Alec Coppen came up with a theory. What if, he asked, all these drugs were increasing levels of serotonin in the brain? If that were true, it would suggest that depression might be caused by low levels of serotonin.

“It’s hard to overstate just how far out on a limb these scientists were climbing,” Dr. Gary Greenberg, who has written the history of this period, explains. “They really had no idea what serotonin was doing in the brain.” To be fair to the scientists who first put forward the idea, he says, they put it forward tentatively, as a suggestion. One of them said it was “at best a reductionist simplification,” and said it couldn’t be shown to be true “on the basis of data currently available.”

But a few years later, in the 1970s, it was finally possible to start testing these theories. It was discovered that you can give people a chemical brew that lowers their serotonin levels. So if this theory was right, if low serotonin caused depression, what should happen? After taking this brew, people should become depressed. So they tried it. They gave people a drug to lower their serotonin levels and watched to see what would happen. And, unless they had already been taking powerful drugs they didn’t become depressed. In fact, in the vast majority of patients, it didn’t affect their mood at all.

I went to see one of the first scientists to study these new antidepressants in Britain, Professor David Healy, in his clinic in Bangor, a town in the north of Wales. He has written the most detailed history of antidepressants we have. When it comes to the idea that depression is caused by low serotonin, he told me: “There was never any basis for it, ever. It was just marketing copy. At the time the drugs came out in the early 1990s, you couldn’t have got any decent expert to go on a platform and say, ‘Look, there’s a lowering of serotonin in the brains of people who are depressed’ There wasn’t ever any evidence for it.” It hasn’t been discredited, he said, because “it didn’t ever get ‘credited,’ in a sense. There wasn’t ever a point in time when 50 percent of the field actually believed it.” In the biggest study of serotonin’s effects on humans, it found no direct relationships with depression. Professor Andrew Skull of Princeton has said attributing depression to low serotonin is “deeply misleading and unscientific.“

It had been useful in only one sense. When the drug companies wanted to sell antidepressants to people like me and Tipper Gore, it was a great metaphor. It’s easy to grasp, and it gives you the impression that what antidepressants do is restore you to a natural state, the kind of balance that everyone else enjoys.

Irving learned that once serotonin was abandoned by scientists (but certainly not by drug company PR teams) as an explanation for depression and anxiety, there was a shift in scientific research. Okay, they said: if it’s not low serotonin that’s causing depression and anxiety, then it must be the lack of some other chemical. It was still taken for granted that these problems are caused by a chemical imbalance in the brain, and antidepressants work by correcting that chemical imbalance. If one chemical turns out not to be the psychological killer, they must start searching for another one.

But Irving began to ask an awkward question. If depression and anxiety are caused by a chemical imbalance, and antidepressants work by fixing that imbalance, then you have to account for something odd that he kept finding. Antidepressant drugs that increase serotonin in the brain have the same modest effect, in clinical trials, as drugs that reduce serotonin in the brain. And they have the same effect as drugs that increase another chemical, norepinephrine. And they have the same effect as drugs that increase another chemical, dopamine. In other words, no matter what chemical you tinker with, you get the same outcome.

So Irving asked: What do the people taking these different drugs actually have in common? Only, he found, one thing: the belief that the drugs work. It works, Irving believes, largely for the same reason that John Haygarth’s wand worked: because you believe you are being looked after and offered a solution.

After twenty years researching this at the highest level, Irving has come to believe that the notion depression is caused by a chemical imbalance is just “an accident of history,” produced by scientists initially misreading what they were seeing, and then drug companies selling that misperception to the world to cash in.

And so, Irving says, the primary explanation for depression offered in our culture starts to fall apart. The idea you feel terrible because of a “chemical imbalance” was built on a series of mistakes and errors. It has come as close to being proved wrong, he told me, as you ever get in science. It’s lying broken on the floor, like a neurochemical Humpty Dumpty with a very sad smile.

I had traveled a long way with Irving on his journey but I stopped there, startled. Could this really be true? I am trained in the social sciences, which is the kind of evidence that I’ll be discussing in the rest of this book. I’m not trained in the kind of science he is a specialist in. I wondered if I was misunderstanding him, or if he was a scientific outlier. So I read all that I could, and I got as many other scientists to explain it to me as possible. “There’s no evidence that there’s a chemical imbalance” in depressed or anxious people’s brains, Professor Joanna Moncrieff, one of the leading experts on this question-explained to me bluntly in her office at the University College of London. The term doesn’t really make any sense, she said: we don’t know what a “chemically balanced” brain would look like. People are told that drugs like antidepressants restore a natural balance to your brain, she said, but it’s not true-they create an artificial state. The whole idea of mental distress being caused simply by a chemical imbalance is “a myth,” she has come to believe, sold to us by the drug companies.

The clinical psychologist Dr. Lucy Johnstone was more blunt still. “Almost everything you were told was bullshit,” she said to me over coffee. The serotonin theory “is a lie. I don’t think we should dress it up and say, ‘Oh, well, maybe there’s evidence to support that.’ There isn’t.”

Yet it seemed wildly implausible to me that something so huge, one of the most popular drugs in the world, taken by so many people all around me, could be so wrong. Obviously, there are protections against this happening: huge hurdles of scientific testing that have to take place before a drug gets to our bathroom cabinets. I felt as if I had just landed in a flight from JFK to LAX, only to be told that the plane had been flown by a monkey the whole way. Surely there are procedures in place to stop something like this from happening? How could these drugs have gotten through the procedures in place, if they were really as limited as this deeper research suggested?

I discussed this with one of the leading scientists in this field, Professor John Ioannidis, who the Atlantic Monthly has said “may be one of the most influential scientists alive.” He says it is not surprising that the drug companies could simply override the evidence and get the drugs to market anyway, because in fact it happens all the time. He talked me through how these antidepressants got from the development stage to my mouth.

It works like this: “The companies are often running their own trials on their own products,” he said. That means they set up the clinical trial, and they get to decide who gets to see any results. So “they are judging their own products. They’re involving all these poor researchers who have no other source of funding, and who have little control over how the results will be written up and presented.” Once the scientific evidence is gathered, it’s not even the scientists who write it up much of the time. “Typically, it’s the company people who write up the published scientific reports.”

This evidence then goes to the regulators, whose job is to decide whether to allow the drug onto the market. But in the United States, 40 percent of the regulators’ wages are paid by the drug companies, and in Britain, it’s 100 percent. When a society is trying to figure out which drug is safe to put on the market, there are meant to be two teams: the drug company making the case for it, and a referee working for us, the public, figuring out if it properly works. But Professor Ioannidis was telling me that in this match, the referee is paid by the drug company team, and that team almost always wins.

The rules they have written are designed to make it extraordinarily easy to get a drug approved. All you have to do is produce two trials, any time, anywhere in the world, that suggest some positive effect of the drug. If there are two, and there is some effect, that’s enough. So you could have a situation in which there are one thousand scientific trials, and 998 find the drug doesn’t work at all, and two find there is a tiny effect, and that means the drug will be making its way to your local pharmacy.

“I think that this is a field that is seriously sick,” Professor Ioannidis told me. “The field is just sick and bought and corrupted, and I can’t describe it otherwise.” I asked him how it made him feel to have learned all of this. “It’s depressing,” he said. That’s ironic, I replied. “But it’s not depressing,” he responded, “to the severe extent that I would take SSRIs [antidepressants].”

I tried to laugh, but it caught in my throat.

Some people said to Irving, so what? Okay, so say it’s a placebo effect. Whatever the reason, people still feel better. Why break the spell? He explained: the evidence from the clinical trials suggests that the antidepressant effects are largely a placebo, but the side effects are mostly the result of the chemicals themselves, and they can be very severe.

“Of course,” Irving says, there’s “weight gain.” I massively ballooned, and saw the weight fall off almost as soon as I stopped. “We know that SSRIs [the new type of antidepressants] in particular contribute to sexual dysfunction, and the rates for most SSRIs are around 75 percent of treatment-engendered sexual dysfunction,” he continued. Though it’s painful to talk about, this rang true for me, too. In the years I was taking Paxil, I found my genitals were a lot less sensitive, and it took a really long time to ejaculate. This made sex painful and it reduced the pleasure I took from it. It was only when I stopped taking the drug and I started having more pleasurable sex again that I remembered regular sex is one of the best natural antidepressants in the world.

“In young people, these chemical antidepressants increase the risk of suicide. There’s a new Swedish study showing that it increases the risk of violent criminal behavior,” Irving continued. “In older people it increases the risk of death from all causes, increases the risk of stroke. In everybody, it increases the risk of type 2 diabetes. In pregnant women, it increases the risk of miscarriage and of having children born with autism or physical deformities. So all of these things are known.” And if you start experiencing these effects, it can be hard to stop, about 20 percent of people experience serious withdrawal symptoms.

So, he says, “if you want to use something to get its placebo effect, at least use something that’s safe.” We could be giving people the herb St. John’s Wort, Irving says, and we’d have all the positive placebo effects and none of these drawbacks. Although, of course, St. John’s Wort isn’t patented by the drug companies, so nobody would be making much profit off it.

By this time, Irving was starting, he told me softly, to feel “guilty” for having pushed those pills for all those years.

In 1802, John Haygarth revealed the true story of the wands to the public. Some people are really recovering from their pain for a time, he explained, but it’s not because of the power in the wands. It’s because of the power in their minds. It was a placebo effect, and it likely wouldn’t last, because it wasn’t solving the underlying problem.

This message angered almost everyone? Some felt duped by the people who had sold the expensive wands in the first place, but many more felt furious with Haygarth himself, and said he was clearly talking rubbish. “The intelligence excited great commotions, accompanied by threats and abuse,” he wrote. “A counterdeclaration was to be signed by a great number of very respectable persons”, including some leading scientists of the day, explaining that the wand worked, and its powers were physical, and real.

Since Irving published his early results, and as he has built on them over the years, the reaction has been similar. Nobody denies that the drug companies’ own data, submitted to the FDA, shows that antidepressants have only a really small effect over and above placebo. Nobody denies that my own drug company admitted privately that the drug I was given, Paxil, was not going to work for people like me, and they had to make a payout in court for their deception.

But some scientists, a considerable number, do dispute many of Kirsch’s wider arguments. I wanted to study carefully what they say. I hoped the old story could still, somehow, be saved. I turned to a man who, more than anyone else alive, successfully sold antidepressants to the wider public, and he did it because he believed it: he never took a cent from the drug companies.

In the 1990s, Dr. Peter Kramer was watching as patient after patient walked into his therapy office in Rhode Island, transformed before his eyes after they were given the new antidepressant drugs. It’s not just that they seemed to have improved; they became, he argued, “better than well”, they had more resilience and energy than the average person. The book he wrote about this, Listening to Prozac, became the bestselling book ever about antidepressants. I read it soon after I started taking the drugs. I was sure the process Peter described so compellingly was happening to me. I wrote about it, and I made his case to the public in articles and interviews.

So when Irving started to present his evidence, Peter, by then a professor at Brown Medical School, was horrified. He started taking apart Irving’s critique of antidepressants at length, in public, both in books and in a series of charged public debates.

His first argument is that Irving is not giving antidepressants enough time. The clinical trials he has analyzed, almost all the ones submitted to the regulator, typically last for four to eight weeks. But that isn’t enough. It takes longer for these drugs to have a real effect.

This seemed to me to be an important objection. Irving thought so, too. So he looked to see if there were any drug trials that had lasted longer, to find their results. It turns out there were two, and in the first, the placebo did the same as the drug, and in the second, the placebo did better.

Peter then pointed to another mistake he believed Irving had made. The antidepressant trials that Irving is looking at lump together two groups: moderately depressed people and severely depressed people. Maybe these drugs don’t work much for moderately depressed people, Peter concedes, but they do work for severely depressed people. He’s seen it. So when Irving adds up an average for everyone, lumping together the mildly depressed and the severely depressed, the effect of the drugs looks small, but that’s only because he’s diluting the real effect, as surely as Coke will lose its flavor if you mix it with pints and pints of water.

Again, Irving thought this was a potentially important point, and one he was keen to understand, so he went back over the studies he had drawn his data from. He discovered that, with a single exception, he had looked only at studies of people classed as having very severe depression.

This then led Peter to turn to his most powerful argument. It’s the heart of his case against Irving and for antidepressants.

In 2012, Peter went to watch some clinical trials being conducted, in a medical center that looked like a beautiful glass cube, and gazed out over expensive houses.

When the company there wants to conduct trials into antidepressants, they have two headaches. They have to recruit volunteers who will swallow potentially dangerous pills over a sustained period of time, but they are restricted by law to paying only small amounts: between $40 and $75. At the same time, they have to find people who have very specific mental health disorders, for example, if you are doing a trial for depression, they have to have only depression and no other complicating factors. Given all that, it’s pretty difficult for them to find anyone who will take part, so they often turn to quite desperate people, and they have to offer other things to tempt them. Peter watched as poor people were bused in from across the city to be offered a gorgeous buffet of care they’d never normally receive at home, therapy, a whole community of people who’d listen to them, a warm place to be during the day, medication, and money that could double their poverty-level income.

As he watched this, he was struck by something. The people who turn up at this center have a strong incentive to pretend to have any condition they happen to be studying there, and the for-profit companies conducting the clinical trials have a strong incentive to pretend to believe them. Peter looked on as both sides seemed to be effectively bullshitting each other. When he saw people being asked to rate how well the drugs had worked, he thought they were often clearly just giving the interviewer whatever answer they wanted.

So Peter concluded that the results from clinical trials of antidepressants, all the data we have, are meaningless. That means Irving is building his conclusion that their effect is very small (at best) on a heap of garbage, Peter declared. The trials themselves are fraudulent.

It’s a devastating point, and Peter has proved it quite powerfully. But it puzzled Irving when he heard it, and it puzzled me. The leading scientific defender of antidepressants, Peter Kramer, is making the case for them by saying that the scientific evidence for them is junk.

When I spoke to Peter, I told him that if he is right (and I think he is), then that’s not a case for the drugs. It’s a case against them. It means that, by law, they should never have been brought to market.

When I started to ask about this, in a friendly tone Peter became quite irritable, and said even bad trials can yield usable results. He soon changed the subject. Given that he puts so much weight on what he’s seen with his own eyes, I asked Peter what he would say to the people who claimed that John Haygarth’s wand worked, because they, too, were just believing what they saw with their own eyes. He said that in cases like that, “the collection of experts isn’t as expert or as numerous as what we’re talking about here. I mean, this would be [an] orders-of-magnitude bigger scandal if these were [like] just bones wrapped in cloth.”

Shortly after, he said: “I think I want to cut off this conversation.”

Even Peter Kramer had one note of caution to offer about these drugs. He stressed to me that the evidence he has seen only makes the case for prescribing antidepressants for six to twenty weeks. Beyond that, he said, “I think that the evidence is thinner, and my dedication to the arguments is less as you get to long-term use. I mean, does anyone really know about what fourteen years of use does in terms of harm and benefit? I think the answer is we don’t really know.” I felt anxious as he said that, I had already told him that I used the drugs for almost that long. Perhaps because he sensed my anxiety, he added: “Although I do think we’ve been reasonably lucky. People like you come off and function.”

Very few scientists now defend the idea that depression is simply caused by low levels of serotonin, but the debate about whether chemical antidepressants work for some other reason we don’t fully understand, is still ongoing. There is no scientific consensus. Many distinguished scientists agree with Irving Kirsch; many agree with Peter Kramer. I wasn’t sure what to take away from all of this, until Irving led me to one last piece of evidence. I think it tells us the most important fact we need to know about chemical antidepressants.

In the late 1990s, a group of scientists wanted to test the effects of the new SSRI antidepressants in a situation that wasn’t just a lab, or a clinical trial. They wanted to look at what happens in a more everyday situation, so they set up something called the Star-D Trial. It was pretty simple. A normal patient goes to the doctor and explains he’s depressed. The doctor talks through the options with him, and if they both agree, he starts taking an antidepressant. At this point, the scientists conducting the trial start to monitor the patient. If the antidepressant doesn’t work for him, he’s given another one. If that one doesn’t work, he’s given another one, and on and on until he gets one that feels as though it works. This is how it works for most of us out there in the real world: a majority of people who get prescribed antidepressants try more than one, or try more than one dosage, until they find the effect they’re looking for.

And what the trial found is that the drugs worked. Some 67 percent of patients did feel better, just like I did in those first months.

But then they found something else. Within a year, half of the patients were fully depressed again. Only one in three of the people who stayed on the pills had a lasting, proper recovery from their depression. (And even that exaggerates the effect, since we know many of those people would have recovered naturally without the pills.)

It seemed like my story, played out line by line. I felt better at first; the effect wore off; I tried increasing the dose, and then that wore off, too. When I realized that antidepressants weren’t working for me any more, that no matter how much I jacked up the dose, the sadness would still seep back through, I assumed there was something wrong with me.

Now I was reading the Star-D Trial’s results, and I realized I was normal. My experience was straight from the textbook: far from being an outlier, I had the typical antidepressant experience.

This evidence has been followed up several times since, and the proportion of people on antidepressants who continue to be depressed is found to be between 65 and 80 percent.

To me, this seems like the most crucial piece of evidence about antidepressants of all: most people on these drugs, after an initial kick, remain depressed or anxious.

I want to stress, some reputable scientists still believe that these drugs genuinely work for a minority of people who take them, due to a real chemical effect. It’s possible. Chemical antidepressants may well be a partial solution for a minority of depressed and anxious people, I certainly don’t want to take away anything that’s giving relief to anyone. If you feel helped by them, and the positives outweigh the side effects, you should carry on. (And if you are going to stop taking them, then it’s essential that you don’t do it overnight, because you can experience severe physical withdrawal symptoms and a great deal of panic as a result. I gradually reduced my dose very slowly, over six months, in consultation with my doctor, to prevent this from happening.)

But it is impossible, in the face of this evidence, to say they are enough, for a big majority of depressed and anxious people.

I couldn’t deny it any longer: for the vast majority we clearly needed to find a different story about what is making us feel this way, and a different set of solutions. But what, asked myself, bewildered, could they be?

The Emperor’s New Drugs

Irving Kirsch

Everyone knows that antidepressant drugs are miracles of modern medicine. Professor Irving Kirsch knew this as well as anyone. But, as he discovered during his research, there is a problem with what everyone knows about antidepressant drugs. It isn’t true.

How did antidepressant drugs gain their reputation as a magic bullet for depression? And why has it taken so long for the story to become public? Answering these questions takes us to the point where the lines between clinical research and marketing disappear altogether.

Using the Freedom of Information Act, Kirsch accessed clinical trials that were withheld, by drug companies, from the public and from the doctors who prescribe antidepressants. What he found, and what he documents here, promises to bring revolutionary change to the way our society perceives, and consumes, antidepressants.

The Emperor’s New Drugs exposes what we have failed to see before: depression is not caused by a chemical imbalance in the brain; antidepressants are significantly more dangerous than other forms of treatment and are only marginally more effective than placebos; and, there are other ways to combat depression, treatments that don’t only include the empty promise of the antidepressant prescription.

This is not a book about alternative medicine and its outlandish claims. This is a book about fantasy and wishful thinking in the heart of clinical medicine, about the seductions of myth, and the final stubbornness of facts.

Irving Kirsch is a lecturer in medicine at the Harvard Medical School and a professor of psychology at Plymouth University, as well as professor emeritus of psychology at the University of Hull, and the University of Connecticut. He has published eight books and numerous scientific articles on placebo effects, antidepressant medication, hypnosis, and suggestion. His work has appeared in Science, Science News, New Scientist, New York Times, Newsweek, and BBC Focus and many other leading magazines, newspapers, and television documentaries.

Like most people, I used to think that antidepressants worked. As a clinical psychologist, I referred depressed psychotherapy clients to psychiatric colleagues for the prescription of medication, believing that it might help. Sometimes the antidepressant seemed to work; sometimes it did not. When it did work, I assumed it was the active ingredient in the antidepressant that was helping my clients cope with their psychological condition.

According to drug companies, more than 80 per cent of depressed patients can be treated successfully by antidepressants. Claims like this made these medications one of the most widely prescribed class of prescription drugs in the world, with global sales that make it a $19-billion-a-year industry. Newspaper and magazine articles heralded antidepressants as miracle drugs that had changed the lives of millions of people. Depression, we were told, is an illness a disease of the brain that can be cured by medication. I was not so sure that depression was really an illness, but I did believe that the drugs worked and that they could be a helpful adjunct to psychotherapy for very severely depressed clients. That is why I referred these clients to psychiatrists who could prescribe antidepressants that the clients could take while continuing in psychotherapy to work on the psychological issues that had made them depressed.

But was it really the drug they were taking that made my clients feel better? Perhaps I should have suspected that the improvement they reported might not have been a drug effect. People obtain considerable benefits from many medications, but they also can experience symptom improvement just by knowing they are being treated. This is called the placebo effect. As a researcher at the University of Connecticut, I had been studying placebo effects for many years. I was well aware of the power of belief to alleviate depression, and I understood that this was an important part of any treatment, be it psychological or pharmacological. But I also believed that antidepressant drugs added something substantial over and beyond the placebo effect.

As I wrote in my first book, ‘comparisons of antidepressive medication with placebo pills indicate that the former has a greater effect, the existing data suggest a pharmacologically specific effect of imipramine on depression’. As a researcher, I trusted the data as it had been presented in the published literature. I believed that antidepressants like imipramine were highly effective drugs, and I referred to this as ‘the established superiority of imipramine over placebo treatment’.

When I began the research that I describe in this book, I was not particularly interested in investigating the effects of antidepressants. But I was definitely interested in investigating placebo effects wherever I could find them, and it seemed to me that depression was a perfect place to look. Why did I expect to find a large placebo effect in the treatment of depression? If you ask depressed people to tell you what the most depressing thing in their lives is, many answer that it is their depression. Clinical depression is a debilitating condition. People with severe depression feel unbearably sad and anxious, at times to the point of considering suicide as a way to relieve the burden. They may be racked with feelings of worthlessness and guilt. Many suffer from insomnia, whereas others sleep too much and find it difficult to get out of bed in the morning. Some have difficulty concentrating and have lost interest in all of the activities that previously brought pleasure and meaning into their lives. Worst of all, they feel hopeless about ever recovering from this terrible state, and this sense of hopelessness may lead them to feel that life is not worth living. In short, depression is depressing. John Teasdale, a leading researcher on depression at Oxford and Cambridge universities, labelled this phenomenon ‘depression about depression’ and claimed that effective treatments for depression work at least in part by altering the sense of hopelessness that comes from being depressed about one’s own depression?!

Whereas hopelessness is a central feature of depression, hope lies at the core of the placebo effect. Placebos instil hope in patients by promising them relief from their distress. Genuine medical treatments also instil hope, and this is the placebo component of their effectiveness.

When the promise of relief instils hope, it counters a fundamental attribute of depression. Indeed, it is difficult to imagine any treatment successfully treating depression without reducing the sense of hopelessness that depressed people feel. Conversely, any treatment that reduces hopelessness must also assuage depression. So a convincing placebo ought to relieve depression.

It was with that in mind that one of my postgraduate students, Guy Sapirstein, and I set out to investigate the placebo effect in depression, an investigation that I describe in the first chapter of this book, and that produced the first of a series of surprises that transformed my views about antidepressants and their role in the treatment of depression. In this book I invite you to share this journey in which I moved from acceptance to dissent, and finally to a thorough rejection of the conventional view of antidepressants.

The drug companies claimed and still maintain that the effectiveness of antidepressants has been proven in published clinical trials showing that the drugs are substantially better than placebos (dummy pills with no active ingredients at all). But the data that Sapirstein and I examined told a very different story. Although many depressed patients improve when given medication, so do many who are given a placebo, and the difference between the drug response and the placebo response is not all that great.

What the published studies really indicate is that most of the improvement shown by depressed people when they take antidepressants is due to the placebo effect.

Our finding that most of the effects of antidepressants could be explained as a placebo effect was only the first of a number of surprises that changed my views about antidepressants. Following up on this research, I learned that the published clinical trials we had analysed were not the only studies assessing the effectiveness of antidepressants. I discovered that approximately 40 per cent of the clinical trials conducted had been withheld from publication by the drug companies that had sponsored them. By and large, these were studies that had failed to show a significant benefit from taking the actual drug. When we analysed all of the data, those that had been published and those that had been suppressed my colleagues and I were led to the inescapable conclusion that antidepressants are little more than active placebos, drugs with very little specific therapeutic benefit, but with serious side effects. I describe these analyses and the reaction to them in Chapters 3 and 4.

How can this be? Before a new drug is put on the market, it is subjected to rigorous testing. The drug companies sponsor expensive clinical trials, in which some patients are given medication and others are given placebos. The drug is considered effective only if patients given the real drug improve significantly more than patients given the placebos. Reports of these trials are then sent out to medical journals, where they are subjected to rigorous peer review before they are published. They are also sent to regulatory agencies, like the Food and Drug Administration (FDA) in the US, the Medicines and Healthcare products Regulatory Agency (MHRA) in the UK and the European Medicine Agency (EMEA) in the EU. These regulatory agencies carefully review the data on safety and effectiveness, before deciding whether to approve the drugs for marketing. So there must be substantial evidence backing the effectiveness of any medication that has reached the market.

And yet I remain convinced that antidepressant drugs are not effective treatments and that the idea of depression as a chemical imbalance in the brain is a myth. When I began to write this book, my claim was more modest. I believed that the clinical effectiveness of antidepressants had not been proven for most of the millions of patients to whom they are prescribed, but I also acknowledged that they might be beneficial to at least a subset of depressed patients. During the process of putting all of the data together, those that I had analysed over the years and newer data that have just recently seen the light of day, I realized that the situation was even worse than I thought.

The belief that antidepressants can cure depression chemically is simply wrong.

In this book I will share with you the process by which I came to this conclusion and the scientific evidence on which it is based. This includes evidence that was known to the pharmaceutical companies and to regulatory agencies, but that was intentionally withheld from prescribing physicians, their patients and even from the National Institute for Health and Clinical Excellence (NICE) when it was drawing up treatment guidelines for the National Health Service (NHS).

My colleagues and I obtained some of these hidden data by using the Freedom of Information Act in the US. We analysed the data and submitted the results for peer review to medical and psychological journals, where they were then published. Our analyses have become the focus of a national and international debate, in which many doctors have changed their prescribing habits and others have reacted with anger and incredulity.

My intention in this book is to present the data in a plain and straightforward way, so that you will be able to decide for yourself whether my conclusions about antidepressants are justified.

The conventional view of depression is that it is caused by a chemical imbalance in the brain. The basis for this idea was the belief that antidepressant drugs were effective treatments. Our analysis showing that most if not all of the effects of these medications are really placebo effects challenges this widespread view of depression. In Chapter 4 I examine the chemical-imbalance theory. You may be surprised to learn that it is actually a rather controversial theory and that there is not much scientific evidence to support it. While writing this chapter I came to an even stronger conclusion. It is not just that there is not much supportive evidence; rather, there is a ton of data indicating that the chemical-imbalance theory is simply wrong.

The chemical effect of antidepressant drugs may be small or even non-existent, but these medications do produce a powerful placebo effect. In Chapters 5 and 6 I examine the placebo effect itself. I look at the myriad of effects that placebos have been shown to have and explore the theories of how these effects are produced. I explain how placebos are able to produce substantial relief from depression, almost as much as that produced by medication, and the implications that this has for the treatment of depression.

Finally, in Chapter 7, I describe some of the alternatives to medication for the treatment of depression and assess the evidence for their effectiveness. One of my aims is to provide essential scientifically grounded information for making informed choices between the various treatment options that are available.

Much of what I write in this book will seem controversial, but it is all thoroughly grounded on scientific evidence, evidence that I describe in detail in this book. Furthermore, as controversial as my conclusions seem, there has been a growing acceptance of them. NICE has acknowledged the failure of antidepressant treatment to provide clinically meaningful benefits to most depressed patients; the UK government has instituted plans for providing alternative treatments; and neuroscientists have noted the inability of the chemical-imbalance theory to explain depression. We seem to be on the cusp of a revolution in the way we understand and treat depression.

Learning the facts behind the myths about antidepressants has been, for me, a journey of discovery. It was a journey filled with shocks and surprises, surprises about how drugs are tested and how they are approved, what doctors are told and what is kept hidden from them, what regulatory agencies know and what they don’t want you to know, and the myth of depression as a brain disease. I would like to share that journey with you. Perhaps you will find it as surprising and shocking as I did. It is my hope that making this information public will foster changes in the way new drugs are tested and approved in the future, in the public availability of the data and in the treatment of depression.

1

Listening to Prozac, but Hearing Placebo

In 1995 Guy Sapirstein and I set out to assess the placebo effect in the treatment of depression. Instead of doing a brand-new study, we decided to pool the results of previous studies in which placebos had been used to treat depression and analyse them together. What we did is called a meta-analysis, and it is a common technique for making sense of the data when a large number of studies have been done to answer a particular question. It was once considered somewhat controversial, but meta-analyses are now common features in all of the leading medical journals. Indeed, it is hard to see how one could interpret the results of large numbers of studies without the aid of a meta-anaiysis.

In doing our meta-analysis, it was not enough to find studies in which depressed patients had been given placebos. We also needed to find studies in which depression had been tracked in patients who were not given any treatment at all. This was to make sure that any effect we found was really due to the administration of the placebo. To better understand the reason for this, imagine that you are investigating a new remedy for colds. If the patients are given the new medicine, they get better, if they are given placebos, they also get better. Seeing these data, you might be tempted to think that the improvement was a placebo effect. But people recover from colds even if you give them nothing at all. So when the patients in our imaginary study took a dummy pill and their colds got better, the improvement may have had nothing to do with the placebo effect. It might simply have been due to the passage of time and the fact that colds are short-lasting illnesses.

Spontaneous improvement is not limited to colds. It can also happen when people are depressed. Because people sometimes recover from bouts of depression with no treatment at all, seeing that a person has become less depressed after taking a placebo does not mean that the person has experienced a placebo effect. The improvement could have been due to any of a number of other factors. For example, people can get better because of positive changes in life circumstances, such as finding a job after a period of unemployment or meeting a new romantic partner. Improvement can also be facilitated by the loving support of friends and family. Sometimes a good friend can function as a surrogate therapist. In fact, a very influential book on psychotherapy bore the title Psychotherapy: The Purchase of Friendship. The author did not claim that psychotherapy was merely friendship, but the title does make the point that it can be very therapeutic to have a friend who is empathic and knows how to listen.

The point is that without comparing the effect of placebos against rates of spontaneous recovery, it is impossible to assess the placebo effect. Just as we have to control for the placebo effect to evaluate the effect of a drug, so too we have to control for the passage of time when assessing the placebo effect. The drug effect is the difference between what happens when people are given the active drug and what happens when they are given the placebo. Analogously, the placebo effect is the difference between what happens when people are given placebos and what happens when they are not treated at all.

It is rare for a study to focus on the placebo effect or on the effect of the simple passage of time, for that matter. So where were we to find our placebo data and no-treatment data? We found our placebo data in clinical studies of antidepressants, and our no-treatment data in clinical studies of psychotherapy. It is common to have no-treatment or wait-list control groups in studies of the effects of psychotherapy. These groups consist of patients who are not given any treatment at all during the course of the study, although they may be placed on a wait list and given treatment after the research is concluded.

For the purpose of our research, Sapirstein and I were not particularly interested in the effects of the antidepressants or psychotherapy. What we were interested in was the placebo effect. But since we had the treatment data to hand, we looked at them as well. And, as it turned out, it was the comparison of drug and placebo that proved to be the most interesting part of our study.

All told, we analysed 38 clinical trials involving more than 3,000 depressed patients. We looked at the average improvement during the course of the study in each of the four types of groups: drug, placebo, psychotherapy and no-treatment. I am going to use a graph here (Figure 1.1) to show what the data tell us. Although the text will have a couple more such charts, I am going to keep them to a minimum. But this is one that I think we need, to make the point clearly. What the graph shows is that there was substantial improvement in both the drug and psychotherapy groups. People got better when given either form of treatment, and the difference between the two was not significant. People also got better when given placebos, and here too the improvement was remarkably large, although not as great as the improvement following drugs or psychotherapy. In contrast, the patients who had not been given any treatment at all showed relatively little improvement.

The first thing to notice in this graph is the difference in improvement between patients given placebos and patients not given any treatment at all. This difference shows that most of the improvement in the placebo groups was produced by the fact that they had been given placebos. The reduction in depression that people experienced was not just caused by the passage of time, the natural course of depression or any of the other factors that might produce an improvement in untreated patients. It was a placebo effect. and it was powerful.

Figure 1.1. Average improvement on drug, psychotherapy, placebo and no treatment. ‘lmprovement’ refers to the reduction of symptoms on scales used to measure depression. The numbers are called ‘effect sizes’. They are commonly used when the results of different studies are pooled together. Typically, effect sizes of 0.5 are considered moderate, whereas effect sizes of 0.8 are considered large. So the graph shows that antidepressants, psychotherapy and placebos produce large changes in the symptoms of depression, but there was only a relatively small average improvement in people who were not given any treatment at all.
.

One thing to learn from these data is that doing nothing is not the best way to respond to depression. People should not just wait to recover spontaneously from clinical depression, nor should they be expected just to snap out of it. There may be some improvement that is associated with the simple passage of time, but compared to doing nothing at all, treatment even if it is just placebo treatment provides substantial benefit.

Sapirstein and I were not surprised to find that there was a powerful placebo effect in the treatment of depression. Actually, we were quite pleased. That was our hypothesis and our reason for doing the study. What did surprise us, however, was how small the difference was between the response to the drug and the response to the placebo. That difference is the drug effect. Although the drug effect in the published clinical trials that we had analysed was statistically significant, it was much smaller than we had anticipated. Much of the therapeutic response to the drug was due to the placebo effect.

The relatively small size of the drug effect was the first of a series of surprises that the antidepressant data had in store for us.

One way to understand the size of the drug effect is to think about it as only a part of the improvement that patients experience when taking medication. Part of the improvement might be spontaneous that is, it might have occurred without any treatment at all and part may be a placebo effect. What is left over after you subtract spontaneous improvement and the placebo effect is the drug effect. You can see in Figure 1.1 that improvement in patients who had been given a placebo was about 75 per cent of the response to the real medication. That means that only 25 per cent of the benefit of antidepressant treatment was really due to the chemical effect of the drug. It also means that 50 per cent of the improvement was a placebo effect. In other words, the placebo effect was twice as large as the drug effect.

The drug effect seemed rather small to us, considering that these medications had been heralded as a revolution in the treatment of depression, blockbuster drugs that have been prescribed to hundreds of millions of patients, with annual sales totalling billions of pounds: Sapirstein and I must have done something wrong in either collecting or analysing the data. But what? We spent months trying to figure it out.

ARE ALL DRUGS CREATED EQUAL? DOUBLEBLIND OR DOUBLE-TALK

One thing that occurred to us, when considering how surprisingly small the drug effect was in the clinical trials we had analysed, was that a number of different medications had been assessed in those studies. Perhaps some of them were effective, whereas others were not. If this were the case, we had underestimated the benefits of effective drugs by lumping them together with ineffective medications. So before we sent our paper out for review, we went back to the data and examined the type of drugs that had been administered in each of the clinical trials in our meta-analysis.

We found that some of these trials had assessed tricyclic antidepressants, an older type of medication that was the most commonly used antidepressant in the 1960s and 1970s. In other trials, the focus was on selective serotonin reuptake inhibitors (SSRIs) like Prozac (fluoxetine), the first of the ‘new-generation’ drugs that replaced tricyclics as the top-selling type of antidepressant. And there were other types of antidepressants investigated in these trials as well. When we reanalysed the data, examining the drug effect and the placebo effect for each type of medication separately, we found that the diversity of drugs had not affected the outcome of our analysis. In fact, the data were remarkably consistent much more so than is usually the case when one analyses different groups of data. Not only did all of these medications produce the same degree of improvement in depression, but also, in each case, only 25 per cent of the improvement was due to the effect of the drug. The rest could be explained by the passage of time and the placebo effect.

The lack of difference we found between one class of antidepressants and another is now a rather frequent finding in antidepressant research. The newer antidepressants (SSRIs, for example) are no more effective than the older medications. Their advantage is that their side effects are less troubling, so that patients are more likely to stay on them rather than discontinue treatment. Still, the consistency of the size of the drug effect was surprising. It was not just that the percentages were close; they were virtually identical. They ranged from 24 to 26 per cent. At the time I thought, ‘What a nice coincidence! It will look great in a PowerPoint slide when I am invited to speak on this topic.’ But since then I have been struck by similar instances in which the consistency of the data is remarkable, and it is part of what has transformed me from a doubter to a disbeliever. I will note similar consistencies as we encounter them in this book.

The consistency of the effects of different types of antidepressants meant that we had not underestimated the antidepressant drug effect by lumping together the effects of more effective and less effective drugs. But our re-examination of the data in our meta-analysis held another surprise for us. Some of the medications we had analysed were not antidepressants at all, even though they had been evaluated for their effects on depression. One was a barbiturate, a depressant that had been used as a sleeping aid, before being replaced by less dangerous medications. Another was a benzodiazepine a sedative that has largely replaced the more dangerous barbiturates. Yet another was a synthetic thyroid hormone that had been given to depressed patients who did not have a thyroid disorder. Although none of these drugs are considered antidepressants, their effects on depression were every bit as great as those of antidepressants and significantly better than placebos. Joanna Moncrieff, a psychiatrist at University College London, has since listed other drugs that have been shown to be as effective as medications for depression. These include antipsychotic drugs, stimulants and herbal remedies. Opiates are also better than placebos, but I have not seen them compared to antidepressants.

If sedatives, barbiturates, antipsychotic drugs, stimulants, opiates and thyroid medications all outperform inert placebos in the treatment of depression, does this mean that any active drug can function as an antidepressant? Apparently not. In September 1998 the pharmaceutical company Merck announced the discovery of a novel antidepressant with a completely different mode of action than other medications for depression. This new drug, which they later marketed under the trade name Emend for the prevention of nausea and vomiting due to chemotherapy, seemed to show considerable promise as an antidepressant in early clinical trials. Four months later the company announced its decision to pull the plug on the drug as a treatment for depression. The reason? It could not find a significant benefit for the active drug over placebos in subsequent clinical trials.

This was unfortunate for a number of reasons. One is that the announcement caused a 5 per cent drop in the value of the company’s stock. Another is that the drug had an important advantage over current antidepressants, it produced substantially fewer side effects. The relative lack of side effects had been one reason for the enthusiasm about Merck’s new antidepressant. However, it may also have been the reason for its subsequent failure in controlled clinical trials. It seems that easily noticeable side effects are needed to show antidepressant benefit for an active drug compared to a placebo.

. . .

from

THE EMPEROR’S NEW DRUGS

by Irving Kirsch

get it at Amazon.com

ANGER CORRODES THE VESSEL THAT CONTAINS IT. Self Compassion and Anger in Relationships – Kristin Neff and Christopher Germer.

Our deepest need as human beings is the need to be loved. Our brains communicate emotions to one another, regardless of how carefully we chose our words.

Much of our relationship suffering is unnecessary and can be prevented by cultivating a loving relationship with ourselves. Cultivating self-compassion is one of the best things we can do for our relationship interactions.

Anger has a way of popping up around disconnection and can sometimes linger for years, long after the relationship has ended.

Sometimes we turn the anger against ourselves in the form of harsh self-criticism, which is a surefire way to become depressed. And if we get stuck in angry rumination, who did what to whom and what they deserve for it, we live with an agitated state of mind and may end up getting angry at others for no apparent reason.

“Anger corrodes the vessel that contains it.”

To have the type of close, connected relationships we really want with others, we first need to feel close and connected to ourselves. Cultivating self-compassion is far from selfish.

Much of our suffering arises in relationship with others. As Sartre famously wrote, “Hell is other people.” The good news is that much of our relationship suffering is unnecessary and can be prevented by cultivating a loving relationship with ourselves.

There are at least two types of relational pain. One is the pain of connection, when those we care about are suffering.

The other type is the pain of disconnection, when we experience loss or rejection and feel hurt, angry, or alone.

Our capacity for emotional resonance means that emotions are contagious. This is especially true in intimate relationships. If you are irritated with your partner but try to hide it, for instance, your partner will often pick up on your irritation. He might say, “Are you angry at me?” Even if you deny it, your partner will feel the irritation; it will affect his mood, leading to an irritated tone of voice. You will feel this, in turn, and become even more irritated, and your responses will have a harsher tone, and on it goes. This is because our brains would have been communicating emotions to one another regardless of how carefully we chose our words.

In social interactions, there can be a downward spiral of negative emotions, when one person has a negative attitude, the other person becomes even more negative, and so on. This means that other people are partly responsible for our state of mind, but we are also partly responsible for their state of mind. The good news is that emotional contagion gives us more power than we realize to change the emotional tenor of our relationships. Self-compassion can interrupt a downward spiral and start an upward spiral instead.

Compassion is actually a positive emotion and activates the reward centers of our brain, even though it arises in the presence of suffering. A very useful way to change the direction of a negative relationship interaction, therefore, is to have compassion for the pain we’re feeling in the moment. The positive feelings of compassion we have for ourselves will also be felt by others, manifested in our tone and subtle facial expressions, and help to interrupt the negative cycle, in this way cultivating self-compassion is one of the best things we can do for our relationship interactions as well as for ourselves.

Not surprisingly, research shows that self-compassionate people have happier and more satisfying romantic relationships. In one study, for instance, individuals with higher levels of self-compassion were described by their partners as being more accepting and nonjudgmental than those who lacked self-compassion. Rather than trying to change their partners, self-compassionate people tended to respect their opinions and consider their point of view. They were also described as being more caring, connected, affectionate, intimate, and willing to talk over relationship problems than those who lacked self-compassion. At the same time, self-compassionate people were described as giving their partners more freedom and autonomy in their relationships. They tended to encourage partners to make their own decisions and to follow their own interests. In contrast, people who lacked self-compassion were described as being more critical and controlling of their partners. They were also described as being more self-centered, inflexibly wanting everything their own way.

Steve met Sheila in college, and after 15 years of marriage he still loved her dearly. He hated to admit this to himself, but she was also starting to drive him crazy. Sheila was terribly insecure and constantly needed Steve to reassure her of his love and affection. Wasn’t sticking around for 15 years enough? If he didn’t tell her “I love you ” every day, she would start to worry, and if a few days went by she got into a proper sulk. He felt controlled by her need for reassurance and resented the fact that she didn’t honor his own need to express himself authentically. Thair relationship was starting to suffer.

To have the type of close, connected relationships we really want with others, we first need to feel close and connected to ourselves. By being supportive toward ourselves in times of struggle, we gain the emotional resources needed to care for our significant others. When we meet our own needs for love and acceptance, we can place fewer demands on our partners, allowing them to be more fully themselves. Cultivating self-compassion is far from selfish.

It gives us the resilience we need to build and sustain happy and healthy relationships in our lives.

Over time Sheila was able to see how her constant need for reassurance from Steve was driving him away. She realized that she had become a black hole and that Steve would never be able to fully satisfy her insecurity by giving her “enough” love. It would never be enough. So Sheila started a practice of journaling at night to give herself the love and affection she craved. She would write the type of tender words to herself that she was hoping to hear from Steve, like “I love you sweetheart. I won’t ever leave you.” Then, first thing in the morning, she would read what she had written and let it soak in. She began giving herself the reassurance she was desperately seeking from Steve and let him off the hook. It wasn’t quite as nice, she had to admit, but she liked the fact that she wasn’t so dependent. As the pressure eased, Steve started to be more naturally expressive in their relationship, and they became closer. The more secure she felt in her own self-acceptanee, the more she was able to accept his love as it was, not just how she wanted it to be. Ironically, by meeting her own needs she became less self-focused and started to feel an independence that was new and delicious.

Self-Compassion and Anger in Relationships

Another type of relational pain is disconnection, which occurs whenever there is a loss or rupture in a relationship. Anger is a common reaction to disconnection. We might get angry when we feel rejected or dismissed, but also when disconnection is unavoidable, such as when someone dies. The reaction may not be rational, but it still happens. Anger has a way of popping up around disconnection and can sometimes linger for years, long after the relationship has ended.

Although anger gets a bad rap, it isn’t necessarily bad. Like all emotions, anger has positive functions. For instance, anger can give us information that someone has overstepped our boundaries or hurt us in some way, and it may be a powerful signal that something needs to change. Anger can also provide us with the energy and determination to protect ourselves in the face of threat, take action to stop harmful behavior, or end a toxic relationship.

While anger in and of itself is not a problem, we often have an unhealthy relationship with anger. For instance, we may not allow ourselves to feel our anger and suppress it instead. This can be especially true for women, who are taught to be “nice,” i.e., not angry. When we try to stuff down our anger, it can lead to anxiety, emotional constriction, or numbness. Sometimes we turn the anger against ourselves in the form of harsh self-criticism, which is a surefire way to become depressed. And if we get stuck in angry rumination, who did what to whom and what they deserve for it, we live with an agitated state of mind and may end up getting angry at others for no apparent reason.

Nate was an electrician who lived in Chicago. He had split from his wife, Lila, over five years ago, but he still got enraged every time he thought about her. It turns out that Lila had an affair with a close friend of theirs, someone they often socialized with, and that this went on behind his back for almost a year. As soon as Nate found out about it, he was seething with anger. He somehow managed to refrain from calling her every name in the book, but he was sick to his stomach whenever he thought about what had happened. He filed for divorce almost immediately, thank goodness they didn’t have children, so the process was relatively quick and easy. Although he hadn’t had any contact with Lila for several years, his anger never really subsided. And the trauma of the affair kept Nate from forming new relationships because he had such a hard time trusting anyone.

If we continually harden our emotions in an attempt to protect ourselves against those we’re angry at, over time we may develop bitterness and resentment. Anger, bitterness, and resentment are “hard feelings.” Hard feelings are resistant to change and often stick with us long past the time when they are useful. (How many of us are still angry at someone we are unlikely to ever see again?) Furthermore, chronic anger causes chronic stress, which is bad for all the systems of the body, cardiovascular, endocrine, nervous, even the reproductive system. As the saying goes, “Anger corrodes the vessel that contains it.” Or “Anger is the poison we drink to kill another person.” When anger is no longer helpful to us, the most compassionate thing we can do is change our relationship to it, especially by applying the resources of mindfulness and self compassion.

How? The first step is to identify the soft feelings behind the hard feelings of anger. Often anger is protecting more tender, sensitive emotions, such as feeling hurt, scared, unloved, alone, or vulnerable. When we peel back the outer layer of anger to see what is underneath, we are often surprised by the fullness and complexity of our feelings. Hard feelings are difficult to work with directly because they are typically defensive and outward focused. When we identify our soft feelings, however, we turn inward and can begin the transformation process.

To truly heal, however, we need to peel back the layers even further and discover the unmet needs that are giving rise to our soft feelings. Unmet needs are universal human needs, those experiences that are core to any human being. The Center for Nonviolent Communication offers a comprehensive list of needs at http://www.cm/cnrg/ training/needs inventory. Some examples are the need to be safe, connected, validated, heard, included, autonomous, and respected. And our deepest need as human beings is the need to be loved.

By having the courage to turn toward and experience our authentic feelings and needs, we can begin to have insight into what is really going on for us. Once we contact the pain and respond with self-compassion, things can start to transform on a deep level. We can use self-compassion to meet our needs directly.

Self-compassion in response to unmet needs means that we can begin to give ourselves what we have yearned to receive from others, perhaps for many years. We can be our own source of support, respect, love, validation, or safety. Of course, we need relationships and connection with others. We aren’t automatons. But when others are unable to meet our needs, for whatever reason, and have harmed us in the process, we can recover by holding the hurt, the soft feelings, in a compassionate embrace and fill the hole in our hearts with loving, connected presence.

Nate worked hard at transforming his anger because he realized it was holding him back. He had tried catharsis to get it out, punching pillows, yelling at the top of his lungs but it didn’t work. Eventually Nate signed up for an MSC course because a friend was very enthusiastic about it and said it would reduce his stress.

When Nate came to the part of the MSC course that focused on transforming anger by meeting his unmet needs, he felt nervous but did it anyway. It was easy to get in touch with his anger, and even the hurt behind it, and feel it in his body. The toughest part was identifying his unmet need. Certainly Nate felt betrayed and unloved, but that wasn’t what seemed to be holding him back. Nate stuck with the exercise, and finally the unmet need revealed itself, and his whole body relaxed. Respect!

Nate came from a hardworking hlue-collar family, and his parents were still happily married after 30 years. He tried to do everything right in his own marriage, to the best of his ability, and he took his vows very seriously. Honesty and respect were core values for Nate. Knowing that Lila would never give him the respect he needed, it was too late for that, he took the plunge and tried to give it to himself. “I respect you,” he told himself. At first it felt silly and empty and hollow. So he paused and tried to say the words as if they were true. He thought about how much he had sacrificed to get his master electrician’s certification and open a business, the long hours he had put in to pay the mortgage and build a savings account. “I respect you,” he repeated, over and over, though it still just sounded like words. Then he thought of how honest and hardworking he had tried to be in his marriage, even though that wasn’t enough for Lila.

Very, very slowly, Nate started to take it in. Finally he put his hand on his heart and said it like he really meant it: “I respect you.” He started to tear up, because he actually felt it. Once he did, the anger at his wife started to melt away. He began to see her unmet needs, different from his, for more closeness and affection. Not that what Lila did was okay, but Nate realized that her behavior had nothing to do with his worth or value as a person. He couldn’t rely on any outside person, even one who was reliable and faithful, to give him the respect he needed. It had to come from within.

Self-Compassion and Forgiveness

When someone has harmed us and we still feel anger and bitterness, sometimes the most compassionate thing to do is to forgive. Forgiveness involves letting go of anger at someone who has caused us harm. But forgiveness must involve grieving before letting go. The central point of forgiveness practice is that we cannot forgive others without first opening to the hurt that we have experienced. Similarly, to forgive ourselves, we must first open to the pain, remorse, and guilt of hurting others.

Forgiveness doesn’t mean condoning bad behavior or resuming a relationship that causes harm. If we are being harmed in a relationship, we need to protect ourselves before we can forgive. If we are harming another in a relationship, we cannot forgive ourselves if we are using this as an excuse for acting badly. We must first stop the behavior, then acknowledge and take responsibility for the harm we have caused.

At the same time, it’s helpful to remember that the harm done is usually the product of a universe of interacting causes and conditions stretching back through time. We have partly inherited our temperament from our parents and grandparents, and our actions are shaped by our early childhood history, culture, health status, current events, and so forth. Therefore, we don’t have complete control over precisely what we say and do from one moment to the next.

Sometimes we cause pain in life without intending it, and we may still feel sorry about causing such pain. An example is when we move across the country to start a new life, leaving friends and family behind, or when we can’t give our elderly parents the attention they need because of our work situation. This kind of pain is not the fault of anyone, but it can still be acknowledged and healed with self compassion.

The capacity to forgive requires keen awareness of our common humanity. We are all imperfect human beings whose actions stem from a web of interdependent conditions that are much larger than ourselves. In other words, we don’t have to take our mistakes so personally.

Paradoxically, this understanding helps us take more responsibility for our actions because we feel more emotionally secure. One research study asked participants to recall a recent action they felt guilty about, such as cheating on an exam, lying to a romantic partner, saying something harmful, that still made them feel bad about themselves when they thought about it. The researchers found that participants who were helped to be self-compassionate about their transgression reported being more motivated to apologize for the harm done, and more committed to not repeating the behavior, than those who were not helped to be selfcompassionate.

Anneka really struggled to forgive herself after getting super angry at her friend and coworker Hilde, whom she told to f-off. Anneka had been under a tremendous amount of pressure at work to secure a contract with new clients and was all set to close the deal at a dinner that they were hosting. The clients were pretty conservative, and Anneka knew she had to be on time and look appropriate for them to trust her. Hilde was supposed to pick her up for the dinner, but she wasn’t there at the appointed time. Frantic, Anneka called her. “Where are you?” Hilde had completely forgotten about the event. “Oh, I ’m so sorry,” she offered lamely. Anneka dropped the f bomb, said a few more unpleasant things, then hung up and called a taxi. Immediately after ward, Anneka felt terrible. This was her friend! Hilde hadn’t done anything purposefully harmful, she simply forgot, and Anneka has been too busy to remind her. The truth was that Anneka was so anxious about closing the deal that she lost perspective and ouerreacted.

There are five steps to forgiveness:

1. Opening to pain, being present with the distress of what happened.

2. Self Compassion, allowing our hearts to melt with sympathy for the pain, no matter what caused it.

3. Wisdom, beginning to recognize that the situation wasn’t entirely personal, but was the consequence of many interdependent causes and conditions.

4. Intention to forgive. “May I begin to forgive myself [another] for what I [he/she] did, wittingly or unwittingly, to have caused them [me] pain.”

5. Responsibility to protect, committing ourselves to not repeat the same mistake; to stay out of harm’s way, to the best of our ability.

At first Anneka harshly berated herself for her behavior, but she knew that heating up on herself wouldn’t help anyone. Instead, Anneka needed to forgive herself for having made a mistake, just as everyone makes mistakes.

Anneka had learned the five steps to forgiveness from her MSC course, so she knew what to do. First, she had to accept the pain she had caused Hilde. This was really tough for Anneka, especially since she didn’t get the contract she was hoping for. Her mind wanted to pin all the blame on Hilde. It was Hilde’s fault! But Anneka knew the truth. There was no excuse for talking to Hilde that way. It was wrong.

Anneka allowed herself to feel in her bones what it must have been like for Hilde to hear those words, from someone she considered a friend. That took some courage because Anneka felt so bad about it. Then Anneka gave herself compassion for the pain of hurting someone she loved. “Everyone makes mistakes. I’m so sorry you wounded your friend in this manner. I know you deeply regret it.” Giving herself compassion provided a bit of perspective, and Anneka was able to acknowledge the incredible stress she was under. The circumstances brought out the worst in her. Then Anneka tried to forgive herself, at least in a preliminary way, for her behavior. “May I begin to forgive myself for the pain I unwittingly inflicted on my dear friend Hilde.” Anneka also made a commitment to take at least one deep breath before speaking when she felt angry. Anneka knew this might take some time because she didn’t always know when she felt angry, but she was determined to try to be less reactive when under stress.

The central point of forgiveness is first opening to the hurt that we experienced or caused to others. Timing is very important because we are naturally ambivalent about feeling the guilt of hurting others or making ourselves vulnerable to being hurt again. As the saying goes, first we need to “give up all hope of a better past.”

Embracing the Good

One of the biggest benefits of self compassion is that it doesn’t just help you cope with negative emotions, it actively generates positive emotions. When we embrace ourselves and our experience with loving, connected presence, it feels good. It doesn’t feel good in a saccharine way, nor does it resist or avoid what feels bad. Rather, self compassion allows us to have the full range of experience, the bitter and the sweet.

Typically, however, we tend to focus much more on what’s wrong than on what’s right in our lives. For example, when you get an annual review at work, what do you remember the most, the points of praise or criticism? Or if you go shopping at the mall and interact with five polite salespeople and one rude one, which is most likely to stick in your mind?

The psychological term for this is negativity bias. Rick Hanson says the brain is like “Velcro for bad experiences and Teflon for good ones.” Evolutionarily speaking, the reason we have a negativity bias is that our ancestors who fretted and worried at the end of the day, wondering where that pack of hyenas was yesterday and where it might be hanging out tomorrow, were more likely to survive than our ancestors who kicked back and relaxed. This is evolutionarily adaptive when we face physical danger. However, since most of the dangers we face nowadays are threats to our sense of self, it is self-compassionate to correct the negativity bias because it distorts reality.

We need to intentionally recognize and absorb positive experiences to develop more realistic, balanced awareness that is not skewed toward the negative. This requires some training, just like mindfulness and self-compassion require training. Furthermore, since compassion training includes opening to pain, we may need the energy boost of focusing on positive experience to support our compassion practice.

Focusing on the positive also has important benefits. Barbara Fredrickson, who developed the “broaden and build” theory, posits that the evolutionary purpose of positive emotions is to broaden attention. In other words, when people feel safe and content, they become curious and start exploring their environment, noticing opportunities for food, shelter, or rest. This allows us to take advantage of opportunities that would otherwise go unnoticed.

“When one door of happiness closes, another opens, but often we look so long at the closed door that we do not see the one that has been opened for us.” Helen Keller

Recently there has been a movement in psychology that focuses on finding the most effective ways to help people cultivate positive emotions, and two powerful practices that have been identified are savoring and gratitude.

Savoring

Savoring involves noticing and appreciating the positive aspects of life, taking them in, letting them linger, and then letting them go. It is more than pleasure, savoring involves mindful awareness of the experience of pleasure. In other words, being aware that something good is happening while it’s happening.

Given our natural tendency to skip over what’s right and focus on what’s wrong, we need to plut a little extra effort into paying attention to what gives us pleasure. Luckily, savoring is simple practice, noticing the tart and juicy taste of a fresh apple, a gentle cool breeze on your cheek, the warm smile of your coworker, the hand of your partner gently holding your own. Research suggests that simply taking the time to notice and linger with these sorts of positive experiences can greatly increase our happiness.

Gratitude

Gratitude involves recognizing, acknowledging, and being grateful for the good things in our lives. If we just focus on what we want but don’t have, we’ll remain in a negative state of mind. But when we focus on what we do have, and give thanks for it, we radically reframe our experience.

Whereas savoring is primarily an experiential practice, gratitude is a wisdom practice. Wisdom refers to understanding how everything arises interdependently, The confluence of factors required for even a simple event to occur is mind boggling and can inspire an attitude of awe and reverence. Gratitude involves recognizing the myriad people and events that contribute to the good in our lives. As an MSC participant once remarked, “The texture of wisdom is gratitude.”

Gratitude can be aimed at the big things in life, like our health and family, but the effect of gratitude may be even more powerful when it is aimed at small things, such as when the bus arrives on time or the air conditioning is working on a hot summer day. Research shows that gratitude is also strongly linked to happiness. As the philosopher Mark Nepo wrote: “One key to knowing joy is to be easily pleased.”

The meditation teacher James Baraz tells this wonderful story about the power of gratitude in his book Awakening Joy, which we’ve adapted here by permission.

One year I was visiting my then eighty-nine-year-old mother and brought along a magazine with an article on the beneficial effects of gratitude. As we ate dinner I told her about some of the findings. She said she was impressed by the reports but admitted she had a lifetime habit of looking at the glass half empty. “I know I ’m very fortunate and have so many things to be thankful for, but little things just set me off” She said she wished she could change the habit but had doubts whether that was possible. “I’m just more used to seeing what’s going wrong,” she concluded.

“You know, Mom, the key to gratitude is really in the way we frame a situation,” I began. “For instance, suppose all of a sudden your television isn’t getting good reception.”

“That’s a scenario I can relate to, ” she agreed with a knowing smile.

“One way to describe your experience would be to say, ‘This is so annoying I could scream.” Or you could say, ‘This is so annoying. . . and my life is really very blessed. She agreed that could make a big difference.

“But I don’t think I can remember to do that,” she sighed.

So together we made up a gratitude game to remind her. Each time she complained about something, I would simply say “and . . . ,” to which she would respond “and my life is very blessed.” I was elated to see that she was willing to try it out. Although it had started as just a fun game, after a while it began to have some real impact. Her mood grew brighter as our weeks became filled with gratitude. To my delight and amazement, my mother has continued doing the practice, and the change has been revolutionary.

Self-Appreciation

Most people recognize the importance of expressing gratitude and appreciation toward others. But what about ourselves? That one doesn’t come so easily.

The negativity bias is especially strong toward ourselves. Self appreciation not only feels unnatural it can feel downright wrong. Because our tendency is to focus on our inadequacies rather than appreciate our strengths, we often have a skewed perspective of who we are. Think about it, When you receive a compliment, do you take it in, or does it bounce off you almost immediately? We usually feel uncomfortable just thinking about our good qualities. The counterargument immediately arises: “I’m not always that way” or “I have a lot of bad qualities too.” Again, this reaction demonstrates the negativity bias because when we receive unpleasant feedback, our first thoughts are not typically “Yes, but I’m not aiways that way” or “Are you aware of all my good qualities?”

Many of us are actually afraid to acknowledge our own goodness. Some common reasons given for this are:

– I don’t want to alienate my friends by being arrogant.

– My good qualities are not a problem that needs to be fixed, so I don’t need to focus on them.

– I’m afraid I would be putting myself on a pedestal, only to fall off.

– It will make me feel superior and separate from others.

Of course, there is a big difference between simply acknowledging what’s true, that we have good as well as not so good qualities, and saying that we’re perfect or better than others. It’s important to appreciate our strengths as well as have compassion for our weaknesses so that we embrace the whole of ourselves, exactly as we are.

We can apply the three components of selfcompassion, self kindness, common humanity, and mindfulness, to our positive qualities as well as our negative ones. These three factors together allow us to appreciate ourselves in a healthy and balanced way.

Self Appreciation

Self Kindness: Part of being kind to ourselves involves expressing appreciation for our good qualities, just as we would do with a good friend.

Common Humanity: When we remember that having good qualities is part of being human, we can acknowledge our strengths without feeling isolated or better than others.

Mindfulness: To appreciate ourselves, we need to pay attention to our good qualities rather than taking them for granted.

It’s important to recognize that the practice of self appreciation is not selfish or self centered. Rather, it simply recognizes that good qualities are part of being human, Although some children may have been raised with the belief that humility means not recognizing their accomplishments, that approach can harm children‘s self-concept and get in the way of knowing themselves properly. Self-appreciation is a way to correct our negativity bias toward ourselves and see ourselves more clearly as a whole person. Self-appreciation also provides the emotional resilience and selfconfidence needed to give to others.

The best selling author and spiritual teacher Marianne Williamson writes, “We are all meant to shine, as children do. . . . And as we let our own light shine, we unconsciously give other people permission to do the same. As we are liberated from our own fear, our presence automatically liberates others.”

Wisdom and gratitude are central to selfappreciation as well. These qualities help us to see our good qualities in a broader context. When we appreciate ourselves, we’re also appreciating the causes, conditions, and people, including friends, parents, and teachers, who helped us develop those good qualities in the first place. This means we don’t need to take our own good qualities so personally!

Alice grew up in a stern Protestant family where humility and self effacement were the expected norm. When she was eight years old and came home with a trophy for winning her third-grade spelling bee, she remembers, her mother just raised her eyebrows and said, “Now don’t you be getting too big for your britches.” Every time Alice accomplished anything she felt she had to downplay it or else receive the disapproval of her family.

Later on in life, Alice started dating a man named Theo who thought she was beautiful and kind and smart and wonderful and liked to tell her so. Alice would not only cringe with embarrassment; Theo’s comments made her anxious. What if Theo finds out I’m not perfect? What happens if I let him down? She would continually push aside his comments when he said something nice, leaving Theo feeling perplexed and on the other side of an invisible wall.

Alice was becoming adept at self-compassion, especially the capacity to see her personal inadequacies as part of common humanity. Self-appreciation made sense to Alice, primarily conceptually, but she knew she had a way to go. First Alice made a mental note of everything good that she did during the day, a moment of kindness, a success, a small accomplishment. Then she tried to say something appreciative about it, such as “That was well done, Alice.” When Alice spoke to herself like this, she felt like she was violating an invisible contract from childhood and it made her uneasy, but she persisted. “I’m not saying I’m better than anyone else or that I’m perfect I’m simply acknowledging that this too is true.”

Eventually Alice made a commitment to take in and savor the heartfelt compliments Theo gave her. Theo was so delighted by this turn of events that he bought her a bracelet that said on the inside, I may not be perfect, but parts of me are excellent!

from

The Mindful Self-Compassion Workbook. A proven way to accept yourself, build inner strength, and thrive

by Kristin Neff, PhD and Christopher Germer, PhD

get it at Amazon.com

Also on TPPA = CRISIS

HOW TO ACCEPT YOURSELF, BUILD INNER STRENGTH, AND THRIVE. THE MINDFUL SELF-COMPASSION WORKBOOK – KRISTIN NEFF AND CHRISTOPHER GERMER

TED TALK. SELF-COMPASSION VS SELF-ESTEEM – DR KRISTIN NEFF

CFT: FOCUSING ON COMPASSION IN NEXT GENERATION CBT DENNIS TIRCH PH.D * COMPASSION FOCUSED THERAPY FOR DUMMIES – MARY WELFORD * COMPASSION FOCUSED THERAPY – PAUL GILBERT

THE MINDFUL PATH TO SELF-COMPASSION. FREEING YOURSELF FROM DESTRUCTIVE THOUGHTS AND EMOTIONS – CHRISTOPHER K. GERMER PhD

THE SELF ACCEPTANCE PROJECT. HOW TO BE KIND & COMPASSIONATE TOWARD YOURSELF IN ANY SITUATION – TAMI SIMON

HOW TO ACCEPT YOURSELF, BUILD INNER STRENGTH, AND THRIVE. The Mindful Self-Compassion Workbook – Kristin Neff and Christopher Germer.

“Be kind to yourself in the midst of suffering.”

Western culture places great emphasis on being kind to our friends, family, and neighbors who are struggling. Not so when it comes to ourselves.

Are you kinder to others than you are to yourself? More than a thousand research studies show the benefits of being a supportive friend to yourself, especially in times of need.

In the blink of an eye we can go from “I don’t like this feeling” to “I don’t want this feeling” to “I shouldn’t have this feeling” to “Something is wrong with me for having this feeling” to “I’m bad!”

The seeds of self-compassion already lie within you, learn how you can uncover this powerful inner resource and transform your life.

Self-compassion is the perfect alternative to self-esteem because it offers a sense of self-worth that doesn’t require being perfect or better than others.

This science-based workbook offers a step-by-step approach to breaking free of harsh self-judgments and impossible standards in order to cultivate emotional well-being. The book is based on the authors’ groundbreaking eight-week Mindful Self-Compassion (MSC) program, which has helped tens of thousands of people worldwide. It is packed with guided meditations (with audio downloads); informal practices to do anytime, anywhere; exercises; and vivid stories of people using the techniques to address relationship stress, weight and body image issues, health concerns, anxiety, and other common problems.

Kristin Neff, PhD, is Associate Professor of Human Development and Culture at the University of Texas at Austin and a pioneer in the field of self-compassion research.

Christopher Germer, PhD, has a private practice in mindfulnessand compassionbased psychotherapy in Arlington, Massachusetts, and is a part-time Lecturer on Psychiatry at Harvard Medical School/Cambridge Health Alliance. He is a founding faculty member of the Institute for Meditation and Psychotherapy and of the Center for Mindfulness and Compassion.

Introduction:

How To Approach This Workbook

“Our task is not to seek for love, but merely to seek and find all the barriers within yourself that you have built against it.” Rumi

We have all built barriers to love. We’ve had to in order to protect ourselves from the harsh realities of living a human life. But there is another way to feel safe and protected. When we are mindful of our struggles, and respond to ourselves with compassion, kindness, and support in times of difficulty, things start to change. We can learn to embrace ourselves and our lives, despite inner and outer imperfections, and provide ourselves with the strength needed to thrive.

An explosion of research into self-compassion over the last decade has shown its benefits for well-being. Individuals who are more self-compassionate tend to have greater happiness, life satisfaction, and motivation, better relationships and physical health, and less anxiety and depression. They also have the resilience needed to cope with stressful life events such as divorce, health crises, academic failure, even combat trauma.

When we struggle, however, when we suffer, fail, or feel inadequate, it’s hard to be mindful toward what’s occurring; we’d rather scream and beat our fists on the table. Not only do we not like what’s happening, we think there is something wrong with us because it’s happening. In the blink of an eye we can go from “I don’t like this feeling” to “I don’t want this feeling” to “I shouldn’t have this feeling” to “Something is wrong with me for having this feeling” to “I’m bad!”

That’s where self-compassion comes in. Sometimes we need to comfort and soothe ourselves for how hard it is to be a human being before we can relate to our lives in a more mindful way.

Self-compassion emerges from the heart of mindfulness when we meet suffering in our lives. Mindfulness invites us to open to suffering with loving, spacious awareness. Self-compassion adds, “be kind to yourself in the midst of suffering.” Together, mindfulness and self-compassion form a state of warmhearted, connected presence during difficult moments in our lives.

MINDFUL SELF-COMPASSION

Mindful Self-Compassion (MSC) was the first training program specifically designed to enhance a person’s self-compassion. Mindfulness-based training programs such as mindfulness-based stress reduction and mindfulness-based cognitive therapy also increase self-compassion, but they do so more implicitly, as a welcome byproduct of mindfulness. MSC was created as a way to explicitly teach the general public the skills needed to be self-compassionate in daily life. MSC is an eight-week course where trained teachers lead a group of 8 to 25 participants through the program for 234 hours each week, plus a half-day meditation retreat. Research indicates that the program produces long-lasting increases in self-compassion and mindfulness, reduces anxiety and depression, enhances overall well-being, and even stabilizes glucose levels among people with diabetes.

The idea for MSC started back in 2008 when the authors met at a meditation retreat for scientists. One of us (Kristin) is a developmental psychologist and pioneering researcher into self-compassion. The other (Chris) is a clinical psychologist who has been at the forefront of integrating mindfulness into psychotherapy since the mid-1990s. We were sharing a ride to the airport after the retreat and realized we could combine our skills to create a program to teach self-compassion.

I (Kristin) first came across the idea of self-compassion in 1997 during my last year of graduate school, when, basically, my life was a mess. I had just gotten through a messy divorce and was under incredible stress at school. I thought I would learn to practice Buddhist meditation to help me deal with my stress. To my great surprise the woman leading the meditation class talked about how important it was to develop self-compassion. Although I knew that Buddhists talked a lot about the importance of compassion for others, I never considered that having compassion for myself might be just as important. My initial reaction was “What? You mean I’m allowed to be kind to myself? Isn’t that selfish?” But I was so desperate for some peace of mind I gave it a try. Soon I realized how helpful self-compassion could be. I learned to be a good, supportive friend to myself when I struggled. When I started to be kinder to and less judgmental of myself, my life transformed.

After receiving my PhD, I did two years of postdoctoral training with a leading self-esteem researcher and began to learn about some of the downsides of the self-esteem movement.

Though it’s beneficial to feel good about ourselves, the need to be “special and above average” was being shown to lead to narcissism, constant comparisons with others, ego-defensive anger, prejudice, and so on.

The other limitation of self-esteem is that it tends to be contingent, it’s there for us in times of success but often deserts us in times of failure, precisely when we need it most!

I realized that self-compassion was the perfect alternative to self-esteem because it offered a sense of self-worth that didn’t require being perfect or better than others.

After getting a job as an assistant professor at the University of Texas at Austin, I decided to conduct research on self-compassion. At that point, no one had studied selfcompassion from an academic perspective, so I tried to define what self-compassion is and created a scale to measure it, which started what is now an avalanche of selfcompassion research.

The reason I really know self-compassion works, however, is because I’ve seen the benefits of it in my personal life. My son, Rowan, was diagnosed with autism in 2007, and it was the most challenging experience I had ever faced. I don’t know how I would have gotten through it if it weren’t for my self-compassion practice. I remember the day I got the diagnosis, I was actually on my way to a meditation retreat. I had told my husband that I would cancel the retreat so we could process, and he said, “No, go to your retreat and do that self-compassion thing, then come back and help me.”

So while I was on retreat, I flooded myself with compassion. I allowed myself to feel whatever I was feeling without judgment, even feelings I thought I “shouldn’t” be having. Feelings of disappointment, even of irrational shame. How could I possibly feel this about the person I love most in the world? But I knew I had to open my heart and let it all in. I let in the sadness, the grief, the fear. And fairly soon I realized I had the stability to hold it, that the resource of self-compassion would not only get me through, but would help me be the best, most unconditionally loving parent to Rowan I could be. And what a difference it made!

Because of the intense sensory issues experienced by children with autism, they are prone to violent tantrums. The only thing you can do as a parent is to try to keep your child safe and wait until the storm passes. When my son screamed and flailed away in the grocery store for no discernible reason, and strangers gave me nasty looks because they thought I wasn’t disciplining my child properly, I would practice self-compassion. I would comfort myself for feeling confused, ashamed, stressed, and helpless, providing myself the emotional support I desperately needed in the moment. Self-compassion helped me steer clear of anger and self-pity, allowing me to remain patient and loving toward Rowan despite the feelings of stress and despair that would inevitably arise. I’m not saying that I didn’t have times when I lost it. I had many. But I could rebound from my missteps much more quickly with self-compassion and refocus on supporting and loving Rowan.

I (Chris) also learned self-compassion primarily for personal reasons. I had been practicing meditation since the late ’70s, became a clinical psychologist in the early ’80s, and joined a study group on mindfulness and psychotherapy. This dual passion for mindfulness and therapy eventually led to the publication of Mindfulness and Psychotherapy.

As mindfulness became more popular, I was being asked to do more public speaking. The problem, however, was that I suffered from terrible public speaking anxiety. Despite maintaining a regular practice of meditation my whole adult life and trying every clinical trick in the book to manage anxiety, before any public talk my heart would pound, my hands began to sweat, and I found it impossible to think clearly. The breaking point came when I was scheduled to speak at an upcoming Harvard Medical School conference that I helped to organize. (I still tried to expose myself to every possible speaking opportunity.) I’d been safely tucked in the shadows of the medical school as a clinical instructor but now I’d have to give a speech and expose my shameful secret to all my esteemed colleagues.

Around that time, a very experienced meditation teacher advised me to shift the focus of my meditation to loving-kindness, and to simply repeat phrases such as “May I be safe,” “May I be happy,” “May I be healthy,” “May I live with ease.” So I gave it a try. In spite of all the years I’d been meditating and reflecting on my inner life as a psychologist, I’d never spoken to myself in a tender, comforting way. Right off the bat, I started to feel better and my mind also became clearer. I adopted loving-kindness as my primary meditation practice.

Whenever anxiety arose as I anticipated the upcoming conference, I just said the loving-kindness phrases to myself, day after day, week after week. I didn’t do this particularly to calm down, but simply because there was nothing else I could do. Eventually, however, the day of the conference arrived. When I was called to the podium to speak, the typical dread rose up in the usual way. But this time there was something new, a faint background whisper saying, “May you be safe. May you be happy . . .” In that moment, for the first time, something rose up and took the place of fear, self-compassion.

Upon later reflection, I realized that I was unable to mindfully accept my anxiety because public speaking anxiety isn’t an anxiety disorder after all, it’s a shame disorder, and the shame was just too overwhelming to bear. Imagine being unable to speak about the topic of mindfulness due to anxiety! I felt like a fraud, incompetent, and a bit stupid. What I discovered on that fateful day was that sometimes, especially when we’re engulfed in intense emotions like shame, we need to hold ourselves before we can hold our moment-to-moment experience. I had begun to learn self-compassion, and saw its power firsthand.

In 2009, I published The Mindful Path to Self-Compassion in an effort to share what I had learned, especially in terms of how self-compassion helped the clients I saw in clinical practice. The following year, Kristin published Self-Compassion, which told her personal story, reviewed the theory and research on self-compassion, and provided many techniques for enhancing self-compassion.

Together we held the first public MSC program in 2010. Since then we, along with a worldwide community of fellow teachers and practitioners, have devoted a tremendous amount of time and energy to developing MSC and making it safe, enjoyable, and effective for just about everyone. The benefits of the program have been supported in multiple research studies, and to date tens of thousands of people have taken MSC around the globe.

HOW TO USE THIS WORKBOOK

Most of the MSC curriculum is contained in this workbook, in an easy-to-use format that will help you start to be more self-compassionate right away. Some people who use this workbook will be currently taking an MSC course, some may want to refresh what they previously learned, but for many people this will be their first experience with MSC.

This workbook is designed to also be a stand-alone pathway for you to learn the skills you need to be more self-compassionate in daily life. It follows the general structure of the MSC course, with the chapters organized in a carefully sequenced manner so the skills build upon one another. Each chapter provides basic information about a topic followed by practices and exercises that allow you to experience the concepts firsthand.

Most of the chapters also contain illustrations of the personal experiences of participants in the MSC course, to help you know how the practices may play out in your life. These are composite illustrations that don’t compromise the privacy of any particular participant, and the names are not real. In this book, we also alternate between masculine and feminine pronouns when referring to a single individual. We have made this choice to promote ease of reading as our language continues to evolve and not out of disrespect toward readers who identify with other personal pronouns. We sincerely hope that all will feel included.

We recommend that you go through the chapters in order, giving the time needed in between to do the practices a few times. A rough guideline would be to practice about 30 minutes a day and to do about one or two chapters per week. Go at your own pace, however. If you feel you need to go more slowly or spend extra time on a particular topic, please do so. Make the program your own. If you are interested in taking the MSC course in person from a trained MSC teacher, you can find a program near you at http://www.centerformsc.org. Online training is also available. For professionals who want to learn more about the theory, research, and practice of MSC, including how to teach self-compassion to clients, we recommend reading the MSC professional training manual, to be published by The Guilford Press in 2019.

The ideas and practices in this workbook are largely based on scientific research (notes at the back of the book point to the relevant research). However, they are also based on our experience teaching thousands of people how to be more selfcompassionate. The MSC program is itself an organic entity, continuing to evolve as we and our participants learn and grow together.

Also, while MSC isn’t therapy, it’s very therapeutic, it will help you access the resource of self-compassion to meet and transform difficulties that inevitably emerge as we live our lives. However, the practice of self-compassion can sometimes activate old wounds, so if you have a history of trauma or are currently having mental health challenges, we recommend that you complete this workbook under the supervision of a therapist.

Tips for Practice

As you go through this workbook, it’s important to keep some points in mind to get the most out of it.

– MSC is an adventure that will take you into uncharted territory, and unexpected experiences will arise. See if you can approach this workbook as an experiment in self-discovery and self-transformation. You will be working in the laboratory of your own experience, see what happens.

– While you will be learning numerous techniques and principles of mindfulness and self-compassion, feel free to tailor and adapt them in a way that works for you. The goal is for you to become your own best teacher.

– Know that tough spots will show up as you learn to turn toward your struggles in a new way. You are likely to get in touch with difficult emotions or painful self-judgments. Fortunately, this book is about building the emotional resources, skills, strengths, and capacities to deal with these difficulties.

– While self-compassion work can be challenging, the goal is to find a way to practice that’s pleasant and easy. Ideally, every moment of self-compassion involves less stress, less striving, and less work, not more.

– It is good to be a “slow learner.” Some people defeat the purpose of self compassion training by pushing themselves too hard to become self compassionate. Allow yourself to go at your own pace.

– The workbook itself is a training ground for self-compassion. The way you approach this course should be self-compassionate. In other words, the means and ends are the same.

– It is important to allow yourself to go through a process of opening and closing as you work through this book. just as our lungs expand and contract, our hearts and minds also naturally open and close. It is self-compassionate to allow ourselves to close when needed and to open up again when that naturally happens. Signs of opening might be laughter, tears, or more vivid thoughts and sensations. Signs of closing might be distraction, sleepiness, annoyance, numbness, or self-criticism.

– See if you can find the right balance between opening and closing. Just like a faucet in the shower has a range of water flow between off and full force that you can control, you can also regulate the degree of openness you experience. Your needs will vary: sometimes you may not be in the right space to do a particular practice, and other times it will be exactly what you need. Please take responsibitty for your own emotional safety, and don’t push yourself through something if it doesn’t feel right in the moment. You can always come back to it later, or do the practice with the help and guidance of a trusted friend or therapist.

1. What is Self-Compassion?

Selt-compassion involves treating yourself the way you would treat a friend who is having a hard time, even if your friend blew it or is feeling inadequate, or is just facing a tough life challenge. Western culture places great emphasis on being kind to our friends, family, and neighbors who are struggling. Not so when it comes to ourselves. Self-compassion is a practice in which we learn to be a good friend to ourselves when we need it most, to become an inner ally rather than an inner enemy. But typically we don’t treat ourselves as well as we treat our friends.

The golden rule says “Do unto others as you would have them do unto you.” However, you probably don’t want to do unto others as you do unto yourself! Imagine that your best friend calls you after she just got dumped by her partner, and this is how the conversation goes.

“Hey,” you say, picking up the phone. “How are you?”

“Terrible,” she says, choking back tears. “You know that guy Michael I’ve been dating? Well, he’s the first man I’ve been really excited about since my divorce. Last night he told me that I was putting too much pressure on him and that he just wants to be friends. I’m devastated.”

You sigh and say, “Well, to be perfectly honest, it’s probably because you’re old, ugly, and boring, not to mention needy and dependent. And you’re at least 20 pounds overweight. I’d just give up now, because there’s really no hope of finding anyone who will ever love you. I mean, frankly you don’t deserve it!”

Would you ever talk this way to someone you cared about? Of course not. But strangely, this is precisely the type of thing we say to ourselves in such situations, or worse. With self-compassion, we learn to speak to ourselves like a good friend. “I’m so sorry. Are you okay? You must be so upset. Remember I’m here for you and I deeply appreciate you. Is there anything I can do to help?”

Although a simple way to think about self-compassion is treating yourself as you would treat a good friend, the more complete definition involves three core elements that we bring to bear when we are in pain: self-kindness, common humanity, and mindfulness.

Self-Kindness. When we make a mistake or fail in some way, we are more likely to beat ourselves up than put a supportive arm around our own shoulder. Think of all the generous, caring people you know who constantly tear themselves down (this may even be you). Self-kindness counters this tendency so that we are as caring toward ourselves as we are toward others. Rather than being harshly critical when noticing personal shortcomings, we are supportive and encouraging and aim to protect ourselves from harm. Instead of attacking and berating ourselves for being inadequate, we offer ourselves warmth and unconditional acceptance. Similarly, when external life circumstances are challenging and feel too difficult to bear, we actively soothe and comfort ourselves.

Theresa was excited. “I did it! I can’t believe I did it! I was at an office party last week and blurted out something inappropriate to a coworker. Instead of doing my usual thing of calling myself terrible names, I tried to be kind and understanding. I told myself, ‘Oh well, it’s not the end of the world. I meant well even if it didn’t come out in the best way.”

Common Humanity. A sense of interconnectedness is central to self-compassion. It’s recognizing that all humans are flawed works-in-progress, that everyone fails, makes mistakes, and experiences hardship in life. Self-compassion honors the unavoidable fact that life entails suffering, for everyone, without exception. While this may seem obvious, it’s so easy to forget. We fall into the trap of believing that . . .

from

The Mindful Self-Compassion Workbook. A proven way to accept yourself, build inner strength, and thrive

by Kristin Neff, PhD and Christopher Germer, PhD

get it at Amazon.com

Also on TPPA = CRISIS

TED TALK. SELF-COMPASSION VS SELF-ESTEEM – DR KRISTIN NEFF

CFT: FOCUSING ON COMPASSION IN NEXT GENERATION CBT DENNIS TIRCH PH.D * COMPASSION FOCUSED THERAPY FOR DUMMIES – MARY WELFORD * COMPASSION FOCUSED THERAPY – PAUL GILBERT

THE MINDFUL PATH TO SELF-COMPASSION. FREEING YOURSELF FROM DESTRUCTIVE THOUGHTS AND EMOTIONS – CHRISTOPHER K. GERMER PhD

THE SELF ACCEPTANCE PROJECT. HOW TO BE KIND & COMPASSIONATE TOWARD YOURSELF IN ANY SITUATION – TAMI SIMON

MIGRAINE AND DEPRESSION: It’s All The Same Brain – Gale Scott * Migraine May Permanently Change Brain Structure – American Academy of Neurology * Migraine: Multiple Processes, Complex Pathophysiology – Rami Burstein, Rodrigo Noseda, and David Borsook.

The symptoms that accompany migraine suggest that multiple neuronal systems function abnormally. Neuroimaging studies show that brain networks, brain morphology, and brain chemistry are altered in episodic and chronic migraineurs. As a consequence of the disease itself or its genetic underpinnings, the migraine brain is altered structurally and functionally.

Migraine tends to run in families and as such is considered a genetic disorder. Genetic predisposition to migraine resides in multiple susceptible gene variants, many of which encode proteins that participate in the regulation of glutamate neurotransmission and proper formation of synaptic plasticity.

Migraine is a leading cause of suicide, an indisputable proof of the severity of the distress that the disease may inflict on the individual. 40% of migraine patients are also depressed.

Migraine and Depression: It’s All The Same Brain

Gale Scott

When a patient suffers from both migraines and depression or other psychiatric comorbidities, physicians have to treat both. It’s a common situation, since 40% of migraine patients are also depressed. Anxiety is even more prevalent in these patients. An estimated 50% of migraine patients are anxious whether with generalized anxiety, phobias, panic attacks. or other forms of anxiety, said Mia Minen, MD Director of Headache Services at NYU Langoni Medical Center.

Health care costs in treating these co-morbid patients are 1.5 times higher than for migraine patients without accompanying psychiatric disorders.

But sorting out whether one problem is causing the other is not always easy, she said in a recent interview at NYU Langone. “it’s really interesting, which came first,” she said, “We really don’t know.”

There may be a bidirectional relationship with depression. Anxiety may precede migraines, then depression may follow.

Fortunately, she said, the question of which problem came first doesn’t really matter that much.

“It’s all one brain, one organ, and some of the same neurotransmitters are implicated in both disorders.” Serotonin is affected in migraine just as it is in depression and anxiety, she said. Dopamine and norepinephrine are also related both to migraines and psychiatric comorbidities.

“So it’s really one organ that’s controlling all these things,” Minen said.

The first step in treatment is having patients keep a headache diary to track the intensity and frequency and what they take when they feel it coming on.

For a mild migraine that might be ibuprofen or another over-the-counter pain killer.

If the migraine is moderately severe there are 7 migraine-specifuc medications that are effective, she said. There are oral, nasal, and injectable forms of triptans a family of tryptamine-based drugs. “We sometimes tell patients to combine the triptan with Naprosyn,” she said.

If triptans are contraindicated because the patient has other health problems, there are still more pharmaceutical options.

Those include some classes of beta blockers, antiseizure medications, and tricyclic antidepressants at low doses.

The drug regimen may vary with the particular comorbidity. For instance, for migraines with anxiety, venlafaxine might work. If patients have sleep disturbances, amitriptyline might be effective. “Lack of sleep is also a trigger for migraine,” she noted.

The toughest co-morbidity to treat in patients with migraine is finding a regimen that works for patients who are taking a lot of psychiatric medications, like SSRIs and antipsychotics.

For older patients with migraines plus cardiovascular disease, drug choices are also limited.

Botox injections seem promising, but Minen is cautious. “It’s a great treatment for patients with chronic migraines but they have to have failed 2 or 3 medications before they qualify for Botox.” Treatment involves 31 injections over the forehead, the back of the head and the neck. Relief lasts about 3 months, she said.

In addition to pharmaceutical treatment, there are cognitive behavior approaches that can work, like biofeedback and progressive muscle relaxation therapy.

Opioids are not the treatment of choice, she said. They have not been shown to be effective, Minen said and reduce the body’s ability to respond to triptans.

“For chronic migraine, studies don’t show opioids enable patients to return to work; there is no objective study showing they work,” and their uses raises other problems. Patients used to taking opioids who go to an emergency room and request them may find themselves suspected of drugseeking behavior. “It’s hard for doctors and patients,” she said, when patients ask for opioids “It puts doctors in a predicament.”

New drugs are on the horizon, she said. “Calcitonin gene related peptide antagonists look good,” and unlike triptans are not contraindicated for people at risk of strokes or heart attacks.

For now, said Minen, treating migraine and comorbidities “is more an art than a science,” she said, “But a large majority of patients do get better.”

Migraine May Permanently Change Brain Structure

American Academy of Neurology

Migraine may have longlasting effects on the brain’s structure, according to a study published in the August 28, 2013, online issue of Neurology®, the medical journal of the American Academy of Neurology.

“Traditionally, migraine has been considered a benign disorder without long-term consequences for the brain,” said study author Messoud Ashina, MD, PhD, with the University of Copenhagen in Denmark. “Our review and meta-analysis study suggests that the disorder may permanently alter brain structure in multiple ways.”

The study found that migraine raised the risk of brain lesions, white matter abnormalities and altered brain volume compared to people without the disorder. The association was even stronger in those with migraine with aura.

Migraine with aura
A common type of migraine featuring additional neurological symptoms. Aura is a term used to describe a neurological symptom of migraine, most commonly visual disturbances.
People who experience ‘migraine with aura’ will have many or all the symptoms of a ‘migraine without aura‘ and additional neurological symptoms which develop over a 5 to 20 minute period and last less than an hour.
Visual disturbances can include: blind spots in the field of eyesight, coloured spots, sparkles or stars, flashing lights before the eyes, tunnel vision, zig zag lines, temporary blindness.
Other symptoms include: numbness or tingling, pins and needles in the arms and legs, weakness on one side of the body, dizziness, a feeling of spinning (vertigo).
Speech and hearing can be affected and some people have reported memory changes, feelings of fear and confusion and, more rarely, partial paralysis or fainting.
These neurological symptoms usually happen before a headache, which could be mild, or no headache may follow.

For the meta-analysis, researchers reviewed six population-based studies and 13 clinic-based studies to see whether people who experienced migraine or migraine with aura had an increased risk of brain lesions, silent abnormalities or brain volume changes on MRI brain scans compared to those without the conditions.

The results showed that migraine with aura increased the risk of white matter brain lesions by 68 percent and migraine with no aura increased the risk by 34 percent, compared to those without migraine. The risk for infarct-like abnormalities increased by 44 percent for those without aura. Brain volume changes were more common in people with migraine and migraine with aura than those with no migraines.

“Migraine affects about 10 to 15 percent of the general population and can cause a substantial personal, occupational and social burden,” said Ashina. “We hope that through more study, we can clarify the association of brain structure changes to attack frequency and length of the disease. We also want to find out how these lesions may influence brain function.”

The study was supported by the Lundbeck Foundation and the Novo Nordisk Foundation.

To learn more about migraine, please visit American Academy of Neurology.

Migraine: Multiple Processes, Complex Pathophysiology

Rami Burstein (1,3), Rodrigo Noseda (1,3) and David Borsook (2,3)
1 – Department of Anesthesia, Critical Care, and Pain Medicine, Beth Israel Deaconess Medical Center, Boston
2 – Department of Anesthesiology, Perioperative and Pain Medicine, Boston Children’s Hospital
3 – Harvard Medical School

Migraine is a common, multifactorial, disabling, recurrent, hereditary neurovascular headache disorder. It usually strikes sufferers a few times per year in childhood and then progresses to a few times per week in adulthood, particularly in females. Attacks often begin with warning signs (prodromes) and aura (transient focal neurological symptoms) whose origin is thought to involve the hypothalamus, brainstem, and cortex.

Once the headache develops, it typically throbs, intensifies with an increase in intracranial pressure, and presents itself in association with nausea, vomiting, and abnormal sensitivity to light, noise, and smell. It can also be accompanied by abnormal skin sensitivity (anodynia) and muscle tenderness.

Collectively, the symptoms that accompany migraine from the prodromal stage through the headache phase suggest that multiple neuronal systems function abnormally.

As a consequence of the disease itself or its genetic underpinnings, the migraine brain is altered structurally and functionally. These molecular, anatomical, and functional abnormalities provide a neuronal substrate for an extreme sensitivity to fluctuations in homeostasis, a decreased ability to adapt, and the recurrence of headache.

Homeostasis is the state of steady internal conditions maintained by living things.

Advances in understanding the genetic predisposition to migraine, and the discovery of multiple susceptible gene variants (many of which encode proteins that participate in the regulation of glutamate neurotransmission and proper formation of synaptic plasticity) define the most compelling hypothesis for the generalized neuronal hyperexcitability and the anatomical alterations seen in the migraine brain.

Regarding the headache pain itself, attempts to understand its unique qualities point to activation of the trigeminovascular pathway as a prerequisite for explaining why the pain is restricted to the head, often affecting the periorhital area and the eye, and intensities when intracranial pressure increases.

Introduction

Migraine is a recurrent headache disorder affecting 15% of the population during the formative and most productive periods of their lives, between the ages of 22 and 55 years. It frequently starts in childhood, particularly around puberty, and affects women more than men.

It tends to run in families and as such is considered a genetic disorder.

In some cases, the headache begins with no warning signs and ends with sleep. In other cases, the headache may be preceded by a prodromal phase that includes fatigue; euphoria; depression; irritability; food cravings; constipation; neck stiffness; increased yawning; and/or abnormal sensitivity to light, sound, and smell and an aura phase that includes a variety of focal cortically mediated neurological symptoms that appear just before and/or during the headache phase. Symptoms of migraine aura develop gradually, feature exeitatory and inhibitory phases, and resolve completely. Positive (gain of function) and negative (loss of function) symptoms may present as scintillating lights and scotomas when affecting the visual cortex; paresthesia, and numbness of the face and hands when affecting the somatosensory cortex; tremor and unilateral muscle weakness when affecting the motor cortex or basal ganglia; and difficulty saying words (aphasia) when affecting the speech area.

The pursuant headache is commonly unilateral, pulsating, aggravated by routine physical activity, and can last a few hours to a few days (Headache Classification Committee of the International Headache Society, 2013). As the headache progresses, it may be accompanied by a variety of autonomic symptoms (nausea, vomiting, nasallsinus congestion, rhinorrhea, lacrimation, ptosis, yawning, frequent urination, and diarrhea), affective symptoms (depression and irritability), cognitive symptoms (attention deficit, difficulty finding words, transient amnesia, and reduced ability to navigate in familiar environments), and sensory symptoms (photophobia, phonophobia, osmophobia, muscle tenderness, and cutaneous allodynia).

The extent of these diverse symptoms suggests that migraine is more than a headache. It is now viewed as a complex neurological disorder that affects multiple cortical, subcortical, and brainstem areas that regulate autonomic, affective, cognitive, and sensory functions. As such, it is evident that the migraine brain differs from the non-migraine brain and that an effort to unravel the pathophysiology of migraine must expand beyond the simplistic view that there are “migraine generator” areas.

In studying migraine pathophysiology, we must consider how different neural networks interact with each other to allow migraine to commence with stressors such as insufficient sleep, skipping meals, stressful or post stressful periods, hormonal fluctuations, alcohol, certain foods, flickering lights, noise, or certain scents, and why migraine attacks are sometimes initiated by these triggers and sometimes not.

We must tackle the enigma of how attacks are resolved on their own or just weaken and become bearable by sleep, relaxation, food, and/or darkness. We must explore the mechanisms by which the frequency of episodic migraine increases over time (from monthly to weekly to daily), and why progression from episodic to chronic migraine is uncommon.

Disease mechanisms

In many cases, migraine attacks are likely to begin centrally, in brain areas capable of generating the classical neurological symptoms of prodromes and aura, whereas the headache phase begins with consequential activation of meningeal nociceptors at the origin of the trigeminovascular system.

A nociceptor is a sensory neuron that responds to damaging or potentially damaging stimuli by sending “possible threat” signals to the spinal cord and the brain. If the brain perceives the threat as credible, it creates the sensation of pain to direct attention to the body part, so the threat can hopefully be mitigated; this process is called nociception.
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The meninges are the three membranes that envelop the brain and spinal cord. In mammals, the meninges are the dura mater, the arachnoid mater, and the pia mater. Cerebrospinal fluid is located in the subarachnoid space between the arachnoid mater and the pia mater. The primary function of the meninges is to protect the central nervous system.

While some clues about how the occurrence of aura can activate nociceptors in the meninges exist, nothing is known about the mechanisms by which common prodromes initiate the headache phase or what sequence of events they trigger that results in activation of the meningeal nociceptors. A mechanistic search for a common denominator in migraine symptomatology and characteristics points heavily toward a genetic predisposition to generalized neuronal hyperexcitability. Mounting evidence for alterations in brain structure and function that are secondary to the repetitive state of headache can explain the progression of disease.

Prodromes

In the context of migraine, prodromes are symptoms that precede the headache by several hours. Examination of symptoms that are most commonly described by patients point to the potential involvement of the hypothalamus (fatigue, depression, irritability, food cravings, and yawning), brainstem (muscle tenderness and neck stiffness), cortex (abnormal sensitivity to light, sound, and smell), and limbic system (depression and anhedonia) in the prodromal phase of a migraine attack. Given that symptoms such as fatigue, yawning, food craving, and transient mood changes occur naturally in all humans, it is critical that we understand how their occurrence triggers a headache; whether the routine occurrence of these symptoms in migraineurs (i.e., when no headache develops) differs mechanistically from their occurrence before the onset of migraine; and why yawning, food craving, and fatigue do not trigger a migraine in healthy subjects.

Recently, much attention has been given to the hypothalamus because it plays a key role in many aspects of human circadian rhythms (wake sleep cycle, body temperature, food intake, and hormonal fluctuations) and in the continuous effort to maintain homeostasis. Because the migraine brain is extremely sensitive to deviations from homeostasis, it seems reasonable that hypothalamie neurons that regulate homeostasis and circadian cycles are at the origin of some of the migraine prodromes.

Unraveling the mechanisms by which hypothalamic and brainstem neurons can trigger a headache is central to our ability to develop therapies that can intercept the headache during the prodromal phase (i.e., before the headache begins. The ongoing effort to answer this question focuses on two very different possibilities (Fig. 1). The first suggests that hypothalamic neurons that respond to changes in physiological and emotional homeostasis can activate meningeal nociceptors by altering the balance between parasympathetic and sympathetic tone in the meninges toward the predominance of parasympathetic tone. Support for such a proposal is based on the following: (1) hypothalamic neurons are in a position to regulate the firing of preganglionic parasympathetic neurons in the superior salivatory nucleus (SSN) and sympathetic preganglionic neurons in the spinal intermediolateral nucleus. (2) the SSN can stimulate the release of acetylcholine, vasoactive intestinal peptide, and nitric oxide from meningeal terminals of postganglionic parasympathetic neurons in the Spheno palatine ganglion (SPG), leading to dilation of intracranial blood vessels, plasma protein extravasation, and local release of inflammatory molecules capable of activating pial and dural branches of meningeal nociceptors; (3) meningeal blood vessels are densely innervated by para sympathetic fibers. (4) activation of SSN neurons can modulate the activity of central trigeminovascular neurons in the spinal trigeminal nucleus. (5) activation of meningeal nociceptors appears to depend partially on enhanced activity in the SPG. (6) enhanced cranial parasympathetic tone during migraine is evident by lacrimation and nasal congestion, and, finally, (7) blockade of the sphenopalatine ganglion provides partial or complete relief of migraine pain.

The second proposal suggests that hypothalamic and brainstem neurons that regulate responses to deviation from physiological and emotional homeostasis can lower the threshold for the transmission of nociceptive trigeminovascular signals from the thalamus to the cortex, a critical step in establishing the headache experience. This proposal is based on understanding how the thalamus selects, amplifies, and prioritizes information it eventually transfers to the cortex, and how hypothalamic and brainstem nuclei regulate relay thalamocortical neurons. It is constructed from recent evidence that relay trigeminothalamic neurons in sensory thalamie nuclei receive direct input from hypothalamic neurons that contain dopamine, histamine, orexin, and melanin concentrating hormone (MCH), and brainstem neurons that contain noradrenaline and serotonin. In principle, each of these neuropeptides/neurotransmitters can shift the activity of thalamic neurons from burst to tonic mode if it is excitatory (dopamine, and high concentration of serotonin, noradrenaline, histamine, orexin, and from tonic to burst mode if it is inhibitory (MCH and low concentration of serotonin). The opposing factors that regulate the firing of relay trigeminovascular thalamic neurons provide an anatomical foundation for explaining why prodromes give rise to some migraine attacks but not to others, and why external (e.g., exposure to strong perfume) and internal conditions (e.g., skipping a meal and feeling hungry, sleeping too little and being tired, or simple stress) trigger migraine attacks so inconsistently.

In the context of migraine, the convergence of these hypothalamic and brainstem neurons on thalamic trigeminovascular neuruns can establish high and low set points for the allostatic load of the migraine brain. The allostatic load, defined as the amount of brain activity required to appropriately manage the level of emotional or physiological stress at any given time, can explain why external and internal conditions only trigger headache some of the times, when they coincide with the right circadian phase of cyclic rhythmicity of brainstem, and hypothalamic and thalamic neurons that preserve homeostasis.

Cortical spreading depression

Clinical and preclinical studies suggest that migraine aura is caused by cortical spreading depression (CSD), a slowly propagating wave of depolarization/excitation followed by hyperpolarization/inhibition in cortical neurons and glia. While specific processes that initiate CSD in humans are not known, mechanisms that invoke inflammatory molecules as a result of emotional or physiological stress, such as lack of sleep, may play a role. In the cortex, the initial membrane depolarization is associated with a large efflux of potassium; influx of sodium and calcium; release of glutamate, ATP, and hydrogen ions; neuronal swelling ; upregulation of genes involved in inflammatory processing; and a host of changes in cortical perfusion and enzymatic activity that include opening of the megachannel Panxl, activation of caspase-1, and a breakdown of the blood brain barrier.

Outside the brain, caspase-1 activation can initiate inflammation by releasing high mobility group protein B1 and interleukin-1 into the CSF, which then activates nuclear factor KB in astrocytes, with the consequential release of cyclooxygenase-2 and inducible nitric oxide swithase (iNOS) into the subarach noid space. The introduction into the meninges of these proinflammatory molecules, as well as calcitonin gene related peptide (CGRP) and nitric oxide, may be the link between aura and headache because the meninges are densely innervated by pain fibers whose activation distinguishes headaches of intracranial origin (e.g., migraine, meningitis, and subaraeh noid bleeds) from headaches of extracranial origin (e.g., tension type headache, cervicogenic headache, or headaches caused by mild trauma to the cranium).

Anatomy and physiology of the trigeminovascular pathway: from activation to sensitization

Anatomical description

The trigeminovascular pathway conveys nociceptive information from the meninges to the brain. The pathway originates in trigeminal ganglion neurons whose peripheral axons reach the pia, dura, and large cerebral arteries, and whose central axons reach the nociceptive dorsal horn laminae of the SpV. In the SpV, the nociceptors converge on neurons that receive additional input from the periorbital skin and pericranial muscles. The ascending axonal projections of trigeminovascular SpV neurons transmit monosynaptic nocieeptive signals to (1) brainstem nuclei, such as the ventro lateral periaqueductal gray, reticular for mation, superior salivatory, parabrachial, cuneiform, and the nucleus of the solitary tract; (2) hypothalamic nuclei, such as the anterior, lateral, perifornical, dorsome dial, suprachiasmatic, and supraoptic; and (3) basal ganglia nuclei, such as the caudate putamen, globus pallidus, and sub stantia innominata. These projections maybe critical for the initiation of nausea, vomiting, yawning, lacrimation, urination, loss of appetite, fatigue, anxiety, irritability, and depression by the headache itself.

Additional projections of trigeminovascular SpV neurons are found in the thalamic ventral posteromedial (VPM), posterior (PO), and parafascicular nuclei. Relay trigeminovascular thalamic neurons that project to the somatosensory, insular, motor, parietal association, retrosplenial, auditory, visual, and olfactory cortices are in a position to construct the specific nature of migraine pain (i.e., location, intensity, and quality) and many of the cortically mediated symptoms that distinguish between migraine headache and other pains. These include transient symptoms of motor clumsiness, difficulty focusing, amnesia, allodynia, phonophobia, photophobia, and osmophobia. Figure 2A illustrates the complexity of the trigeminovascular pathway.

Activation

Studies in animals show that CSD initiates delayed activation (Fig. 2D, 2B,C) and immediate activation (Fig. 2D) of peripheral and central trigeminovascular neurons in a fashion that resembles the classic delay and occasional immediate onset of headache after aura, and that systemic administration of the M type potassium channel opener KCNQ2/3 can prevent the CSD induced activation of the nociceptors.

These findings support the notion that the onset of the headache phase of migraine with aura coincides with the activation of meningeal nociceptors at the peripheral origin of the trigeminovascular pathway. Whereas the vascular, cellular, and molecular events involved in the activation of meningeal nocieeptors by CSD are not well under stood, a large body of data suggests that transient constriction and dilatation of pial arteries and the development of dural plasma protein extravasation, neurogenic inflammation, platelet aggregation, and mast cell degranulation, many of which may be driven by CSD dependent peripheral CGRP release, can introduce to the meninges proinflammatory molecules, such as histamine, bradykinin, serotonin, and prostaglandins (prostaglandin E2), and a high level of hydrogen ions thus altering the molecular environment in which meningeal nociceptors exist.

Sensitization

When activated in the altered molecular environment described above, peripheral trigeminovascular neurons become sensitized (their response threshold decreases and their response magnitude increases) and begin to respond to dura stimuli to which they showed minimal or no response at base line. When central trigeminovascular neurons in laminae I and V of SpV (Fig. 2F) and in the thalamic PO/VPM nuclei (Fig. 2G) become sensitized, their spontaneous activity increases, their receptive fields expand, and they begin to respond to innocuous mechanical and thermal stimulation of cephalic and extracephalic skin areas as if it were noxious. The human correlates of the electrophysiological measures of neuronal sensitization in animal studies are evident in contrast analysis of BOLD signals registered in MRI scans of the human trigeminal ganglion (Fig. 2H), spinal trigeminal nucleus (Fig. 2I), and the thalamus (Fig. 2J), all measured during migraine attacks.

The clinical manifestation of peripheral sensitization during migraine, which takes roughly 10 mins to develop, includes the perception of throbbing headache and the transient intensiflcation of headache while bending over or coughing, activities that momentarily increase intracranial pressure.

The clinical manifestation of sensitization of central trigeminovascular neurons in the SpV, which takes 30-60 min to develop and 120 min to reach full extent, include the development of cephalic allodynia signs such as scalp and muscle tenderness and hypersensitivity to touch. These signs are often recognized in patients reporting that they avoid wearing glasses, earrings, hats, or any other object that come in contact with the facial skin during migraine.

The clinical manifestation of thalamic sensitization during migraine, which takes 2-4 h to develop, also includes extracephalic allodynia signs that cause patients to remove tight clothing and jewelry, and avoid being touched, massaged, or hugged.

Evidence that triptans, 5HT agonists that disrupt communications between peripheral and central trigeminovascular neurons in the dorsal horn, are more effective in aborting migraine when administered early (i.e., before the development of central sensitization and allodynia) rather than late (i.e., after the development of allodynia) provides further support for the notion that meningeal nociceptors drive the initial phase of the headache. Further support for this concept was provided recently by studies showing that humanized monoclonal antihodies against CGRP, molecules that are too big to penetrate the bloodbrain barrier and act centrally (according to the companies that developed them), are effective in preventing migraine. Along this line, it was also reported that drugs that act on central trigeminovascular neurons, e.g., dihydroergotamine (DHE), are equally effective in reversing an already developed central sensitization a possible explanation for DHE effectiveness in aborting migraine after the failure of therapy with triptans.

Genetics and the hyperexcitable brain

Family history points to a genetic predisposition to migraine. A genetic association with migraine was first observed and defined in patients with familial hemiplegic migraine (FHM).

The three genes identified with FHM encode proteins that regulate glutamate availability in the synapse. FHM1 (CACNAIA) encodes the pore-forming a1 subunit of the P/Q type calcium channel; FHM2 (ATP1A2) encodes the 112 subunit of the Na+/K+ ATPase pump; and the FHM3 (SCNIA) encodes the a1 sub unit of the neuronal voltage gated Nav1.1 channel.

Collectively, these genes regulate transmitter release, glial ability to clear (reuptake) glutamate from the synapse, and the generation of action potentials.

Since these early findings, large genome wide association studies have identified 13 susceptibility gene variants for migraine with and without aura, three of which regulate glutaminergic neurotransmission (MTDH/AEG-1 downregulates glutamate transporter, LPRI modulates synaptic transmission through the NMDA receptor, and MEF-2D regulates the glutamatergic excitatory synapse), and two of which regulate synaptic development and plasticity (ASTN2 is involved in the structural development of cortical layers, and FHI5 regulates cAMP sensitive CREB proteins involved msynaptic plasticity).

These findings provide the most plausible explanation for the “generalized” neuronal hyperexcitability of the migraine brain.

In the context of migraine, increased activity in glutamalergic systems can lead to excessive occupation of the NMDA receptor, which in turn may amplify and reinforce pain transmission, and the development of allodynia and central sensitization. Network wise, wide spread neuronal hyperexcitability may also be driven by thalamocortical dysrhythmia, defective modulatory brainstem circuits that regulate excitability at multiple levels along the neuraxis; and inherently improper regulation/habituation of cortical, thalamic, and brainstem functions by limbic structures, such as the hypothalamus, amygdala, nucleus accumbens, caudate, putamen, and globus pallidus. Given that 2 of the 13 susceptibility genes regulate synaptic development and plasticity, it is reasonable to speculate that some of the networks mentioned above may not be properly wired to set a normal level of habituation throughout the brain, thus explaining the multi factorial nature of migraine. Along this line, it is also tempting to propose that at least some of the structural alterations seen in the migraine brain may be inherited and, as such, may be the “cause” of migraine, rather than being secondary to (i.e., being caused by) the repeated headache attacks. But this concept awaits evidence.

Structural and functional brain alterations

Brain alterations can be categorized into the following two processes: (1) alteration in brain function and (2) alterations in brain structure (Fig. 3). Functionally, a variety of imaging techniques used to measure relative activation in different brain areas in migraineurs (vs control subjects) revealed enhanced activation in the periaqueductal gray; red nucleus and substantia nigra; hypothalamus; posterior thalamus; cerebellum, insula, cingulate and prefrontal cortices, anterior temporal pole, and the hippocampus; and decreased activation in the somatosensory cortex, nucleus cuneiformis, caudate, putamen, and pallidum. All of these activity changes occurred in response to nonrepetitive stimuli, and in the cingulate and prefrontal cortex they occurred in response to repetitive stimuli.

Collectively, these studies support the concept that the migraine brain lacks the ability to habituate itself and consequently becomes hyperexcitable. It is a matter of debate, however, if such changes are unique to migraine headache. Evidence for nearly identical activation patterns in other pain conditions, such as lower back pain, neuropathic pain, Hbromyalgia, irritable bowel syndrome, and cardiac pain, raises the possibility that differences between somatic pain and migraine pain are not due to differences in central pain processing.

Anatomically, voxel based morphometry and diffusion sensor imaging studies in migraine patients (vs control subjects) have revealed thickening of the somatosensory cortex; increased gray matter density in the caudate; and gray matter volume loss in the superior temporal gyms, inferior frontal gyms, precentral gyms, anterior cingulate cortex, amygdala, parietal operculum, middle and inferior frontal gyrus, inferior frontal gyrus, and bilateral insula.

Changes in cortical and subcortical structures may also depend on the frequency of migraine attacks for a number of cortical and subcortical regions. As discussed above, it is unclear whether such changes are genetically predetermined or simply a result of the repetitive exposure to pain/stress. Favoring the latter are studies showing that similar gray matter changes occurring in patients experiencing other chronic pain conditions are reversible and that the magnitude of these changes can be correlated with the duration of disease.

Further complicating our ability to determine how the migraine brain differs from the brain of a patient experiencing other chronic pain conditions are anatomical findings showing decreased gray matter density in the prefrontal cortex, thalamus, posterior insula, secondary somatosensory cortex, precentral and posteentral gyms, hippocampus, and temporal pole of chronic back pain patients; anterior insula and orbitofrontal cortex of complex regional pain syndrome patients; and the insula, midanterior cingulate cortex, hippocampus and inferior temporal coxtex in osteoarthritis pa tients with chronic back pain.

Whereas some of the brain alterations seen in migraineurs depend on the sex of the patient, little can he said about the role played by the sex of patients who experience other pain conditions.

Treatments in development

Migraine therapy has two goals: to terminate acute attacks; and to prevent the next attack from happening. The latter can potentially prevent the progression from episodic to chronic state. Regarding the effort to terminate acute attacks, migraine represents one of the few pain conditions for which a specific drug (i.e., triptan) has been developed based on understanding the mechanisms of the disease. In contrast, the effort to prevent migraine from happening is likely to face a much larger challenge given that migraine can originate in an unknown number of brain areas (see above), and is associated with generalized functional and structural brain abnormalities.

A number of treatments that attract attention are briefly reviewed below.

Medications The most exciting drug currently under development is humanized monoclonal antibodies against CGRP. The development of these monoclonal antibodies are directed at both CGRP and its receptors. The concept is based on CGRP localization in the trigeminal ganglion and its relevance to migaine patho-physiology. In recent phase II randomized placebo-controlled trials, the neutralizing humanized monoclonal antibodies against CGRP administered by injection for the prevention of episodic migraine, showed promising results. Remarkably, a single injection may prevent or significantly reduce migraine attacks for 3 months.

Given our growing understanding of the importance of prodromes (likely representing abnormal sensitivity to the fluctuation in hypothalamically regulated homeostasis) and aura (likely representing the inherited conical hyperexcitability) in the pathophysiology of migraine, drugs that target ghrelin, leptin, and orexin receptors may be considered for therapeutic development which is based on their ability to restore proper hypothalamic control of stress, hyperphagia, adiposity, and sleep. All may be critical in reducing allostatic load and, consequently, in initiating the next migraine attack.

Brain modification

Neuroimaging studies showing that brain networks, brain morphology, and brain chemistry are altered in episodic and chronic migraineurs justify attempts to develop therapies that widely modify brain networks and their functions. Transcranial magnetic stimulation, which is thought to modify cortical hyperexcitability, is one such approach. Another approach for generalized brain modification is cognitive behavioral therapy.

Conclusions

Migraine is a common and undertreated disease. For those who suffer, it is a major cause of disability, including missing work or school, and it frequently has associated comorbidities such as anxiety and depression. To put this in context, it is a leading cause of suicide, an indisputable proof of the severity of the distress that the disease may inflict on the individual.

There is currently no objective diagnosis or treatment that is universally effective in aborting or preventing attacks. As an intermittent disorder, migraine represents a neurological condition wherein systems that continuously evaluate errors (error detection) frequently fail, thus adding to the allostatic load of the disease.

Given the enormous burden to society, there is an urgent imperative to focus on better understanding the neurobiology of the disease to enable the discovery of novel treatment approaches.

AN ANXIOUS PARADISE. Crisis in New Zealand mental health services as depression and anxiety soar – Eleanor Ainge Roy * World in mental health crisis of monumental suffering – Sarah Broseley.

System neglects ‘missing middle’ of the population who face common problems.
50-80% of New Zealanders experience mental distress or addiction challenges at some point in their lives, while each year one in five people experience mental illness or significant mental distress.

A landmark inquiry has found New Zealand’s mental health services are overwhelmed and geared towards crisis care rather than the wider population who are experiencing increasing rates of depression, trauma and substance abuse.

It has urged the government to widen provision of mental health care from 3% of the population in critical need to “the missing middle” – the 20% of the population who struggle with “common, disabling problems” such as anxiety.

New Zealand has one of the highest rates of suicide in the OECD, especially among young people. In 2017, 20,000 people tried to take their own life.

. . . The Guardian

Also on TPPA = CRISIS

World in mental health crisis of ‘monumental suffering’, say experts – Sarah Broseley.

“Mental health problems kill more young people than any other cause around the world.” Prof. Vikram Patel, Harvard Medical School
Lancet report says 13.5 million lives could be saved every year if mental illness addressed.

OFC, Brain Stimulation for Depression – Janice Wood * Direct Electrical Stimulation of Lateral OFC Acutely Improves Mood.

“You could see the improvements in patients’ body language. They smiled, they sat up straighter, they started to speak more quickly and naturally. They said things like ‘Wow, I feel better,’ ‘I feel less anxious,’ ‘I feel calm, cool and collected.”

An important step toward developing a therapy for people with treatment-resistant depression.

Converging lines of evidence from lesion studies, functional neuroimaging, and intracranial physiology point to a role of OFC in emotion processing. Clinically depressed individuals have abnormally high levels of activity in OFC as ascertained by functional neuroimaging, and recovery from depression is associated with decreased OFC activity.

We found that lateral OFC stimulation acutely improved mood in subjects with baseline depression and that these therapeutic effects correlated with modulation of large-scale brain networks implicated in emotion processing.

Our results suggest that lateral OFC stimulation improves mood state at least partly through mechanisms that underlie natural mood variation, and they are consistent with the notion that OFC integrates multiple streams of information relevant to affective cognition.

Unilateral stimulation of lateral OFC consistently produced acute, dose-dependent mood-state improvement across subjects with baseline depression traits.

In a new study, patients with moderate to severe depression reported significant improvements in mood when researchers stimulated the orbitofrontal cortex (OFC).

The orbitofrontal cortex (OFC) is a prefrontal cortex region in the frontal lobes in the brain, which is involved in the cognitive processing of decision-making.

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Researchers at the University of California San Francisco say the study’s findings are “an important step toward developing a therapy for people with treatment-resistant depression, which affects as many as 30 percent of depression patients.”

Using electrical current to directly stimulate affected regions of the brain has proven to be an effective therapy for treating certain forms of epilepsy and Parkinson’s disease, but efforts to develop therapeutic brain stimulation for depression have so far been inconclusive, according to the researchers.

“The OFC has been called one of the least understood regions in the brain, but it is richly connected to various brain structures linked to mood, depression, and decision making, making it very well positioned to coordinate activity between emotion and cognition.”

Two additional observations suggested that OFC stimulation could have therapeutic potential.

First, the researchers found that applying current to the lateral OFC triggered wide-spread patterns of brain activity that resembled what had naturally occurred in volunteers’ brains during positive moods in the days before brain stimulation. Equally promising was the fact that stimulation only improved mood in patients with moderate to severe depression symptoms but had no effect on those with milder symptoms.

“These two observations suggest that stimulation was helping patients with serious depression experience something like a naturally positive mood state, rather than artificially boosting mood in everyone.

This is in line with previous observations that OFC activity is elevated in patients with severe depression and suggests electrical stimulation may affect the brain in a way that removes an impediment to positive mood that occurs in people with depression.”

Psych Central

Direct Electrical Stimulation of Lateral Orbitofrontal Cortex Acutely Improves Mood in Individuals with Symptoms of Depression

Vikram R. Rao, Kristin K. Sellers, Deanna L. Wallace, Maryam M. Shanechi, Heather E. Dawes, Edward F. Chang.

Mood disorders cause significant morbidity and mortality, and existing therapies fail 20%–30% of patients. Deep brain stimulation (DBS) is an emerging treatment for refractory mood disorders, but its success depends critically on target selection. DBS focused on known targets within mood-related frontostriatal and limbic circuits has been variably efficacious.

Here, we examine the effects of stimulation in orbitofrontal cortex (OFC), a key hub for mood-related circuitry that has not been well characterized as a stimulation target. We studied 25 subjects with epilepsy who were implanted with intracranial electrodes for seizure localization. Baseline depression traits ranged from mild to severe. We serially assayed mood state over several days using a validated questionnaire. Continuous electrocorticography enabled investigation of neurophysiological correlates of mood-state changes.

We used implanted electrodes to stimulate OFC and other brain regions while collecting verbal mood reports and questionnaire scores. We found that unilateral stimulation of the lateral OFC produced acute, dose-dependent mood-state improvement in subjects with moderate-to-severe baseline depression. Stimulation suppressed low-frequency power in OFC, mirroring neurophysiological features that were associated with positive mood states during natural mood fluctuation. Stimulation potentiated single-pulse-evoked responses in OFC and modulated activity within distributed structures implicated in mood regulation.

Behavioral responses to stimulation did not include hypomania and indicated an acute restoration to non-depressed mood state.

Together, these findings indicate that lateral OFC stimulation broadly modulates mood-related circuitry to improve mood state in depressed patients, revealing lateral OFC as a promising new target for therapeutic brain stimulation in mood disorders.

Experimental Design and Locations of Stimulated Sites

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Introduction

A modern conception of mood disorders holds that the signs and symptoms of emotional dysregulation are manifestations of abnormal activity within large-scale brain networks. This view, evolved from earlier hypotheses based on chemical imbalances in the brain, has fueled interest in selective neural network modulation with deep brain stimulation (DBS). Although the potential for precise therapeutic intervention with DBS is promising, its efficacy is sensitive to target selection. In treatment-resistant depression (TRD), for example, well-studied targets for DBS include the subgenual cingulate cortex (SCC) and subcortical structures, but the benefits of DBS in these areas are not clearly established.

A major challenge in this regard relates to the fact that clinical manifestations of mood disorders like TRD are heterogeneous and involve dysfunction in cognitive, affective, and reward systems. Therefore, brain regions that represent a functional confluence of these systems are attractive targets for therapeutic brain stimulation.

Residing within prefrontal cortex, the orbitofrontal cortex (OFC) shares reciprocal connections with amygdala, ventral striatum, insula, and cingulate cortex, areas implicated in emotion regulation. As such, OFC is anatomically well positioned to regulate mood. Functionally, OFC serves as a nexus for sensory integration and has myriad roles related to emotional experience, including predicting and evaluating outcomes, representing reward-driven learning and behavior, and mediating subjective hedonic experience.

Converging lines of evidence from lesion studies, functional neuroimaging, and intracranial physiology point to a role of OFC in emotion processing. Clinically depressed individuals have abnormally high levels of activity in OFC as ascertained by functional neuroimaging, and recovery from depression is associated with decreased OFC activity.

Repetitive transcranial magnetic stimulation (rTMS) of OFC was shown to improve mood in a single-subject case study and in a series of patients who otherwise did not respond to rTMS delivered to conventional (non-OFC) targets, but whether intracranial OFC stimulation can reliably alleviate mood symptoms is not known.

Furthermore, OFC is relatively large, and functional distinctions between medial and lateral subregions are known, raising the possibility that subregions of OFC may play distinct roles in mood regulation.

More generally, it remains poorly understood how direct brain stimulation affects local and network-level neural activity to produce complex emotional responses.

We hypothesized that brain networks involved in emotion processing include regions, like OFC, that represent previously unrecognized stimulation targets for alleviation of neuropsychiatric symptoms. To test this hypothesis, we developed a system for studying mood-related neural activity in subjects with epilepsy who were undergoing intracranial electroencephalography (iEEG) for seizure localization. In addition to direct recording of neural activity, iEEG allows delivery of defined electrical stimulation pulses with high spatiotemporal precision and concurrent measurement of behavioral correlates.

Using serial quantitative mood assessments and continuous iEEG recordings, we investigated the acute effects of OFC stimulation on mood state and characterized corresponding changes in neural activity locally and in distributed brain regions. We found that lateral OFC stimulation acutely improved mood in subjects with baseline depression and that these therapeutic effects correlated with modulation of large-scale brain networks implicated in emotion processing.

Our results suggest that lateral OFC stimulation improves mood state at least partly through mechanisms that underlie natural mood variation, and they are consistent with the notion that OFC integrates multiple streams of information relevant to affective cognition.

Discussion

Here, we show that human lateral OFC is a promising target for brain stimulation to alleviate mood symptoms. Unilateral stimulation of lateral OFC consistently produced acute, dose-dependent mood-state improvement across subjects with baseline depression traits. Locally, lateral OFC stimulation increased cortical excitability and suppressed low-frequency power, a feature we found to be negatively correlated with mood state. At the network level, lateral OFC stimulation modulated activity within a network of limbic and paralimbic structures implicated in mood regulation.

Relief of mood symptoms afforded by lateral OFC stimulation may arise from OFC acting as a hub within brain networks that mediate affective cognition.

Previous studies identify OFC as a key node within an emotional salience network activated by anticipation of aversive events. Within this network, OFC is thought to integrate multimodal sensory information and guide emotion-related decisions by evaluating expected outcomes.

Stimulation of other brain regions that encode value information, such as SCC and ventral striatum, has also been found to improve mood, highlighting the relevance of reward circuits to mood state.

Here, using iEEG, we extend previous studies that employed indirect imaging biomarkers, such as glucose metabolism or blood oxygen level, to show that direct OFC stimulation modulates neural activity within a distributed network of brain regions. Our finding that lateral OFC stimulation was more effective than medial OFC stimulation for mood symptom relief advances the idea that these regions have differential contributions to depression, likely due to differences in network connectivity.

We did not observe consistent differences based on laterality of stimulation, but future studies powered to discern such differences may reveal additional layers of specificity.

Although few behavioral variables have been identified to predict which individuals will respond to stimulation of a given target for depression, we found that only patients with significant trait depression experienced mood-state improvement with lateral OFC stimulation. Based on speech-rate analysis, lateral OFC stimulation did not produce supraphysiological mood states, as can be seen with stimulation of other targets, but did specifically elevate speech rate in trait-depressed subjects, resulting in a level similar to that of the non-depressed subjects. Local neurophysiological changes induced by stimulation were opposite of those observed during spontaneous negative mood states. Taken together, these findings suggest that the effect of lateral OFC stimulation is to normalize or suppress pathological activity in circuits that mediate natural mood variation.

Our observations provide potential clues about how lateral OFC stimulation may impact mood. Although functional imaging biomarkers of depression are not firmly established, increased activity in lateral OFC is seen in patients with depression and normalizes with effective antidepressant treatment, and lateral OFC hyperactivity has been proposed as a mood-state marker of depression.

Thus, a speculative possibility is that our stimulation paradigm works by decreasing OFC theta power in a way that may impact baseline hyperactivity. We cannot exclude the possibility that the mechanisms underlying mood improvement with lateral OFC stimulation involve multiple regions and may at least partially overlap with mechanisms responsible for mood improvement with stimulation of SCC. In fact, based on anatomic and functional connectivity between these regions, and the constellation of white matter tracts likely affected by stimulation of these sites, some mechanistic overlap seems probable.

Our results have potential implications for interventional treatments for psychiatric disorders like TRD and anxiety. DBS efficacy for TRD is inconsistent, and a major thrust of the field has been to understand and circumvent inter-subject variability. For example, the heterogeneous responses seen with SCC stimulation may relate to laterality and precise anatomic electrode position. In our study, positive mood responses were induced by unilateral stimulation of the OFC in either hemisphere, and although stimulation of lateral OFC improved mood more than stimulation of medial OFC, we observed mood improvement with stimulation across lateral OFC and did not see evidence of fine subregion specificity. These findings suggest that lateral OFC may be a more forgiving site for therapeutic stimulation than previously reported targets.

Another practical advantage of OFC relative to other targets is that the cortical surface is generally more surgically accessible than deep brain targets and that the ability to forego parenchymal penetration may impart lower risk during electrode implantation. Although seizures are a theoretical risk with any cortical stimulation, this risk is thought to be acceptably low, and we did not observe seizures during OFC stimulation.

Despite the widespread use of DBS in clinical and research applications, the mechanisms by which focal brain stimulation modulates network activity to produce complex behavioral changes remain largely unknown. The effects of stimulation are not limited to the targeted region, and stimulation-induced activity can propagate through anatomical connections to influence distributed networks in the brain. Previous studies have shown that target connectivity may determine likelihood of response to DBS.

Deciphering the precise mechanism of mood improvement with OFC stimulation requires future study, but our observation that stimulation suppresses low-frequency activity broadly across multiple sites suggests a possible local inhibitory effect that reverberates through connected brain regions. Consistent with this, inhibitory transcranial magnetic stimulation of OFC was recently reported to improve mood in one depressed patient. Since the OFC is relatively large and bilateral, it is possible that the mood effects we observed could be improved by more widespread stimulation.

Our study has limitations. The sample size was relatively small, reflecting the rare opportunity to directly and precisely target brain stimulation in human subjects. Although electrode coverage was generally extensive in our subjects, basal ganglia structures known to be important for mood are not typically implanted with electrodes for the purposes of seizure localization. Subjective self-report of mood has intrinsic limitations but remains the best instrument available to measure internal experience.

Our subjects, who had medically refractory epilepsy, may not be representative of all patients with mood disorders. While we cannot rule out the possibility that mood symptoms in our subjects had a seizure-specific etiology, the observed effects of lateral OFC stimulation were robust in a patient group with diverse underlying seizure pathology. To establish generalizability, our findings will need to be replicated in other cohorts.

Finally, it is possible that the acute effects of stimulation we observed may not translate into chronic efficacy for mood disorders in clinical settings. Indeed, rapid mood changes have been previously reported in TRD patients treated with bilateral DBS of SCC and subcortical targets. Whether chronic OFC stimulation can produce durable mood improvement is an important question for future study, ideally under controlled clinical trial conditions with appropriate monitoring of relevant outcomes and adverse events.

The clinical heterogeneity of mood disorders suggests that brain stimulation paradigms may need to be tailored for individual patients. Importantly, this study is one of few to assess the functional consequences of brain stimulation with direct neural recordings. The approach we used for serial quantitative mood state assessment may be useful for sensitively tracking symptoms of mood disorders during clinical interventions, including DBS trials. Our identification of a novel, robust stimulation target and our observation of stimulation-induced changes in endogenous mood-related neural features together set the stage for the next generation of stimulation therapies. OFC theta power may be useful for optimization of stimulation parameters for non-invasive stimulation modalities targeting the OFC in depression, and further characterization of mood biomarkers might enable personalized closed-loop stimulation devices that ameliorate debilitating mood symptoms.

Although the OFC is currently among the least understood brain regions, it may ultimately prove important for the treatment of refractory mood disorders.

Study: Current Biology

University of California, San Francisco (UCSF)

OUR EARLIEST EXPERIENCES SHAPE WHO WE ARE. Babies, Their Wonderful World – Dr Guddi Singh * The Six Faces of Maternal Narcissism – Karyl McBride Ph.D.

Love and attention.

One of the most important things that we know about early brain development is that the first two years of life are crucial.

Our brains are literally built on experience from the moment we are born. Experiences help build strong neural pathways between brain cells and allow brain material to expand.

Strong initial attachment bonds are crucial to making a happy secure adult.

Babies aren’t just eating and sleeping machines. Instead, we know they are like mini computers taking in everything that is going on around them.

In the first few months of life, personality traits start to show like caution, or bravery.

Babies who are not exposed to enough stimulation in their environment do not have the chance to develop the ‘hardware’ they need to be effective adults. Our brains are literally built on experience from the moment we are born. Experiences help build strong neural pathways between brain cells and allow brain material to expand. Stress and neglect can also inhibit brain growth because high levels of the stress hormone cortisone inhibits brain cells, although ironically it may encourage the over development of areas that are involved in the fight or flight response, increasing the likelihood that an individual will be prone to anxiety.

When it comes to smart phones and screens in baby cots, the issue is not so much that technology inhibits brain growth but that it causes a problem when it is a stand-in for parental involvement and love. That’s when we see problems when mobile phones and screens are used as babysitters for long periods while carers divert their attention elsewhere. From observational studies, it seems that it interferes with normal attachment and socialisation as well as inhibiting sleep, and the brain needs sleep for normal growth.

Babies who have siblings may benefit from socialisation and to a baby, nothing is funnier than a sibling. But single children can also be stimulated in a busy, challenging environment where they can still get this type of input including in a nursery environment.

The strongest evidence we have about developmental milestones early in life surround attachment theory. It has been shown time and time again that strong initial attachment bonds are crucial to making a happy secure adult. This is why paediatricians advocate close skin to skin contact in the early days and weeks of life. And we know that babies who are separated from a strong parental figure early on can have all sorts of emotional and social problems later in life.

However, that figure does not have to be the parent but can be someone from an extended family or even the community. It is really helpful to look at different cultures and how they parent their kids, there isn’t a one perfect solution and it can be done in different ways. In the west, there is a fetishisation of biological bonds, but adopted or looked after children can benefit from this strong bond as long as it includes love and attention.

Hippocratic Post

Dr Guddi Singh is a paediatrician based at East London NHS Foundation Trust. She is one of the advisers on the new BBC 2 series, Babies – Their Wonderful World. She is a member of the Royal Society of Medicine’s Paediatrics and Child Health Section Council.

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Also on TPPA = CRISIS

The Six Faces of Maternal Narcissism – Karyl McBride Ph.D.

“We Will Change The World , Starting From The Very Beginning.” Building Babies Brains . Criança Feliz, Brazil’s Audacious Plan To Fight Poverty – Jenny Anderson

Life After Severe Childhood Trauma . I Think I’ll Make It. A True Story Of Lost And Found – Kat Hurley

Chronic Childhood Stress And A Dysfunctional Family – Kylie Matthews * Different Adversities Lead To Similar Health Problems – Donna Jackson Nakazawa

How Our Brains Grow – Ruby Wax

The Deepest Well. Healing The Long Term Effects Of Childhood Adversity – Dr Nadine Burke Harris

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 Disrupted . How Your Biography Becomes Your Biology , And How You Can Heal – Donna Jackson Nakazawa * The Origins Of Addiction . Evidence From The Adverse Childhood Experiences Study – Vincent J. Felitti MD.

THE HAPPINESS EQUATION. The Surprising Economics of Our Most Valuable Asset – Nick Powdthavee.

What do we do, then? What do we do when our lives are a series of trade-offs between different combinations of ‘what ifs”? What do we do when there is an endless horizon of time and resource constraints constantly telling us that whatever we do, we can’t possibly have it all?

“Happiness is not having what you want, but wanting what you have.” Rabbi Hyman Schachtel.

Why is marriage worth £200,000 a year? Why will having children make you unhappy?

Why does happiness from winning the lottery take two years to arrive?

Why does time heal the pain of divorce or the death of a loved one but not unemployment?

Everybody wants to be happy. But how much happiness precisely will each life choice bring? Should I get married? Am I really going to feel happy about the career that I picked? How can we decide not only which choice is better for us, but how much it’s better for us?

The result of new, unique research, The Happiness Equation brings to a general readership for the first time the new science of happiness economics.

It describes how we can measure emotional reactions to different life experiences and present them in ways we can relate to. How, for instance, monetary values can be put on things that can’t be bought or sold in the market such as marriage, friendship, even death so that we can objectively rank them in order of preference. It also explains why some things matter more to our happiness than others (like why seeing friends is worth more than a Ferrari) while others are worth almost nothing (like sunny weather).

Nick Powdthavee whose work on happiness has been discussed on both the Undercover Economist and Freakanomics blogs brings cutting-edge research on how we value our happiness to a general audience with a style that wears its learning lightly and is a joy to read.

Dr Nattavudh (Nick) Powdthavee is a behavioural economist at the University of York (shortly to move to the Department of Economics, Nanyang Technological University, Singapore). Discussions of his work on the economics of happiness have appeared in over 50 major international newspapers in the past five years, including the New York Times and the Guardian, as well as on TV, including Channel 5 News and The Wright Stuff. He is originally from Thailand.

CHAPTER 1

THE PURSUIT

Most of us go through life believing we know exactly what we need to make us happy. For the most part, we believe that all we ever need is to have someone we love loving us back. Or it’s a combination of more money, a good job, a stable marriage and perfect health. Sometimes it’s the little things in life, like a day off work; a clear blue sky on an autumn afternoon; a nice cup of cool mochaccino on a hot day; an hour-long foot rub; a day spent laughing with friends and family; 45 minutes of uninterrupted sex with our partner, and the energy to last for the best part of it.

But unfortunately in the words of Mick Jagger and Keith Richards we can’t always get what we want. At least, we can’t always get what we want all the time. A day off work every so often sounds like a good idea until, of course, we realise that we will become a little poorer because of it. And that’s no good because, according to the abstract idea we have in our heads of what makes a good life, money matters a lot. Okay then, in that case, we’ll put in more hours at work. But wait. That will also mean less time to be spent with friends and family, and that doesn’t seem so good either.

So what do we do, then? What do we do when our lives are a series of trade-offs between different combinations of ‘what ifs”? What do we do when there is an endless horizon of time and resource constraints constantly telling us that whatever we do, we can’t possibly have it all? Well, according to economists, who are supposedly experts on decision-making, what usually happens is that we try to do the best we can with our choices. We gather all necessary information about our options. We engage in rationalisation and mental calculations. We quietly argue and debate within ourselves over the potential impacts of each individual decision on our happiness. We cross-refer them to the rule-book of ‘All the things that make me happy’, put each possibility into an order of preference, and then, subject to both time and resource constraints, choose the best combination of bundles that we know would optimise our wellbeing. Easy.

Bounded rationality

But of course, if that were true if we always chose the best possible combination of options according to stable preference functions and the constraints facing them then the way we led our lives would literally be disappointment-free. Whatever decisions we made, we would know exactly well in advance what we were getting ourselves into. After all, our rationality would have already done the homework for us: we would be getting the greatest reward at the lowest cost.

How could we possibly not be happy with that?

The reality, however, is that our lives are too often filled with disappointing and regrettable decisions, whether big or small. The holiday we went on last summer; that antique car we bought; or even the job or college degrees we picked. The following anecdotal evidence from a chance meeting between two economists and a dentist makes it all too clear.

Two economics professors and friends, John Bennett and Chuck Blackorby, were attending an economics conference. On the first evening, they met a dentist at the hotel bar who was at an annual conference for dentists just next door to them. After a brief introduction and a couple of drinks, Chuck, who was known for his sometimes brash and direct manner, decided to ask the dentist, by then a little tipsy, a somewhat personal question.

‘So, tell me, are you very happy being a dentist?’

‘Happy? I’m miserable as a dentist’, replied the man.

Chuck smiled to himself. ‘What? If you’re so unhappy, why on earth did you choose to become a dentist in the first place?’

‘I didn’t choose to become a dentist.’ The man took another swig of his drink before delivering the final hammer blow. ‘It’s that stupid kid eighteen years ago that chose to become a dentist. Not me.’

And even when we’re not too disappointed; when we actually think we’re fairly satisfied with the choices we made, sometimes there’s just no way for us to know for certain whether or not we would have been happier if we’d gone with the alternatives. Take having children, for example. For most parents, a natural and genuine response to the question, ‘Would you be happier without children?’ would be a screaming ‘No!’ However, there’s no real way of knowing precisely what life would have been like if these parents had decided not to have their little David or Sarah simply because the childless alternative didn’t take place for them. The same argument holds true for partners who choose not to become parents.

One of the main reasons why we aren’t always able to choose the best options for ourselves is that our rationality is often bounded by the amount of information it possesses, the cognitive limitations of our brains, and the finite amount of time we have to make a decision. According to the so-called ‘bounded rationality’ concept, we human beings are only partly rational and downright irrational in the remaining part of our actions. While economists believe that all human beings are approximately Homo economicus (economic man), rational and broadly self-interested by nature, the reality is that we are just as likely, if not more likely, to let emotions overrule rationality and completely dictate the way we behave.

That we are not wholly rational is shown by studies that have identified two distinct sides to our brains: one that is rational controlled, slow, deliberative and deductive; and one that is emotional automatic, rapid, associative and affective. The mesh between the two is extremely complex, and one does not always dominate the other. And while economic theories of decision making have tended to emphasise the operation of the rational side of our brain in guiding choice behaviour, it’s often the case that, when making decisions under pressure or under conditions where information is incomplete or overly complex, we tend to rely on simplifying heuristics or ‘gut feelings’ rather than extensive algorithmic processing. These ‘rules of thumb’ are far from perfect, and it’s precisely why we sometimes spend too much money on food when we go grocery shopping with an empty stomach, or find it increasingly difficult to walk away from a bus stop the longer we have been waiting for a bus to come even if it would have been a lot quicker to walk than to wait for that damn bus to arrive.

The adaptive unconscious and past experiences

But maybe it’s not always such a bad thing to trust our emotions. Research carried out by psychology professor Timothy Wilson suggests that, in situations where we have had a lot of experience, decisions made without thinking (those made on impulses and gut feelings) can often lead to better and happier outcomes than if they had been made under a strict rule of optimisation, simply because this is when the emotional part of our brain works best at detecting that something is out of the ordinary even if we may not know ourselves what that something is at the time and alerts us in the form of emotional alarm bells such as sweaty palms and butterflies in our stomach. And it’s in these scenarios that practice really makes perfect. It’s also where thinking too much about our past experiences can actually hurt rather than help us.

The question is: Why?

One reason. According to psychologist and Nobel laureate Daniel Kahneman, the cognitive part of our brain tends to suffer from what he called the ‘peak-end’ effect, which is the tendency to judge past experiences both pleasant and unpleasant almost entirely on how they were at their peak and how they ended.

Kahneman and his colleagues illustrated the core concept of the peak-end theory in a series of experiments, most notably that involving hospital patients and the very painful colonoscopy procedure. While undergoing a colonoscopy, the patients reported their level of discomfort every 60 seconds throughout the procedure. Afterwards, the patients were asked to remember how unpleasant the procedure was, using several different scales including a ten-point scale, and also about the relative unpleasantness of the colonoscopy compared to other unpleasant experiences such as stubbing a toe, or an average visit to the dentist.

What Kahneman and his colleagues found was astonishing. While there was almost zero correlation between the duration of the colonoscopies that different patients experienced and the global rating of the procedure, the relationship between the peak-end average (the average of the peaks and how the patients felt at the end of the procedure) and the global rating of the procedure was simply undeniable. In other words, we are more likely to remember our experience of a colonoscopy as being awful if the peaks of unpleasantness were very high or if it ended awfully for us, than if the entire procedure itself took a long time to finish. What matters is not the duration of an experience; we hardly ever think about it when we try to recall and judge how happy or unhappy we were in the past. It’s how we were feeling at the peaks and at the end of our experience that count the most.

What about frequency? Surely having experienced something often can teach us to repeat only the things that we remember with pleasure and fondness, and avoid those that we remember with embarrassment and regret? The trouble is, according to Harvard psychologist Daniel Gilbert, we are just not very good at remembering them correctly. He illustrates his point by prompting the readers of his book Stumbling on Happiness to think about where they were, whom they were with, and what they were doing when they first heard the news about the 9/11 attacks in 2001.

Okay, that sounds easy enough. Closing my eyes, I can still remember that I was standing at one of the check-in counters at London Heathrow airport, trying to get on the evening flight to Bangkok. Sitting behind the Finnair counter was a man in his late 50s who, as I recall, spoke with a very thick Glaswegian accent.

‘So you’re off to Thailand then, eh? Ah, what a beautiful country! Lovely food, gorgeous beaches, very pretty women!’ His eyes twinkled as he said this.

I smiled politely, acknowledging his appreciation of my country of birth. I knew he was just trying to be friendly in what seemed to be a surprisingly empty airport on a Tuesday afternoon.

‘Okay, sir. Here’s your boarding pass. Have a nice flight. Oh, and have you heard? Two planes hit the World Trade Center not half an hour ago. Probably a terrorist attack. But since you’re flying to Finland first, I’m sure you’ll be just fine.’ He ended with a beam while I stood there, rigid as a board.

Like me, most people will be able to remember in fine detail what they were doing when they first heard the news. But, Gilbert added, would the same people also remember precisely where they were, whom they were with, and what they were doing on the morning of 10 September 2001, one day before the attacks?

I personally couldn’t, of course. And I’m confident enough to bet that not many people could either, a fact that is also true for most Americans.

The main reason why it’s relatively easier for us to recall the exact details of 11 September 2001, but nearly impossible to remember what happened a day earlier, is because momentous events like the 9/11 attacks do not happen frequently in our lifetime. While 11 September 2001 defied our every sense of normality, 10 September, by contrast, was like almost any other day. And unless we religiously keep a diary of everything that ever happened in our lives, any other day is nothing more than a blob in our memory bank.

Daniel Gilbert’s message is clear: it is the infrequent and unusual experiences that are most memorable. These are the ones that stick like glue to the clipboard of our memory cortex. Not the other way round.

Conventional wisdom and imagination

There are two lessons we can draw at this stage. The first is that, in situations where we have had a lot of experience, it’s perhaps better to trust our instincts when it comes to making a decision. And the second lesson, related to the first, is that it seems important not to rely completely on emotions in situations where we have had little or no prior experience. The explanation is simple: in these circumstances, the emotional part of our brain will not have had enough chances to adapt and learn from our past experiences, which will inevitably make it impossible for it to distinguish which decision is better for us.

That sounds perfectly reasonable. All we need to do now is follow any great professional’s advice and just practise, practise, practise. Then afterwards, we can sit back in situations where we have had a lot of these experiences and just make snap decisions without having to think too much about the best outcomes.

Two problems, though. First, how do we know when we have had enough practice doing something? How do we know when we can let the rational brain take a back seat and the emotional brain do all the work? Will 10,000 hours of doing something repetitively be enough? Or will it take a lifetime of experience? Second, what about other, more novel situations? How do we know that we will be happier being married than staying single? How do we know whether we will be happier in a job that pays less but is nevertheless much closer to home? How can we be sure that rationality will not fail us when we have to face dilemmas that we have never faced before?

So now we’ve come full circle: economists’ description of how the world works though somewhat incomplete actually turns out to be useful advice on what we should do in situations where we have had little or no prior experience. According to theories on rational choice, there are perhaps two essential ingredients to successful decision-making when a degree of rationality is involved. The first is time. Unlike the emotional part of our brain where all decision-making is done instantaneously, the rational part of our brain needs time to think things over, to mull over the information. The second ingredient is getting the right information. It’s important that we have perfect awareness of all relevant information regarding the outcome of our choice before making a decision, especially one that could change our lives.

Since we can often find time to think things over before coming up with a solution for many of our life problems, could it just be the case that we don’t always have the right information about the choices we plan to make? Going back to the unhappy dentist, could it be possible that he decided to obtain a degree in dentistry on a whim or, worse, on a dare? Maybe. Nevertheless, considering the potentially life-changing impact of choosing the right career, it’s perhaps more likely that he did try to seek all the available information about how happy a career in dentistry would make him in eighteen years’ time. How could he then have been so wrong?

There are usually two ways of getting the information we need about the potential impacts of a novel experience. First, we can do some research about the experience. So in the case of the unhappy dentist, his decision to study dentistry could have been influenced by what he was expecting to get objectively from becoming a dentist, such as financial return, or by other people’s accounts of their subjective experiences as dentists, or even by conventional wisdom passed down from generation to generation.

Second, if all else fails, we can still use our imagination to conjure up the information we need to undertake a decision. We can try, for example, to picture ourselves in the future: what life would be like being married, or having kids, or having so much money we don’t know what to do with it.

. . .

from

THE HAPPINESS EQUATION. The Surprising Economics of Our Most Valuable Asset

by Nick Powdthavee

get it at Amazon.com

MIND IN THE MIRROR * Neuroplasticity in a Nutshell * Mindsight, Change Your Brain and Your Life – Daniel J. Siegel MD.

We come to know our own minds through our interactions with others.

As we welcome the neural reality of our interconnected lives, we can gain new clarity about who we are, what shapes us, and how we in turn can shape our lives.

Riding the Resonance Circuits

It’s folk wisdom that couples in long and happy relationships look more and more alike as the years go by. Peer closely at those old photographs, and you’ll see that the couples haven’t actually grown similar noses or chins. Instead, they have reflected each other’s expressions so frequently and so accurately that the hundreds of tiny muscle attachments to their skin have reshaped their faces to mirror their union. How this happens gives us a window on one of the most fascinating recent discoveries about the brain, and about how we come to “feel felt” by one another.

Some of what I’ll describe here is still speculative, but it can shed light on the most intimate ways we experience mindsight in our daily lives.

Neurons That Mirror Our Minds

In the mid-1990s, a group of Italian neuroscientists were studying the premotor area of a monkey’s cortex. They were using implanted electrodes to monitor individual neurons, and when the monkey ate a peanut, a certain electrode fired. No surprise there, that’s what they expected. But what happened next has changed the course of our insight into the mind. When the monkey simply watched one of the researchers eat a peanut, that same motor neuron fired. Even more startling: The researchers discovered that this happened only when the motion being observed was goal-directed. Somehow, the circuits they had discovered were activated only by an intentional act.

This mirror neuron system has since been identified in human beings and is now considered the root of empathy. Beginning from the perception of a basic behavioral intention, our more elaborated human prefrontal cortex enables us to map out the minds of others. Our brains use sensory information to create representations of others’ minds, just as they use sensory input to create images of the physical world. The key is that mirror neurons respond only to an act with intention, with a predictable sequence or sense of purpose. If I simply lift up my hand and wave it randomly, your mirror neurons will not respond. But if I carry out any act you can predict from experience, your mirror neurons will “figure out” what I intend to do before I do it. So when I lift up my hand with a cup in it, you can predict at a synaptic level that I intend to drink from the cup. Not only that, the mirror neurons in the premotor area of your frontal cortex will get you ready to drink as well.

We see an act and we ready ourselves to imitate it. At the simplest level, that’s why we get thirsty when others drink, and why we yawn when others yawn. At the most complex level, mirror neurons help us understand the nature of culture and how our shared behaviors bind us together, mind to mind. The internal maps created by mirror neurons are automatic, they do not require consciousness or effort. We are hardwired from birth to detect sequences and make maps in our brains of the internal state, the intentional stance, of other people. And this mirroring is “cross-modal”, it operates in all sensory channels, not just vision, so that a sound, a touch, a smell, can cue us to the internal state and intentions of another.

By embedding the mind of another into our own firing patterns, our mirror neurons may provide the foundation for our mindsight maps.

Now let’s take another step. Based on these sensory inputs, we can mirror not only the behavioral intentions of others, but also their emotional states. In other words, this is the way we not only imitate others’ behaviors but actually come to resonate with their feelings, the internal mental flow of their minds. We sense not only what action is coming next, but also the emotional energy that underlies the behavior. In developmental terms, if the behavioral patterns we see in our caregivers are straightforward, we can then map sequences with security, knowing what might happen next, embedding intentions of kindness and care, and so create in ourselves a mindsight lens that is focused and clear. If, on the other hand, we’ve had parents who are confusing and hard to “read,” our own sequencing circuits may create distorted maps.

So from our earliest days, the basic circuitry of mindsight can be laid down with a solid foundation, or created on shaky ground.

Knowing Me, Knowing You

I once organized an interdisciplinary think tank of researchers to explore how the mind might use the brain to perceive itself. One idea we discussed is that we make maps of intention using our cortically based mirror neurons and then transfer this information downward to our subcortical regions. A neural circuit called the insula seems to be the information superhighway between the mirror neurons and the limbic areas, which in turn send messages to the brainstem and the body proper. This is how we can come to resonate physiologically with others, how even our respiration, blood pressure, and heart rate can rise and fall in sync with another’s internal state.

These signals from our body, brainstem, and limbic areas then travel back up the insula to the middle prefrontal areas. I’ve come to call this set of circuits, from mirror neurons to subcortical regions, back up to the middle prefrontal areas, the “resonance circuits.” This is the pathway that connects us to one another. Notice what happens when you’re at a party with friends. If you approach a group that is laughing, you’ll probably find yourself smiling or chuckling even before you’ve heard the joke. Or perhaps you’ve gone to dinner with people who’ve suffered a recent loss. Without their saying anything, you may begin to sense a feeling of heaviness in your chest, a welling up in your throat, tears in your eyes. Scientists call this emotional contagion. The internal states of others, from joy and play to sadness and fear, directly affect our own state of mind. This contagion can even make us interpret unrelated events with a particular bias, so that, for example, after we’ve been around someone who is depressed we interpret someone else’s seriousness as sadness.

For therapists, it’s crucial to keep this bias in mind. Otherwise a prior session may shape our internal state so much that we aren’t open and receptive to the new person with whom we need to be resonating.

Our awareness of another person’s state of mind depends on how well we know our own. The insula brings the resonating state within us upward into the middle prefrontal cortex, where we make a map of our internal world. So we feel others’ feelings by actually feeling our own, we notice the belly fill with laughter at the party or with sadness at the funeral home. All of our subcortical data, our heart rate, breathing, and muscle tension, our limbic coloring of emotion, travels up the insula to inform the cortex of our state of mind. This is the main reason that people who are more aware of their bodies have been found to be more empathic.

The insula is the key: When we can sense our own internal state, the fundamental pathway for resonating with others is open as well.

The mind we first see in our development is the internal state of our caregiver. We coo and she smiles, we laugh and his face lights up. So we first know ourselves as reflected in the other. One of the most interesting ideas we discussed in our study group is that our resonance with others may actually precede our awareness of ourselves. Developmentally and evolutionarily, our modern self-awareness circuitry may be built upon the more ancient resonance circuits that root us in our social world.

How, then, do we discern who is “me” and who is “you”? The scientists in our group suggested that we may adjust the location and firing pattern of the prefrontal images to perceive our own mind. Increases in the registration of our own bodily sensations combined with a decrease in our mirror neuron response may help us know that these tears are mine, not yours, or that this anger is indeed from me, not from you. This may seem like a purely philosophical and theoretical question until you are in the midst of a marital conflict and find yourself arguing about who is the angry one, you or your spouse. And certainly, as a therapist, if I do not track the distinction between me and other, I can become flooded with my patients’ feelings, lose my ability to help, and also burn out quickly.

When resonance literally becomes mirroring, when we confuse me with you, then objectivity is lost. Resonance requires that we remain differentiated, that we know who we are, while also becoming linked. We let our own internal states be influenced by, but not become identical with, those of the other person.

It will take much more research to elucidate the exact way our mindsight maps make this distinction, but the basic issues are clear. The energy and information flow that we sense both in ourselves and in others rides the resonance circuits to enable mindsight.

As I consider the resonance circuits, two mind lessons stand out for me. One is that becoming open to our body’s states, the feelings in our heart, the sensations in our belly, the rhythm of our breathing, is a powerful source of knowledge. The insula flow that brings up this information and energy colors our cortical awareness, shaping how we reason and make decisions. We cannot successfully ignore or suppress these subcortical springs. Becoming open to them is a gateway to clear mindsight.

The second lesson is that relationships are woven into the fabric of our interior world. We come to know our own minds through our interactions with others. Our mirror neuron perceptions, and the resonance they create, act quickly and often outside of awareness. Mindsight permits us to invite these fast and automatic sources of our mental life into the theater of consciousness. As we welcome the neural reality of our interconnected lives, we can gain new clarity about who we are, what shapes us, and how we in turn can shape our lives.

Neuroplasticity in a Nutshell – Daniel J. Siegel MD

Change Your Brain and Your life – Daniel J. Siegel MD

from

Mindsight, change your brain and your life

by Daniel J. Siegel MD

get it at Amazon.com

THE HOME OF EMPATHY. The Mirror Neuron System – V. Rajmohan and E. Mohandas.

The Mirror Neuron System (MNS) discovery is considered to be the most important landmark in neuroscience research during the last decade.

The Mirror neuron system is a group of specialized neurons that “mirrors” the actions and behaviour of others.

Theory of mind (ToM) or mentalisation is the ability to recognize that someone else has a mind different from one’s own.

The Mirror neuron system is a group of specialized neurons that “mirrors” the actions and behaviour of others. The involvement of mirror neuron system (MNS) is implicated in neurocognitive functions (social cognition, language, empathy, theory of mind) and neuropsychiatric disorders. MNS discovery is considered to be the most important landmark in neuroscience research during the last decade.

MIRROR NEURON SYSTEM DISCOVERY

The mirror neurons were discovered serendipitously by Giacomo Rizzolatti and colleagues while working on the grasp response of macaques. They observed that a group of neurons in the area F5 of the premotor cortex that fires when a macaque performs an action; also discharges when it observes the same action being performed by another animal. Subsequent research has elucidated the diverse regions involved in the MNS of monkeys. Recently different cortical structures have been described as part of the MNS in humans.

MNS in monkeys

The area F5 of the premotor cortex (premotor area located in the posterior bank of the inferior arcuate sulcus and the cortical convexity immediately caudal to it) in monkeys has two sets of visuomotor neurons namely the ‘canonical’ and the ‘mirror neurons’. The ‘canonical neurons’ (in F5 bank region) respond to presentation of an object while mirror neurons (in F5 convexity) respond to performance of an action and observation of an object directed action. The mirror neurons are triggered by any action that involves the interaction between a biological effector (mouth, hand etc.) and an object. They are stimulated by the observation of the exact same action involving the effector and object (‘strictly congruent’ neurons) and also by actions that are similar but not having exact effect or object interaction (‘broadly congruent’ neurons).

Other areas that form part of the MNS are the superior temporal sulcus (STS) and the area 7b (PF of Von Economo) in the inferior parietal lobule (IPL). The STS codes for a larger number of movements than the F5 neurons but lacks motor properties (i.e., does not discharge while performing the movement). The area 7b neurons in IPL are heterogeneous and have a role in coding sensory stimuli and respond to somatosensory, visual or bimodal stimuli. In addition to this, they also have motor properties and discharge on action observation and performance. The IPL receives inputs from the STS and sends an important output to the ventral premotor cortex including area F5.

Figure 1. Basic mirror neuron circuitry in monkey. F1: Primary motor cortex, F5: Premotor cortex, IPL: inferior parietal lobule, STS: superior temporal sulcus.

MNS in humans

Brain imaging studies reveal that action observation in humans activates the inferior frontal gyrus (IFG), lower part of the precentral gyrus, the rostral part of the IPL and also the temporal, occipital and parietal visual areas. The frontal and the parietal mirror neuron regions are somatotopically organized. The activation of pars opercularis of the IFG reflects the observation of distal hand and mouth actions, whereas the activation of the premotor cortex reflects proximal arm and neck movements [Figure 2]. The mirror neurons in humans, unlike those in monkeys fire even while observing meaningless (intransitive) movements. The observation of transitive actions causes the firing of the frontal and the temporal nodes of the MNS while that of intransitive actions result in the firing of the frontal node only.

Figure 2. Mirror neuron regions in humans

FUNCTIONS OF MNS

Action understanding

Action understanding is the fundamental function of the MNS. Each time the animal observes a certain action being performed by another animal, the mirror neurons representing the performance of that action are activated. The mirror neurons transform visual observation into knowledge. Studies on humans during action observation have shown activation of the IFG, the IPL and a region within the STS. The precentral motor cortex though not activated by action observation is involved indirectly in action understanding as they have a role in motor imagery.

The main hypotheses to explain the phenomenon of action understanding are the visual hypothesis, direct-match hypothesis and the ‘generate and test’ model. Visual hypothesis is based on the visual analysis of the effector, the object and on the context in which the action is going on to draw conclusions as to the meaning of the action. The neural substrates are visual extrastriate areas, inferotemporal lobe and STS region. The direct match hypothesis is based on the mapping of observed action on his/her own motor representation of the observed action. Therefore it involves a process of observation induced motor representation, followed by matching of this to the motor representation generated during active outcome directed action performed by the individual (simulation). If both these motor representations correspond, it leads to action understanding.

A more complex hypothesis suggested for action understanding is the ‘generate and test’ model. According to this model, action understanding involves finding a ‘pretend’ goal that would generate an action plan in the observer’s own motor planning system. This is then matched with the observed action. It is presumed that when the simulated motor action does not match the observed one, a new hypothesis is generated and tested for congruence with the observed action. So actions are understood not just in terms of their outcomes, but also in terms of the mental states and especially the goals, that have generated them.

Imitation

Basic circuit underlying imitation coincides with that which is active during action observation. Imitation requires a perfect matching of the performed action onto the observed one. Mirror neurons are able to recognize the actions of others and the intention associated with them. So they can code for likely future actions of others, thereby observers are able to anticipate the actions of others.

Human imitation involves flow of information through the STS, IPL and the IFG. STS provides higher order visual processing of observed action while the fronto-parietal MNS codes for the goal of the action and the motor plan on how to achieve it. The fronto-parietal system then sends copies of this motor plan to the STS, which matches the predicted sensory consequence of the planned motor action with the visual description of the observed action. The efferent copies to the STS originate from the ventral sector of the pars opercularis of the IFG, the activity of which is specific to imitation.

There is a difference during imitative learning of tasks between novel tasks and the tasks that are part of the observer’s motor repertoire. The frontal and parietal areas are activated during observation of a task that is part of one’s repertoire. The imitation of novel action in addition to the above regions involves the dorsolateral prefrontal cortex (DLPFC) and the cortical areas relevant to motor preparation namely: dorsal premotor cortex (PMd), mesial prefrontal cortex and the superior parietal lobule. So the basic imitation learning circuit consists of IFG, IPL, STS, motor preparation areas and DLPFC.

Figure 3. Mirror neuron structures in imitation

Speech and language

The presence of mirror neurons in Broca’s area of humans suggests that human language may have evolved from a gesture performance/understanding system. The tasks like spontaneous speech and reading activate the hand motor area and the IFG, on the left side. So language mirror neurons seem to be lateralized to the left side involving the dominant hand motor cortex and the higher levels of language network.

Theory of mind

Theory of mind (ToM) or mentalisation is the ability to recognize that someone else has a mind different from one’s own. It involves the ability to infer someone else’s mind by facial expression, tone of voice and non-verbal communication. It involves the area concerned with action imitation, face imitation and intention understanding. The neural structures involved in ToM include IFG, right STS, right IPL, medial prefrontal cortex including the anterior cingulate cortex (ACC) orbitofrontal cortex (OFC), precuneus, somatosensory cortex, amygdala and the occipital cortex. Therefore the MNS is considered integral to the theory of mind.

Social communication and empathy

Social communication and identification involve imitation. The more people tend to imitate each other, the more they are able to develop an empathic relationship. Social mirroring involves the interaction of the core mirror neuron system with the limbic system. Imaging studies have shown that observation and imitation of facial emotional expression involve the fronto-parietal mirror neuron system, STS, insula and the limbic system [Figure 3].

Empathy is a process which involves the affective sharing between self and others, adopting the perspective of others and the ability for self agency and self regulation. The neural correlates empathy include IFG, right STS, right IPL, ACC, ventromedial prefrontal cortex (VMPFC), somatosensory cortex, amygdala, precuneus, insula and the posterior cingulate. Thus empathy involves a significant interaction of the core MNS and its limbic extension.

Table 1. Neural correlates of mirror neuron system, theory of mind and empathy

Social cognition

Social cognition refers to thought processes involved in understanding and dealing with others. It involves regions that mediate face perception, emotional processing, theory of mind, empathy (especially self reference) and working memory. The MNS involvement in mediating empathy and ToM reflects its significant role in social cognition.

Mirror neurons and neuropsychiatric disorders

Autism and autism spectrum disorders (ASD) are characterized by social impairment, the lack of ToM and demonstrable defects in imitation skills. This implies dysfunctional MNS in ASD. Neuroimaging studies have demonstrated lesser activation of Broadman’s area (BA) 44/45, the superior temporal gyrus (BA 22), the right insula and the left amygdala. A recent study also demonstrated the lack of MNS activity during observation and emotional expression in children with ASD.

The mirror neurons may also be involved in the development of disorders with hypersociality like William’s syndrome and Turner’s syndrome. The relevance of mirror neurons in social cognition may account for dysfunctional MNS in social phobia and asociality observed in schizophrenia.

The MNS also plays an important role in bonding and attachment. Dysfunctional MNS may play a role in antisocial and borderline personality disorder. The patients with borderline personality disorder lack the ability to discern the mental states of self and others. They have fractured early attachments leading to a deficiency in learning of the concepts like secure attachment and the capacity to mentalise. Psychotherapeutic processes involve the MNS accounting for empathy and ToM.

CONCLUSION

The fascinating discovery of MNS has generated tremendous enthusiasm among researchers in cognitive neuroscience. The involvement of MNS in social cognition, empathy and ToM has fuelled interest in explaining its role in ASD, schizophrenia, personality disorders and psychotherapeutic processes. The future research may unravel mysteries surrounding MNS.

Indian Journal of Psychiatry

SOUL DAMAGE. The Precious Resources of Our Time and Attention – Linda and Charlie Bloom.

How do we nurture our soul?

Soul-damage occurs when we deny ourselves the kinds of enriching experiences that we need to have in order to thrive, rather than simply survive, experiences that make our heart sing, that infuse our lives with a sense of passion and vitality.

Most of us know that there are certain kinds of experiences that nurture our souls and others that don’t. We also know that “experiences” are not “things,” and that although things, like money, homes, and motor vehicles do matter in our lives, they do not nourish our hearts and spirits. There’s nothing wrong with something that enhances only the material as long as we don’t expect more from it than that. For most of us, separating unrealistic expectations from real ones is not easy.

If we spent even 10% as much of our time and energy on matters of the heart as we do on matters that relate to the fulfillment of our ego’s desires, our quality of life would transform.

For most of us, even 10% would represent a several-fold increase of our time. Many of us give more time and concern towards the maintenance of our cars than to our deeper needs. We may insist that what we most value is love, inner peace, family, or ‘truth”, yet our lives may not reflect this priority.

It has been said that you can know a person by the way in which they spend their time, not by their words. What we truly love is what we give our energies to, and this may not be what we say matters most to us.

It is the first and most critical step in the process of bringing integrity into our lives. Until we have done so, self-deception and rationalization will permeate our daily existence.

Psychology Today

Does using testosterone to treat depression work? – Tim Newman.

Medical professionals have been discussing whether testosterone treatment can actually reduce depressive symptoms in men for many years. A recent meta-analysis attempts to draw a clearer picture.

Depression is a major global concern. Per year, major depressive disorder affects an estimated 16.1 million adults in the United States alone.

The World Health Organization (WHO) describe depression as “the leading cause of ill health and disability worldwide.”

There are drugs available to manage depressive symptoms, but they do not work for everyone. In fact, a significant percentage of people do not experience long-term relief, even after trying multiple drugs. Existing depression therapies only work for a subset of the population. For this reason, it is vital to understand whether testosterone might help in treatment-resistant cases.

. . . Medical News Today

MINDING THE BRAIN. Neuroplasticity in a Nutshell – Daniel J. Siegel MD * Neuroplasticity – Wikipedia.

“The brain is so complicated it staggers its own imagination.”

“Neurons that fire together, wire together”, “neurons that fire out of sync, fail to link”.

We can use the power of our mind to change the firing patterns of our brain and thereby alter our feelings, perceptions, and responses. The power to direct our attention, focus, has within it the power to shape our brain’s firing patterns, as well as the power to shape the architecture of the brain itself.

The causal arrows between brain and mind point in both directions. When we focus our attention in specific ways, we create neural firing patterns that permit previously separated areas to become linked and integrated. The synaptic linkages are strengthened, the brain becomes more interconnected, and the mind becomes more adaptive.

Daniel J. Siegel, MD, is a clinical professor of psychiatry at the UCLA School of Medicine, co-director of the UCLA Mindful Awareness Research Center, and executive director of the Mindsight Institute.

Neuroplasticity

/,njuaraupla’stisiti/ noun

The ability of the brain to form and reorganize synaptic connections, especially in response to learning or experience or following injury. “neuroplasticity offers real hope to everyone from stroke victims to dyslexics”

It’s easy to get overwhelmed thinking about the brain. With more than one hundred billion interconnected neurons stuffed into a small, skull-enclosed space, the brain is both dense and intricate. And as if that weren’t complicated enough, each of your average neurons has ten thousand connections, or synapses, linking it to other neurons. In the skull portion of the nervous system alone, there are hundreds of trillions of connections linking the various neural groupings into a vast spiderweb-like network. Even if we wanted to, we couldn’t live long enough to count each of those synaptic linkages.

Given this number of synaptic connections, the brain’s possible on-off firing patterns, its potential for various states of activation, has been calculated to be ten to the millionth power, or ten times ten one million times. This number is thought to be larger than the number of atoms in the known universe. It also far exceeds our ability to experience in one lifetime even a small percentage of these firing possibilities. As a neuroscientist once said, “The brain is so complicated it staggers its own imagination.” The brain’s complexity gives us virtually infinite choices for how our mind will use those firing patterns to create itself. ‘If we get stuck in one pattern or the other, we’re limiting our potential.

Patterns of neural firing are what we are looking for when we watch a brain scanner “light up” as a certain task is being performed. What scans often measure is blood flow. Since neural activity increases oxygen use, an increased flow of blood to a given area of the brain implies that neurons are firing there. Research studies correlate this inferred neural firing with specific mental functions, such as focusing attention, recalling a past event, or feeling pain.

We can only imagine how a scan of my brain might have looked when I went down the low road in a tense encounter with my son one day: an abundance of limbic firing with increased blood flow to my irritated amygdala and a diminished flow to my prefrontal areas as they began to shut down. Sometimes the out-of-control firing of our brain drives what we feel, how we perceive what is happening, and how we respond. Once my prefrontal region was off-Iine, the firing patterns from throughout my subcortical regions could dominate my internal experience and my interactions with my kids. But it is also true that when we’re not traveling down the low road we can use the power of our mind to change the firing patterns of our brain and thereby alter our feelings, perceptions, and responses.

One of the key practical lessons of modern neuroscience is that the power to direct our attention has within it the power to shape our brain’s firing patterns, as well as the power to shape the architecture of the brain itself.

As you become more familiar with the various parts of the brain, you can more easily grasp how the mind uses the firing patterns in these various parts to create itself. It bears repeating that while the physical property of neurons firing is correlated with the subjective experience we call mental activity, no one knows exactly how this actually occurs. But keep this in the front of your mind:

Mental activity stimulates brain firing as much as brain firing creates mental activity.

When you voluntarily choose to focus your attention, say, on remembering how the Golden Gate Bridge looked one foggy day last fall, your mind has just activated the visual areas in the posterior part of your cortex. On the other hand, if you were undergoing brain surgery, the physician might place an electrical probe to stimulate neural firing in that posterior area, and you’d also experience a mental image of some sort.

The causal arrows between brain and mind point in both directions.

Keeping the brain in mind in this way is like knowing how to exercise properly. As we work out, we need to coordinate and balance the different muscle groups in order to keep ourselves fit. Similarly, we can focus our minds to build the specific “muscle groups” of the brain, reinforcing their connections, establishing new circuitry, and linking them together in new and helpful ways. There are no muscles in the brain, of course, but rather differentiated clusters of neurons that form various groupings called nuclei, parts, areas, zones, regions, circuits, or hemispheres.

And just as we can intentionally activate our muscles by flexing them, we can “flex” our circuits by focusing our attention to stimulate the firing in those neuronal groups. Using mindsight to focus our attention in ways that integrate these neural circuits can be seen as a form of “brain hygiene.”

WHAT FIRES TOGETHER, WIRES TOGETHER

You may have heard this before: As neurons fire together, they wire together. But let’s unpack this statement piece by piece. When we have an experience, our neurons become activated; What this means is that the long length of the neuron, the axon, has a flow of ions in and out of its encasing membrane that functions like an electrical current. At the far end of the axon, the electrical flow leads to the release of a chemical neurotransmitter into the small synaptic space that joins the firing neuron to the next, postsynaptic neuron. This chemical release activates or deactivates the downstream neuron. Under the right conditions, neural firing can lead to the strengthening of synaptic connections. These conditions include repetition, emotional arousal, novelty, and the careful focus of attention! Strengthening synaptic linkages between neurons is how we learn from experience.

One reason that we are so open to learning from experience is that, from the earliest days in the womb and continuing into our childhood and adolescence, the basic architecture of the brain is very much a work in progress.

During gestation, the brain takes shape from the bottom up, with the brainstem maturing first. By the time we are born, the limbic areas are partially developed but the neurons of the cortex lack extensive connections to one another.

This immaturity, the lack of connections within and among the different regions of the brain, is what gives us that openness to experience that is so critical to learning.

A massive proliferation of synapses occurs during the first years of life. These connections are shaped by genes and chance as well as experience, with some aspects of ourselves being less amenable to the influence of experience than others. Our temperament, for example, has a nonexperiential basis; it is determined in large part by genes and by chance. For instance, we may have a robust approach to novelty and love to explore new things, or we may tend to hang back in response to new situations, needing to “warm up” before we can overcome our initial shyness. Such neural propensities are set up before birth and then directly shape how we respond to the worId-and how others respond to us.

From our first days of life, our immature brain is also directly shaped by our interactions with the world, and especially by our relationships. Our experiences stimulate neural firing and sculpt our emerging synaptic connections. This is how experience changes the structure of the brain itself, and could even end up having an influence on our innate temperament.

As we grow, then, an intricate weaving together of the genetic, chance, and experiential input into the brain shapes what we call our “personality,” with all its habits, likes, dislikes, and patterns of response. If you’ve always had positive experiences with dogs and have enjoyed having them in your life, you may feel pleasure and excitement when a neighbor’s new dog comes bounding toward you. But if you’ve ever been severely bitten, your neural firing patterns may instead help create a sense of dread and panic, causing your entire body to shrink away from the pooch. If on top of having had a prior bad experience with a dog you also have a shy temperament, such an encounter may be even more fraught with fear. But whatever your experience and underlying temperament, transformation is possible. Learning to focus your attention in specific therapeutic ways can help you override that old coupling of fear with dogs.

The intentional focus of attention is actually a form of self-directed experience: It stimulates new patterns of neural firing to create new synaptic linkages.

You may be wondering, “How can experience, even a mental activity such as directing attention, actually shape the structure of the brain?” As we’ve seen, experience means neural firing. When neurons fire together, the genes in their nuclei, their master control centers, become activated and “express” themselves. Gene expression means that certain proteins are produced. These proteins then enable the synaptic linkages to be constructed anew or to be strengthened.

Experience also stimulates the production of myelin, the fatty sheath around axons, resulting in as much as a hundredfold increase in the speed of conduction down the neuron’s length. And as we now know, experience can also stimulate neural stem cells to differentiate into wholly new neurons in the brain.

This neurogenesis, along with synapse formation and myelin growth, can take place in response to experience throughout our lives. As discussed before, the capacity of the brain to change is called neuroplasticity. We are now discovering how the careful focus of attention amplifies neuroplasticity by stimulating the release of neurochemicals that enhance the structural growth of synaptic linkages among the activated neurons.

Epigenesis

An additional piece of the puzzle is now emerging. Researchers have discovered that early experiences can change the long-term regulation of the genetic machinery within the nuclei of neurons through a process called epigenesis.

If early experiences are positive, for example, chemical controls over how genes are expressed in specific areas of the brain can alter the regulation of our nervous system in such a way as to reinforce the quality of emotional resilience. If early experiences are negative, however, it has been shown that alterations in the control of genes influencing the stress response may diminish resilience in children and compromise their ability to adjust to stressful events in the future.

The changes wrought through epigenesis will continue to be in the science news as part of our exploration of how experience shapes who we are.

In sum, experience creates the repeated neural firing that can lead to gene expression, protein production, and changes in both the genetic regulation of neurons and the structural connections in the brain. By harnessing the power of awareness to strategically stimulate the brain’s firing, mindsight enables us to voluntarily change a firing pattern that was laid down involuntarily. When we focus our attention in specific ways, we create neural firing patterns that permit previously separated areas to become linked and integrated. The synaptic linkages are strengthened, the brain becomes more interconnected, and the mind becomes more adaptive.

THE BRAIN IN THE BODY

It’s important to remember that the activity of what we’re calling the “brain” is not just in our heads. For example, the heart has an extensive network of nerves that process complex information and relay data upward to the brain in the skull. So, too, do the intestines, and all the other major organ systems of the body. The dispersion of nerve cells throughout the body begins during our earliest development in the womb, when the cells that form the outer layer of the embryo fold inward to become the origin of our spinal cord. Clusters of these wandering cells then start to gather at one end of the spinal cord, ultimately to become the skull-encased brain. But other neural tissue becomes intricately woven with our musculature, our skin, our heart, our lungs, and our intestines. Some of these neural extensions form part of the autonomic nervous system, which keeps the body working in balance whether we are awake or asleep; other circuitry forms the voluntary portion of the nervous system, which allows us to intentionally move our limbs and control our respiration. The simple connection of sensory nerves from the periphery to our spinal cord and then upward through the various layers of the skull-encased brain allows signals from the outer world to reach the cortex, where we can become aware of them. This input comes to us via the five senses that permit us to perceive the outer physical world.

The neural networks throughout the interior of the body, including those surrounding the hollow organs, such as the intestines and the heart, send complex sensory input to the skull-based brain. This data forms the foundation for visceral maps that help us have a “gut feeling” or a “heartfelt” sense. Such input from the body forms a vital source of intuition and powerfully influences our reasoning and the way we create meaning in our lives.

Other bodily input comes from the impact of molecules known as hormones. The body’s hormones, together with chemicals from the foods and drugs we ingest, flow into our bloodstream and directly affect the signals sent along neurai routes. And, as we now know, even our immune system interacts with our nervous system. Many of these effects influence the neurotransmitters that operate at the synapses. These chemical messengers come in hundreds of varieties, some of which, such as dopamine and serotonin, have become household names thanks in part to drug company advertising. These substances have specific and complex effects on different regions of our nervous system. For example, dopamine is involved in the reward systems of the brain; behaviors and substances can become addictive because they stimulate dopamine release. Serotonin helps smooth out anxiety, depression, and mood fluctuations. Another chemical messenger is oxytocin, which is released when we feel close and attached to someone.

Throughout this book, I use the general term brain to encompass all of this wonderful complexity of the body proper as it intimately intertwines with its chemical environment and with the portion of neural tissue in the head. This is the brain that both shapes and is shaped by our mind. This is also the brain that forms one point of the triangle of well-being that is so central to mindsight.

By looking at the brain as an embodied system beyond its skull case, we can actually make sense of the intimate dance of the brain, the mind, and our relationships with one another. We can also recruit the power of neuroplasticity to repair damaged connections and create new, more satisfying patterns in our everyday lives.

from

Mindsight, change your brain and your life

by Daniel J. Siegel MD

get it at Amazon.com

See also: MINDSIGHT, OUR SEVENTH SENSE, an introduction. Change your brain and your life – Daniel J. Siegel MD.

Neuroplasticity – Wikipedia

Neuroplasticity, also known as brain plasticity and neural plasticity, is the ability of the brain to change throughout an individual’s life, e.g., brain activity associated with a given function can be transferred to a different location, the proportion of grey matter can change, and synapses may strengthen or weaken over time.

Research in the latter half of the 20th century showed that many aspects of the brain can be altered (or are “plastic”) even through adulthood.“ However, the developing brain exhibits a higher degree of plasticity than the adult brain.

Neuroplasticity can be observed at multiple scales, from microscopic changes in individual neurons to larger-scale changes such as cortical remapping in response to injury. Behavior, environmental stimuli, thought, and emotions may also cause neuroplastic change through activity-dependent plasticity, which has significant implications for healthy development, learning, memory, and recovery from brain damage.

At the single cell level, synaptic plasticity refers to changes in the connections between neurons, whereas non-synaptic plasticity refers to changes in their intrinsic excitability.

Neurobiology

One of the fundamental principles underlying neuroplasticity is based on the idea that individual synaptic connections are constantly being removed or recreated, largely dependent upon the activity of the neurons that bear them. The activity-dependence of synaptic plasticity is captured in the aphorism which is often used to summarize Hebbian theory: “neurons that fire together, wire together”/”neurons that fire out of sync, fail to link”. If two nearby neurons often produce an impulse in close temporal proximity, their functional properties may converge. Conversely, neurons that are not regularly activated simultaneously may be less likely to functionally converge.

Cortical maps

Cortical organization, especially in sensory systems, is often described in terms of maps. For example, sensory information from the foot projects to one cortical site and the projections from the hand target another site. As a result, the cortical representation of sensory inputs from the body resembles a somatotopic map, often described as the sensory homunculus.

In the late 1970s and early 1980s, several groups began exploring the impact of interfering with sensory inputs on cortical map reorganization. Michael Merzenich, Jon Kaas and Doug Rasmusson were some of those researchers. They found that if the cortical map is deprived of its input, it activates at a later time in response to other, usually adjacent inputs. Their findings have been since corroborated and extended by many research groups. Merzenich’s (1984) study involved the mapping of owl monkey hands before and after amputation of the third digit. Before amputation, there were five distinct areas, one corresponding to each digit of the experimental hand. Sixty-two days following amputation of the third digit, the area in the cortical map formerly occupied by that digit had been invaded by the previously adjacent second and fourth digit zones. The areas representing digit one and five are not located directly beside the area representing digit three, so these regions remained, for the most part, unchanged following amputation. This study demonstrates that only those regions that border a certain area invade it to alter the cortical map. In the somatic sensory system, in which this phenomenon has been most thoroughly investigated, JT Wall and J Xu have traced the mechanisms underlying this plasticity. Reorganization is not cortically emergent, but occurs at every level in the processing hierarchy; this produces the map changes observed in the cerebral cortex.“

Merzenich and William Jenkins (1990) initiated studies relating sensory experience, without pathological perturbation, to cortically observed plasticity in the primate somatosensory system, with the finding that sensory sites activated in an attended operant behavior increase in their cortical representation. Shortly thereafter, Ford Ebner and colleagues (1994) made similar efforts in the rodent whisker barrel cortex (also part of the somatosensory system). These two groups largely diverged over the years. The rodent whisker barrel efforts became a focus for Ebner, Matthew Diamond, Michael Armstrong-James, Robert Sachdev, and Kevin Fox. Great inroads were made in identifying the locus of change as being at cortical synapses expressing NMDA receptors, and in implicating cholinergic inputs as necessary for normal expression. The work of Ron Frostig and Daniel Polley (1999, 2004) identified behavioral manipulations causing a substantial impact on the cortical plasticity in that system.

Merzenich and DT Blake (2002, 2005, 2006) went on to use cortical implants to study the evolution of plasticity in both the somatosensory and auditory systems. Both systems show similar changes with respect to behavior. When a stimulus is cognitively associated with reinforcement, its cortical representation is strengthened and enlarged. In some cases, cortical representations can increase two to threefold in 1-2 days when a new sensory motor behavior is first acquired, and changes are largely finalised within at most a few weeks. Control studies show that these changes are not caused by sensory experience alone: they require learning about the sensory experience, they are strongest for the stimuli that are associated with reward, and they occur with equal ease in operant and classical conditioning behaviors.

An interesting phenomenon involving plasticity of cortical maps is the phenomenon of phantom limb sensation. Phantom limb sensation is experienced by people who have undergone amputations in hands, arms, and legs, but it is not limited to extremities. Although the neurological basis of phantom limb sensation is still not entirely understood it is believed that cortical reorganization plays an important role.

Norman Doidge, following the lead of Michael Merzenich, separates manifestations of neuroplasticity into adaptations that have positive or negative behavioral consequences. For example, if an organism can recover after a stroke to normal levels of performance, that adaptiveness could be considered an example of “positive plasticity”. Changes such as an excessive level of neuronal growth leading to spasticity or tonic paralysis, or excessive neurotransmitter release in response to injury that could result in nerve cell death, are considered as an example of “negative” plasticity. In addition, drug addiction and obsessive-compulsive disorder are both deemed examples of “negative plasticity” by Dr. Doidge, as the synaptic rewiring resulting in these behaviors is also highly maladaptive.

A 2005 study found that the effects of neuroplasticity occur even more rapidly than previously expected. Medical students’ brains were imaged during the period of studying for their exams. In a matter of months, the students’ gray matter increased significantly in the posterior and lateral parietal cortex.

Applications and example

The adult brain is not entirely “hard-wired” with fixed neuronal circuits. There are many instances of cortical and subcortical rewiring of neuronal circuits in response to training as well as in response to injury. There is solid evidence that neurogenesis (birth of brain cells) occurs in the adult mammalian brain, and such changes can persist well into old age. The evidence for neurogenesis is mainly restricted to the hippocampus and olfactory bulb, but current research has revealed that other parts of the brain, including the cerebellum, may be involved as well. However, the degree of rewiring induced by the integration of new neurons in the established circuits is not known, and such rewiring may well be functionally redundant.

There is now ample evidence for the active, experience-dependent reorganization of the synaptic networks of the brain involving multiple inter-related structures including the cerebral cortex. The specific details of how this process occurs at the molecular and ultrastructural levels are topics of active neuroscience research. The way experience can influence the synaptic organization of the brain is also the basis for a number of theories of brain function including the general theory of mind and Neural Darwinism. The concept of neuroplasticity is also central to theories of memory and learning that are associated with experience-driven alteration of synaptic structure and function in studies of classical conditioning in invertebrate animal models such as Aplysia.

Treatment of brain damage

A surprising consequence of neuroplasticity is that the brain activity associated with a given function can be transferred to a different location; this can result from normal experience and also occurs in the process of recovery from brain injury. Neuroplasticity is the fundamental issue that supports the scientific basis for treatment of acquired brain injury with goal-directed experiential therapeutic programs in the context of rehabilitation approaches to the functional consequences of the injury.

Neuroplasticity is gaining popularity as a theory that, at least in part, explains improvements in functional outcomes with physical therapy post-stroke. Rehabilitation techniques that are supported by evidence which suggest cortical reorganization as the mechanism of change include constraint-induced movement therapy, functional electrical stimulation, treadmill training with body-weight support, and virtual reality therapy. Robot assisted therapy is an emerging technique, which is also hypothesized to work by way of neuroplasticity, though there is currently insufficient evidence to determine the exact mechanisms of change when using this method.

One group has developed a treatment that includes increased levels of progesterone injections in brain-injured patients. “Administration of progesterone after traumatic brain injury (TBI) and stroke reduces edema, inflammation, and neuronal cell death, and enhances spatial reference memory and sensory motor recovery.” In a clinical trial, a group of severely injured patients had a 60% reduction in mortality after three days of progesterone injections?” However, a study published in the New England Journal of Medicine in 2014 detailing the results of a multi-center NIH-funded phase III clinical trial of 882 patients found that treatment of acute traumatic brain injury with the hormone progesterone provides no significant benefit to patients when compared with placebo.”

Vision

For decades, researchers assumed that humans had to acquire binocular vision, in particular stereopsis, in early childhood or they would never gain it. In recent years, however, successful improvements in persons with amblyopia, convergence insufficiency or other stereo vision anomalies have become prime examples of neuroplasticity; binocular vision improvements and stereopsis recovery are now active areas of scientific and clinical research.

Brain training

Several companies have offered so-called cognitive training software programs for various purposes that claim to work via neuroplasticity; one example is Fast ForWord which is marketed to help children with learning disabilities. A systematic metaanalytic review found that “There is no evidence from the analysis carried out that Fast ForWord is effective as a treatment for children‘s oral language or reading difficulties”. A 2016 review found very little evidence supporting any of the claims of Fast ForWord and other commercial products, as their task-speciflc effects fail to generalise to other tasks.

Sensory prostheses

Neuroplasticity is involved in the development of sensory function. The brain is born immature and it adapts to sensory inputs after birth. In the auditory system, congenital hearing impairment, a rather frequent inborn condition affecting 1 of 1000 newborns, has been shown to affect auditory development, and implantation of a sensory prostheses activating the auditory system has prevented the deficits and induced functional maturation of the auditory system. Due to a sensitive period for plasticity, there is also a sensitive period for such intervention within the first 2-4 years of life. Consequently, in prelingually deaf children, early cochlear implantation, as a rule, allows the children to learn the mother language and acquire acoustic communication.

Phantom limb sensation

In the phenomenon of phantom limb sensation, a person continues to feel pain or sensation within a part of their body that has been amputated. This is strangely common, occurring in 60-80% of amputees. An explanation for this is based on the concept of neuroplasticity, as the cortical maps of the removed limbs are believed to have become engaged with the area around them in the postcentral gyrus. This results in activity within the surrounding area of the cortex being misinterpreted by the area of the cortex formerly responsible for the amputated limb.

The relationship between phantom limb sensation and neuroplasticity is a complex one. In the early 1990s V.S. Ramachandran theorized that phantom limbs were the result of cortical remapping. However, in 1995 Hertz Flor and her colleagues demonstrated that cortical remapping occurs only in patients who have phantom pain.” Her research showed that phantom limb pain (rather than referred sensations) was the perceptual correlate of cortical reorganization. This phenomenon is sometimes referred to as maladaptive plasticity.

In 2009 Lorimer Moseley and Peter Brugger carried out a remarkable experiment in which they encouraged arm amputee subjects to use visual imagery to contort their phantom limbs into impossible configurations. Four of the seven subjects succeeded in performing impossible movements of the phantom limb. This experiment suggests that the subjects had modified the neural representation of their phantom limbs and generated the motor commands needed to execute impossible movements in the absence of feedback from the body. The authors stated that: “In fact, this finding extends our understanding of the brain’s plasticity because it is evidence that profound changes in the mental representation of the body can be induced purely by internal brain mechanisms, the brain truly does change itself.”

Chronlc pain

Individuals who suffer from chronic pain experience prolonged pain at sites that may have been previously injured, yet are otherwise currently healthy. This phenomenon is related to neuroplasticity due to a maladaptive reorganization of the nervous system, both peripherally and centrally. During the period of tissue damage, noxious stimuli and inflammation cause an elevation of nociceptive input from the periphery to the central nervous system. Prolonged nociception from the periphery then elicits a neuroplastic response at the cortical level to change its somatotopic organization for the painful site, inducing central sensitization.“ For instance, individuals experiencing complex regional pain syndrome demonstrate a diminished cortical somatotopic representation of the hand contralaterally as well as a decreased spacing between the hand and the mouth.

Additionally, chronic pain has been reported to significantly reduce the volume of grey matter in the brain globally, and more specifically at the prefrontal cortex and right thalamus. However, following treatment, these abnormalities in cortical reorganization and grey matter volume are resolved, as well as their symptoms. Similar results have been reported for phantom limb pain, chronic low back pain and carpal tunnel syndrome.

Meditation

A number of studies have linked meditation practice to differences in cortical thickness or density of gray matter. One of the most well-known studies to demonstrate this was led by Sara Lazar, from Harvard University, in 2000. Richard Davidson, a neuroscientist at the University of Wisconsin, has led experiments in cooperation with the Dalai Lama on effects of meditation on the brain. His results suggest that long-term or short-term practice of meditation results in different levels of activity in brain regions associated with such qualities as attention, anxiety, depression, fear, anger, and the ability of the body to heal itself. These functional changes may be caused by changes in the physical structure of the brain.

Fitness and exercise

Aerobic exercise promotes adult neurogenesis by increasing the production of neurotrophic factors (compounds that promote growth or survival of neurons), such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor (IGF-1), and vascular endothelial growth factor (VEGF). Exercise-induced neurogenesis in the hippocampus is associated with measurable improvements in spatial memory. Consistent aerobic exercise over a period of several months induces marked clinically significant improvements in executive function (i.e., the “cognitive control” of behavior) and increased gray matter volume in multiple brain regions, particularly those that give rise to cognitive control. The brain structures that show the greatest improvements in gray matter volume in response to aerobic exercise are the prefrontal cortex and hippocampus; moderate improvements are seen in the anterior cingulate cortex, parietal cortex, cerebellum, caudate nucleus, and nucleus accumbens. Higher physical fitness scores (measured by V02 max) are associated with better executive function, faster processing speed, and greater volume of the hippocampus, caudate nucleus, and nucleus accumbens.

Human echolocation

Human echolocation is a learned ability for humans to sense their environment from echoes. This ability is used by some blind people to navigate their environment and sense their surroundings in detail. Studies in 2010 and 2011 using functional magnetic resonance imaging techniques have shown that parts of the brain associated with visual processing are adapted for the new skill of echolocation. Studies with blind patients, for example, suggest that the click-echoes heard by these patients were processed by brain regions devoted to vision rather than audition.

ADHD stimulants

Reviews of MRI studies on individuals with ADHD suggest that the long-term treatment of attention deficit hyperactivity disorder (ADHD) with stimulants, such as amphetamine or methylphenidate, decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function in several parts of the brain, such as the right caudatenucleus of the basal ganglia.

In children

Neuroplasticity is most active in childhood as a part of normal human development, and can also be seen as an especially important mechanism for children in terms of risk and resiliency. Trauma is considered a great risk as it negatively affects many areas of the brain and puts strain on the sympathetic nervous system from constant activation. Trauma thus alters the brain’s connections such that children who have experienced trauma may be hyper vigilant or overly aroused. However a child’s brain can cope with these adverse effects through the actions of neuroplasticity.

In animals

In a single lifespan, individuals of an animal species may encounter various changes in brain morphology. Many of these differences are caused by the release of hormones in the brain; others are the product of evolutionary factors or developmental stages. Some changes occur seasonally in species to enhance or generate response behaviors.

Seasonal brain changes

Changing brain behavior and morphology to suit other seasonal behaviors is relatively common in animals. These changes can improve the chances of mating during breeding season. Examples of seasonal brain morphology change can be found within many classes and species.

Within the class Aves, black-capped chickadees experience an increase in the volume of their hippocampus and strength of neural connections to the hippocampus during fall months. These morphological changes within the hippocampus which are related to spatial memory are not limited to birds, as they can also be observed in rodents and amphibians?“ In songbirds, many song control nuclei in the brain increase in size during mating season. Among birds, changes in brain morphology to influence song patterns, frequency, and volume are common. Gonadotropin-releasing hormone (GnRH) immunoreactivity, or the reception of the hormone, is lowered in European starlings exposed to longer periods of light during the day.

The California sea hare, a gastropod, has more successful inhibition of egg-laying hormones outside of mating season due to increased effectiveness of inhibitors in the brain. Changes to the inhibitory nature of regions of the brain can also be found in humans and other mammals. In the amphibian Bufo japonicus, part of the amygdala is larger before breeding and during hibernation than it is after breeding.

Seasonal brain variation occurs within many mammals. Part of the hypothalamus of the common ewe is more receptive to GnRH during breeding season than at other times of the year.

Humans experience a change in the size of the hypothalamic suprachiasmatic nucleus and vasopressin-immunoreactive neurons within it during the fall, when these parts are larger. In the spring, both reduce in size.

Traumatic brain injury research

Randy Nudo’s group found that if a small stroke (an infarction) is induced by obstruction of blood flow to a portion of a monkey’s motor cortex, the part of the body that responds by movement moves when areas adjacent to the damaged brain area are stimulated. In one study, intracortical microstimulation (ICMS) mapping techniques were used in nine normal monkeys. Some underwent ischemic-infarction procedures and the others, ICMS procedures. The monkeys with ischemic infarctions retained more finger flexion during food retrieval and after several months this deficit returned to preoperative levels.

With respect to the distal forelimb representation, “postinfarction mapping procedures revealed that movement representations underwent reorganization throughout the adjacent, undamaged cortex.” Understanding of interaction between the damaged and undamaged areas provides a basis for better treatment plans in stroke patients. Current research includes the tracking of changes that occur in the motor areas of the cerebral cortex as a result of a stroke. Thus, events that occur in the reorganization process of the brain can be ascertained. Nudo is also involved in studying the treatment plans that may enhance recovery from strokes, such as physiotherapy, pharmacotherapy, and electrical-stimulation therapy.

Jon Kaas, a professor at Vanderbilt University, has been able to show “how somatosensory area 3b and ventroposterior (VP) nucleus of the thalamus are affected by longstanding unilateral dorsal-column lesions at cervical levels in macaque monkeys.” Adult brains have the ability to change as a result of injury but the extent of the reorganization depends on the extent of the injury. His recent research focuses on the somatosensory system, which involves a sense of the body and its movements using many senses. Usually, damage of the somatosensory cortex results in impairment of the body perception. Kaas’ research project is focused on how these systems (somatosensory, cognitive, motor systems) respond with plastic changes resulting from injury.

One recent study of neuroplasticity involves work done by a team of doctors and researchers at Emory University, specifically Dr. Donald Stein and Dr. David Wright. This is the first treatment in 40 years that has significant results in treating traumatic brain injuries while also incurring no known side effects and being cheap to administer. Dr. Stein noticed that female mice seemed to recover from brain injuries better than male mice, and that at certain points in the estrus cycle, females recovered even better. This difference may be attributed to different levels of progesterone, with higher levels of progesterone leading to the faster recovery from brain injury in mice. However, clinical trials showed progesterone offers no significant benefit for traumatic brain injury human patients.

History

Origin

The term “plasticity” was first applied to behavior in 1890 by William James in The Principles of Psychology. The first person to use the term neural plasticity appears to have been the Polish neuroscientist Jerzy Konorski.

See also: William James’s Revolutionary 1884 Theory of How Our Bodies Affect Our Feelings – Maria Popova * What is an Emotion? – William James (1884).

In 1793, Italian anatomist Michele Vicenzo Malacarne described experiments in which he paired animals, trained one of the pair extensively for years, and then dissected both. He discovered that the cerebellums of the trained animals were substantially larger. But these findings were eventually forgotten.

The idea that the brain and its function are not fixed throughout adulthood was proposed in 1890 by William James in The Principles of Psychology, though the idea was largely neglected. Until around the 1970s, neuroscientists believed that the brain’s structure and function was essentially fixed throughout adulthood.

The term has since been broadly applied:

“Given the central importance of neuroplasticity, an outsider would be forgiven for assuming that it was well defined and that a basic and universal framework served to direct current and future hypotheses and experimentation. Sadly, however, this is not the case. While many neuroscientists use the word neuroplasticity as an umbrella term it means different things to different researchers in different subflelds. In brief, a mutually agreed upon framework does not appear to exist.”

Research and discovery

In 1923, Karl Lashley conducted experiments on rhesus monkeys that demonstrated changes in neuronal pathways, which he concluded were evidence of plasticity. Despite this, and other research that suggested plasticity took place, neuroscientists did not widely accept the idea of neuroplasticity.

In 1945, Justo Gonzalo concluded from his research of brain dynamics, that, contrary to the activity of the projection areas, the “central” cortical mass (more or less equidistant from the visual, tactile and auditive projection areas), would be a “maneuvering mass”, rather unspecific or multisensory, with capacity to increase neural excitability and re-organize the activity by means of plasticity properties. He gives as a first example of adaptation, to see upright with reversing glasses in the Stratton experiment, and specially, several first-hand brain injuries cases in which he observed dynamic and adaptive properties in their disorders, in particular in the inverted perception disorder. He stated that a sensory signal in a projection area would be only an inverted and constricted outline that would be magnified due to the increase in recruited cerebral mass, and re-inverted due to some effect of brain plasticity, in more central areas, following a spiral growth.

Marian Diamond of the University of California, Berkeley, produced the first scientific evidence of anatomical brain plasticity, publishing her research in 1964.

Other significant evidence was produced in the 1960s and after, notably from scientists including Paul Bach-y-Rita, Michael Merzenich along with Jon Kaas, as well as several others.

In the 1960s, Paul Bach-y-Rita invented a device that was tested on a small number of people, and involved a person sitting in a chair, in which were embedded nubs that were made to vibrate in ways that translated images received in a camera, allowing a form of vision via sensory substitution.

Studies in people recovering from stroke also provided support for neuroplasticity, as regions of the brain that remained healthy could sometimes take over, at least in part, functions that had been destroyed; Shepherd Ivory Franz did work in this area.

Eleanor Maguire documented changes in hippocampal structure associated with acquiring the knowledge of London’s layout in local taxi drivers. A redistribution of grey matter was indicated in London Taxi Drivers compared to controls. This work on hippocampal plasticity not only interested scientists, but also engaged the public and media worldwide.

Michael Merzenich is a neuroscientist who has been one of the pioneers of neuroplasticity for over three decades. He has made some of “the most ambitious claims for the field that brain exercises may be as useful as drugs to treat diseases as severe as schizophrenia, that plasticity exists from cradle to the grave, and that radical improvements in cognitive functioning, how we learn, think, perceive, and remember are possible even in the elderly.

Merzenich’s work was affected by a crucial discovery made by David Hubel and Torsten Wiesel in their work with kittens. The experiment involved sewing one eye shut and recording the cortical brain maps. Hubel and Wiesel saw that the portion of the kitten’s brain associated with the shut eye was not idle, as expected. Instead, it processed visual information from the open eye. It was “…as though the brain didn’t want to waste any ‘cortical real estate’ and had found a way to rewire itself.”

This implied neuroplasticity during the critical period. However, Merzenich argued that neuroplasticity could occur beyond the critical period. His first encounter with adult plasticity came when he was engaged in a postdoctoral study with Clinton Woosley. The experiment was based on observation of what occurred in the brain when one peripheral nerve was cut and subsequently regenerated. The two scientists micromapped the hand maps of monkey brains before and after cutting a peripheral nerve and sewing the ends together. Afterwards, the hand map in the brain that they expected to be jumbled was nearly normal. This was a substantial breakthrough. Merzenich asserted that, “If the brain map could normalize its structure in response to abnormal input, the prevailing view that we are born with a hardwired system had to be wrong. The brain had to be plastic.” Merzenich received the 2016 Kavli Prize in Neuroscience “for the discovery of mechanisms that allow experience and neural activity to remodel brain function.”

Global warming will drive up suicide rates, study warns – Sharon Kirkey * How Climate Change Affects Mental Health – Katherine Schreiber * Mental Health and our Changing Climate, A Primer – APA.

The health, economic, political, and environmental implications of climate change affect all of us. The tolls on our mental health are far reaching. They induce stress, depression, and anxiety; strain social and community relationships; and have been linked to increases in aggression, violence, and crime.

Heat profoundly affects the human mind. The more neurotransmitters needed to cool the body, the less available to suppress emotions like aggression, impatience or violence. Heat increases circulating levels of the stress hormone, cortisol. Psychiatric hospital visits increase during hotter weather.

Virtually everywhere around the world we’re facing warmer temperatures, and there is a lot of evidence of direct effects of warming on mental health.

Although the psychological impacts of climate change may not be obvious, they are no less serious because they can lead to disorders, such as depression, antisocial behavior, and suicide. Therefore, these disorders must be considered impacts of climate change as are disease, hunger, and other physical health consequences.

Of the 36% of Americans who are personally concerned a great deal about climate issues, 72% are Democrats, and 27% are Republicans (PEW Research).

Sharon Kirkey

It was Raymond Chandler who wrote of nights with a hot wind blowing into Los Angeles, a wind that makes “your nerves jump.”

“On nights like that every booze party ends in a fight,” he wrote. “Meek little wives feel the edge of the carving knife and study their husbands’ necks. Anything can happen.”

Now there’s research that says climate change may damage our mental health, just like Chandler’s hot wind from the Santa Ana Mountains.

Last week, a team of 28 specialists convened by the Lancet medical journal listed climate change among the greatest threats to mental health globally.

Ferocious storms and more frequent weather extremes will affect the human psyche in costly ways, some scientists predict, from more depression and anxiety to increased suicide rates.

One working theory is that some of the same neurotransmitters used by the brain to regulate the body’s temperature are also used to control emotions. The more neurotransmitters needed to cool the body, the less available to suppress emotions like aggression, impatience or violence.

. . . National Post

How Climate Change Affects Mental Health.

A new report shows global warming affects our psyches just as much as our earth.

Katherine Schreiber

When we talk about climate change, we tend to think about its effects on our environment, melting polar ice caps, extreme swings in weather, more frequent droughts, flooding, and higher incidences of natural disasters. But what about the effect on our moods, thoughts, and feelings? A new report written by the American Psychological Association, Climate for Health, and ecoAmerica argues that our mental wellbeing is just as vulnerable to global warming as is our earth.

. . . Psychology Today

MENTAL HEALTH AND OUR CHANGING CLIMATE:

IMPACTS IMPLICATIONS, AND GUIDANCE

WHY WE OFFER THIS REPORT

When you think about climate change, mental health might not be the first thing that comes to mind. Americans are beginning to grow familiar with climate change and its health impacts: worsening asthma and allergies; heat-related stress: foodborne, waterborne, and vector-borne diseases; illness and injury related to storms; and floods and droughts. However, the connections with mental health are not often part of the discussion.

It is time to expand information and action on climate and health, including mental health. The health, economic, political, and environmental implications of climate change affect all of us. The tolls on our mental health are far reaching. They induce stress, depression, and anxiety; strain social and community relationships; and have been linked to increases in aggression, violence, and crime. Children and communities with few resources to deal with the impacts of climate change are those most impacted.

To compound the issue, the psychological responses to climate change, such as conflict avoidance, fatalism, fear, helplessness, and resignation are growing. These responses are keeping us, and our nation, from properly addressing the core causes of and solutions for our changing climate, and from building and supporting psychological resiliency.

To help increase awareness of these challenges and to address them, the American Psychological Association and ecoAmerica sponsored this report, Mental Health and Our Changing Climate: Impacts, Implications, and Guidance. This is an updated and expanded version of our 2014 report, Beyond Storms & Droughts: The Psychological Impacts of Climate Change, which explored how climate change can impact mental health and provided guidance to engage the public. This updated report is intended to further inform and empower health and medical professionals, community and elected leaders, and the public. Our websites offer webinars and other resources to supplement this report.

On behalf of the authors, the many professionals who contributed directly and indirectly to this work, and all those involved in expanding awareness of and action on climate and mental health, thank you for taking the time to review and share this important resource.

We invite your feedback, and as the field continues to grow, we’ll continue to update this work.

EXECUTIVE SUMMARY

Thus far, most research and communications on the impacts of climate change have emphasized the physical health effects, while mental health has been secondary. Building upon Beyond Storms and Droughts: The Psychological Impacts of Climate Change, the goal of this updated report is to increase awareness of the psychological impacts of climate change on human mental health and well-being. The report provides climate communicators, planners, policymakers, public health professionals, and other leaders the tools and tips needed to respond to these impacts and bolster public engagement on climate solutions.

The impacts of climate change on people’s physical, mental, and community health arise directly and indirectly. Some human health effects stem directly from natural disasters exacerbated by climate change, like floods, storms, wildfires, and heatwaves. Other effects surface more gradually from changing temperatures and rising sea levels that cause forced migration. Weakened infrastructure and less secure food systems are examples of indirect climate impacts on society‘s physical and mental health.

Some communities and populations are more vulnerable to the health-related impacts of climate change. Factors that may increase sensitivity to the mental health impacts include geographic location. presence of pre-existing disabilities or chronic illnesses, and socioeconomic and demographic inequalities, such as education level, income, and age.

In particular, stress from climate impacts can cause children to experience changes in behavior, development, memory, executive function, decision-making, and scholastic achievement.

The connection between changes in the climate and impacts on a person can be difficult to grasp. Although people’s understanding and knowledge of climate change can increase by experiencing the effects directly, perception, politics, and uncertainty can complicate this link. Psychological factors (like psychological distance), a political divide, uncertainty, helplessness, and denial influence the way people comprehend information and form their beliefs on climate change. Research on the impacts of climate change on human well-being is particularly important given the relationship among understanding, experiencing, and comprehending climate change. People’s willingness to support and engage in climate solutions is likely to increase if they can relate them to local experiences or if they see the relevance to their own health and well-being. Additionally, individuals who have higher perceived environmental self-efficacy, or the sense of being able to positively contribute, are more motivated to act on climate solutions.

Climate solutions are available now, are widespread, and support psychological health. Increasing adoption of active commuting, public transportation, green spaces, and clean energy are all solutions that people can choose to support and integrate into their daily lives. These climate solutions, among others, can help to curb the stress, anxiety, and other mental illnesses incurred from the decline of economies, infrastructure, and social identity that comes from damage to the climate.

Major acute mental health impacts include increases in trauma and shock, posttraumatic stress disorder (PTSD), compounded stress, anxiety, substance abuse, and depression. Climate change induced extreme weather, changing weather patterns, damaged food and water resources, and polluted air impact human mental health. Increased levels of stress and distress from these factors can also put strains on social relationships and even have impacts on physical health, such as memory loss, sleep disorders, immune suppression, and changes in digestion.

Major chronic mental health impacts include higher rates of aggression and violence, more mental health emergencies, an increased sense of helplessness, hopelessness, or fatalism, and intense feelings of loss. These feelings of loss may be due to profound changes in a personally important place (such as one’s home) and/or a sense that one has lost control over events in one’s life due to disturbances from climate change. Additionally, a sense of loss regarding one’s personal or occupational identity can arise when treasured objects are destroyed by a disaster or place-based occupations are disrupted by climate change.

Personal relationships and the ways in which people interact in communities and with each other are affected by a changing climate. Compounded stress from a changing environment, ecomigration, and/or ecoanxiety can affect community mental well-being through the loss of social identity and cohesion, hostility, violence, and interpersonal and intergroup aggression.

Psychological well-being includes positive emotions, a sense of meaning and purpose, and strong social connections. Although the psychological impacts of climate change may not be obvious, they are no less serious because they can lead to disorders, such as depression, antisocial behavior, and suicide. Therefore, these disorders must be considered impacts of climate change as are disease, hunger, and other physical health consequences.

Building resilience is essential to address the physical and mental health impacts of climate change. Many local governments within the United States and in other countries have created plans to protect and enhance infrastructure, but these plans tend to overlook the support needed to ensure thriving psychological well-being. There is an opportunity to include the resilience capacity of individuals and communities in the development of preparedness plans.

OUR CHANGING CLIMATE: A PRIMER

Our climate is changing at an accelerated rate and continues to have profound impacts on human health. This change jeopardizes not only physical health but also mental health.

ACCELERATION

From wildfires and drought in California to severe flooding in Maryland to Alaskan communities threatened by rising seas, we are clearly living through some of the most severe weather events in US. history as a result of damage to our climate. Thes impacts on our environment will, in turn, affect human health and community well-being.

CHANGES WORLDWIDE

Climate change is creating visible impacts worldwide, including many here in America. As seen in the tripling of heat waves between 2011 and 2012, weather patterns introduce lasting impacts, such as food insecurity. Similarly, rising sea-surface temperatures have been connected to increasing rates of disease for marine life and humans. Sea levels are estimated to increase anywhere from 8 inches to 6.6 feet due to warmer temperatures by 2100, putting 8 million Americans living in coastal areas at risk for flooding. In terms of our economy, Hurricane Sandy cost the United States around $68 billion in total. Droughts caused by increases in temperature and changing weather patterns cost California $2.7 billion in 2015 and Texas $7.62 billion in 2011. As these climate disturbances become more dramatic and persistent, we must prepare for these climate conditions.

COMMUNITIES ARE IMPACTED

Our communities’ health, infrastructure, and economy are directly connected to our climate. As temperatures increase, we experience higher levels of pollution, allergens, and diseases. Severe weather events threaten our businesses and vulnerable communities. Pollution and drought undermine our food and water supplies, and the latter increases the prevalence of wildfires that can destroy homes and communities. Although all Americans are affected, certain populations of concern will feel the impacts more severely. Together, communities can build resilience to a changing climate.

HEALTH IS IMPACTED

As severe weather events, poorer air quality, degraded food and water systems, and physical illnesses increase, the direct and indirect impacts on health must be understood. The next section highlights the physical health impacts of climate change, and the following sections delve deeper into the mental health impacts, and what can be done to protect human well-being.

THE CLIMATE AND HEALTH IMPACTS ON HUMANS

Health is more than the absence of disease. Health includes mental health, as well as physical well-being, and communities that fail to provide basic services and social support challenge both. As we think about the impacts of climate change on our communities, we need to recognize not only the direct effects but also the indirect consequences for human health based on damage to the physical and social community infrastructure. Regardless of how these impacts surface, whether they occur within a matter of hours or over several decades, the outcomes of climate change are interconnected to all facets of our health.

ACUTE IMPACTS:

DlSASTER-RELATED EFFECTS

Recent increases in natural disasters illustrate the relationship between the acceleration of climate change and severe weather.

Areas that endure a natural disaster face a number of risks and difficulties. Direct physical impacts range from brute physical trauma to more pernicious effects, like increased incidence of infectious disease, asthma, heart disease, and lung problems. These physical health impacts interact with mental health impacts.

Major and minor acute physical injury

Natural disasters lead to increased rates of death and injury. The most common causes of mortality during floods are drowning and acute physical trauma. This past year alone, deaths from flash floods have more than doubled the 10-year average. Many people sustain non-fatal injuries, such as cuts and broken bones.

Infrastructure, food, and water

The direct effect of a natural disaster is often exacerbated by a cascade of indirect consequences that follow. Natural disasters can lead to technological disasters (such as power outages), breakdowns in the water, sewer, and other infrastructure, or urban fires. For instance, the risk of carbon monoxide poisoning related to power outages increases as a result of climate change-induced disasters. Disruptions to medical infrastructure, including the provision of medical supplies, can transform minor issues into major and even fatal problems. In addition, disruptions in other types of services (e.g., cell phone communication, transportation, or waste management) add stress and difficulty during the aftermath of a disaster. These disruptions may impact people’s physical health by making it more difficult to access health care or by potentially increasing exposure to pests or hazardous substances (e.g., when there is no garbage pick-up. Loss of income while businesses are closed due to natural disasters can be a major threat to food security, especially for non-professionals or small business owners.

After effects

Additional health threats follow in the wake of a disaster. Floodwater has been shown to introduce toxic materials, water-borne diseases (e.g., respiratory illnesses, skin infections, and neurologic and gastrointestinal illness where there are poor hygiene resources), and vector-borne illnesses (e.g., West Nile). Other after effects of flooding include heart attack, heat stroke, dehydration, and stroke, particularly when the affected areas lack the necessary medical supplies. In addition, post-flood mold due to fungal growth inside houses can worsen allergy or asthma symptoms.

MORE GRADUAL HEALTH EFFECTS

Ongoing effects of climate change include rising sea levels, increases in temperature, and changes in precipitation that will affect agricultural conditions. The impacts on human health are less dramatic in the short term but in the long run can affect more people and have a fundamental impact on society.

Severe and changing weather

Periods of higher-than-normal heat result in higher rates of heat exhaustion, heat cramps, heat stroke, hospital admission for heart-related illnesses, and death.

It’s estimated that the average American citizen will experience between 4 and 8 times as many days above 95 degrees Fahrenheit each year as he or she does now by the end of the century. This increase will likely push Arizona’s above-95-degree days from 116 today to as many as 205 by 2099. In contrast, extreme winter storms can expose people to hypothermia and frostbite. Altered growing seasons and ocean temperatures change the timing and occurrence of diarrhea, fever, and abdominal cramps from pathogen transmissions in raw food. Additionally, changing weather patterns influence the expansion of the migration patterns of animals and insects. This expansion has already begun to result in the spread of vector-borne illness, such as Lyme disease, malaria, dengue fever, plague, and Zika virus to new U.S. geographic areas. For example, vector-borne illnesses carried by mosquitoes can capitalize on receding floodwater for mosquito breeding.

Respiratory issues and allergens

People exposed to ozone air pollution, which is emitted mostly by cars and industrial facilities and is intensified by warmer temperatures, are more likely to visit the hospital for respiratory issues, suffer from asthma, and die prematurely of strokes or heart attacks. Hotter and drier summers increase the frequency and intensity of large wildfires that contribute to smoke inhalation. Pollution contributes to higher levels of pollen and translates into longer and more prevalent allergy seasons.

Fetal and child development

CIimate-driven physical stress on mothers can cause adverse birth outcomes, such as preterm birth and low birth weight. Scientific research shows that children and developing fetuses are at particular risk from air pollution, heat, malnutrition, infectious diseases, allergies, and mental illnesses, which have detrimental impacts on development.

Water and food supply

Nutrition and food safety can be affected because climate change can lower crop yields, reduce the nutritional quality of food, interrupt distribution chains, and reduce access to food because families lose income. For example, higher C02 concentrations lower the levels of protein and essential minerals of widely consumed crops such as wheat, rice, and potatoes. Barriers to food transport, such as damage to infrastructure and displacement of employees, affect food markets by increasing food costs. Droughts, floods, and changes in the availability of fertile land lead to hunger and malnutrition, though these changes are less likely in wealthy countries, such as the United States. Nevertheless, there will be an increased likelihood of a global food market crisis as climate change accelerates. A two-degree Celsius increase in temperature places 100-400 million people at risk of hunger, according to the World Bank.

General fitness

Increased average temperatures and decreased air quality also lead to changes in the type of activities that people engage in, particularly outdoor activities and recreation. These changes, in turn, may be associated with increased rates of obesity and cardiovascular disease. Although people may compensate by exercising in indoor environments, reduced access to the restorative potential of outdoor environments may indirectly increase stress and bypass the long-term emotional benefits of taking physical activity outdoors.

LINKING PHYSICAL IMPACTS, MENTAL HEALTH, AND COMMUNITY WELL-BEING

MENTAL HEALTH

The ability to process information and make decisions without being disabled by extreme emotional responses is threatened by climate change. Some emotional response is normal, and even negative emotions are a necessary part of a fulfilling life. In the extreme case, however, they can interfere with our ablllty to think rationally, plan our behavior, and consider alternative actions. An extreme weather event can be a source of trauma, and the experience can cause disabling emotions. More subtle and indirect effects of climate change can add stress to people’s lives in varying degrees. Whether experienced indirectly or directly, stressors to our climate translate into impaired mental health that can result in depression and anxiety. Although everyone is able to cope with a certain amount of stress, the accumulated effects of compound stress can tip a person from mentally healthy to mentally ill. Even uncertalnty can be a source of stress and a risk factor for psychological distress. People can be negatively affected by hearing about the negative experiences of others, and by fears, founded or unfounded, about their own potential vulnerability.

PHYSICAL HEALTH AND MENTAL HEALTH

Compromised physical health can be a source of stress that threatens psychological well being. Conversely mental health problems can also threaten physical health, for example, by changing patterns of sleep, eating, or exercise and by reducung immune system function.

COMMUNITY HEALTH

Although resndents‘ mental and physical health affect communlties, the impacts of climate on community health can have a particularly strong effect on community fabric and interpersonal relationships. Altered environmental condtions due to climate change can shift the opportunities people have for social interaction, the ways in which they relate to each other. and their connectlons to the natural world.

COMPREHENDING CLIMATE CHANGE

Witnessing the visible impacts of climate change may help people overcome barriers to grasping the problem; however, comprehension has many facets.

PERCEPTION IS DIFFICULT

Although most people are generally aware that climate change is occurring, it continues to seem distant: something that will happen to others, in another place, at some unspecified future date. Psychologists refer to this idea as psychological distance. Terms such as “climate change” and “global warming” draw attention to the global scale rather than the personal impacts. Additionally, the signal of climate change is obscured by the noise of daily and seasonal weather variation. All this makes the issue easier for people to push aside, particularly when faced with other pressing life issues. When people learn about and experience local climate impacts, their understanding increases. Local effects of climate change are often more personally relevant than the general phenomenon of a warming climate, and particularly when knowledge of direct effects is combined with news stories of the imminent risks of climate change. Perceived experience of impacts is associated with increased concern and awareness about climate change, direct experience also increases people’s understanding of climate change. However, direct experience does not necessarily lead to behavior change. For example, experiencing water shortages may increase behavior changes in water use but not encourage other sustainable behavior. Similarly, research suggests experiencing temperature change has no impact on water use behavior.

A PARTISAN ISSUE

Politically polarized in the United States, climate change is perceived as an issue that belongs with the political left, which can suppress belief and concern and discussions about solutions. For example, of the 36% of Americans who are personally concerned a great deal about climate issues, 72% are Democrats, and 27% are Republicans. Political orientation can make open conversations about climate impacts and solutions difficult, and make those who are concerned about climate change feel isolated or paranoid in some circles.

Concerns about health impacts provide common ground for discussion with both ends of the political spectrum. Describing the health-related impacts of climate change and the relevant benefits of taking action to address the impacts can inspire hope among those who dismiss climate change. For instance, conservatives showed decreased support for climate action when the negative health effects were described as affecting people in a faraway country as opposed to people who live in the United States. Listing several health impacts is overwhelming, causing fatalism and diminished engagement.

UNCERTAINTY AND DENIAL

People feel uncertain about the threat of climate change and how to minimize the damage. The media have been criticized for promoting an inaccurate perception of climate change: for example, that there is more scientific controversy about climate change than actually exists. In some cases, information that increases perceptions of the reality of climate change may feel so frightening that it leads to denial and thus a reduction in concern and support for action. In addition, communicating scientific information is not easy; this complexity itself may be a problem. One study showed that people who received more complex information on environmental problems 1) felt more helpless and more inclined to leave the problem to the government; and 2) those who felt ignorant about the topic were more likely to want to avoid hearing about more negative information.

Worldviews and ideologies act as filters to help increase or decrease concern about climate change and motivate action toward solutions. People do not perceive the world neutraly. Instead, through directionally motivated cognition, individuals strive to maintain a world consistent with the ideology and values of their social groups. Because of this, individuals whose worldviews conflict with climate change realities actually may not perceive certain climate effects. Myers, Maibach, Roser-Renouf, Akerlof, and Leiserowitz (2012) found that individuals who were 1) either very concerned about or skeptical of climate change tended to report personal experience with climate change (or lack thereof) based on their pre-existing beliefs about its existence; and 2) individuals less engaged with the issue of climate change changed their beliefs about the existence of climate change based on perceived personal experience with its impacts. Ideologies of climate change and action may also contribute to widespread psychological denial. The distress of climate change can manifest in negative reactions to climate activism. These reactions are reflected in outlets such as social media, and researchers believe this behavior shifts others to denial.

CLIMATE SOLUTIONS BENEFIT MENTAL HEALTH

Physical commuting enhances a sense of well-being. Choosing to bike and/or walk (assuming it is safe and practical to do so) is one individual step that can help reduce the use of climate change-driving fossil fuels. Physical commuting also directly impacts depression, anxiety, PTSD, and other mental illnesses. People who bike and walk to work, school, appointments, and other activities not only reduce emissions and improve their physical health but also experience lower stress levels than car commuters. For instance, individuals who utilized the Washington DC. bikeshare program reported reduced stress levels and weight loss. Similarly, adolescents who actively commute to school show not only lower levels of perceived stress but also increased cardiovascular fitness, improved cognitive performance, and higher academic achievement.

Public transportation invigorates community mental health. Moving people from individual cars to public transit also results in lower greenhouse gas emissions. In addition, several studies have shown that using public transportation leads to an increase in community cohesion, recreational activities, neighborhood walkability, and reduced symptoms of depression and stress associated with less driving and more exercise. Meanwhile, traffic driving worsens air quality and contributes to reduced productivity and increased healthcare costs. Sound transportation systems and urban planning should be expanded as they lead to beneficial mental health and climate outcomes. Green spaces diminish stress. Parks and green corridors have been connected to improved air quality and can increase mental well-being. For example, trees sequester carbon, and green spaces absorb less heat than paved surfaces and buildings. More time spent interacting with nature has been shown to significantly lower stress levels and reduce stress-related illness. Interestingly, this evidence is supported across socioeconomic status, age, and gender. Likewise, individuals who move to areas with access to more green space showed sustained mental health improvements, while individuals who moved to areas with less access to green space experienced substantial negative mental health impacts. However, although a person’s physical and mental health is determined to a large degree by the neighborhood in which he or she lives, relocating to a greener neighborhood isn’t always an option. As planners and policymakers make decisions that will reshape the landscapes of our cities and communities, it is important to recognize the significance and role green areas have in improving air quality, reducing stress, and ensuring a healthy living environment for everyone.

Clean energy reduces health burdens. Wind, solar, hydro, and other clean energy as well as energy efficiency are not only climate-friendly; they also reduce particulates and pollution in the air. Studies on air quality and children’s lung development have shown that as air pollution is reduced, children display significant lung function improvements. Further research revealed that children exposed to higher levels of urban pollution are more likely to develop attention problems and symptoms of anxiety and depression, as well as lower academic performance and brain function. Clean energy provides an opportunity to protect populations of concern, such as children, who experience these impacts more severely.

Although the co-benefits are clear, more comprehensive research on the positive mental health outcomes of climate solutions is needed to bolster support. Research can further promote dynamic solutions as opportunities to improve our health. It is important to increase awareness of the daily choices we make, from how to get to work to the sources of energy to, the more climate-friendly behaviors become mainstreamed, the more they help populations of concern: children, elderly, sick, low income, etc. Fortunately, tangible and effective climate solutions are available today to implement and build upon.

MENTAL HEALTH IMPACTS

The mental health effects of Climate change are gaining public attention. A 2071 government report (US. Global Change Research Program) reviewed a large body of research to summarize the current state of knowledge. This report builds on that knowledge, and considers the direct and indirect effects of Climate change on mental health.

We start by describing the mental health effects on individuals, both short and long term, acute and chronic, the stressors that accumulate in the aftermath of a disaster, and the impacts that natural disasters have on social relationships, with consequences for health and well-being. We move on to discussing the individual-level impacts of more gradual changes in climate, including impacts on aggression and violence, identity, and the long-term emotional impacts of Climate change. Next, we discuss the impacts of climate change on communities and on intergroup and international relationships. Finally, we address the problem of inequity, the fact that certain populations are relatively more vulnerable to these mental health impacts compared to others.

IMPACTS ON INDIVIDUALS

Climate change has acute and chronic impacts, directly and indirectly, on individual well-being. Acute impacts result from natural disasters or extreme weather events. Chronic impacts result from longer term changes in climate. This discussion emphasizes the impacts experienced directly by individuals; however, it also touches on indirect impacts (witnessing others being impacted), which have profound implications for mental health.

ACUTE IMPACTS

Trauma and shock

Climate change-induced disasters have a high potential for immediate and severe psychological trauma from personal injury, injury or death of a loved one, damage to or loss of personal property (e.g., home) and pets, and disruption in or loss of livelihood. An early meta-analysis of studies on the relationship between disasters and mental health impacts found that between 7% and 40% of all subjects in 36 studies showed some form of psychopathology. General anxiety was the type of psychopathology with the highest prevalence rate, followed by phobic, somatic, and alcohol impairment, and then depression and drug impairment, which were all elevated relative to prevalence in the general population. More recent reviews concluded that acute traumatic stress is the most common mental health problem after a disaster. Terror, anger, shock, and other intense negative emotions are likely to dominate people’s initial response. Interview participants in a study about flooding conducted by Carroll, Morbey, Balogh, and Araoz (2009) used words such as “horrifying,” “panic stricken,” and “petrified“ to describe their experience during the flood

Post-traumatic stress disorder (PTSD)

For most people, acute symptoms of trauma and shock are reduced after conditions of security have been restored. However, many continue to experience problems as PTSD manifests as a chronic disorder. PTSD, depression, general anxiety, and suicide all tend to increase after a disaster.

For example, among a sample of people living in areas affected by Hurricane Katrina, suicide and suicidal ideation more than doubled, one in six people met the diagnostic criteria for PTSD, and 49% of people living in an affected area developed an anxiety or mood disorder such as depression. Similarly, 14.5% showed symptoms of PTSD from Hurricane Sandy, and 15.6% of a highly affected community showed symptoms of PTSD several years after experiencing extreme bushfire. PTSD is often linked to a host of other mental health problems, including higher levels of suicide, substance abuse, depression, anxiety, violence, aggresson, interpersonal difficulties, and job-related difficulties.

Incidence of PTSD is more likely among those who have lost close family members or property. Individuals who experience muitiple or long-lasting acute events, such as more than one disaster or multiple years of drought, are likely to experience more severe trauma and may be even more susceptible to PTSD and the other types of psychiatric symptoms described above. For example, a study showed that refugees exposed to multiple traumatic events experienced a higher rate of immediate and lifetime PTSD and had a lower probability of remission than refugees who had experienced few traumatic events. The likelihood of suicide is higher among those who have been exposed to more severe disasters.

Compounded stress

In general, climate change can be considered an additional source of stress to our everyday concerns, which may be tolerable for someone with many sources of support but can be enough to serve as a tipping point for those who have fewer resources or who are already experiencing other stressors. Stress manifests as a subjective feeling and a physiological response that occur when a person feels that he or she does not have the capacity to respond and adapt to a given situation. Thus, climate-related stress is likely to lead to increases in stress-related problems, such as substance abuse, anxiety disorders, and depression. These problems often carry economic costs incurred by lost work days, increased use of medical services, etc, which, in turn, create additional stress for individuals and society and have their own impacts on mental and physical health. Stress can also be accompanied by worry about future disasters and feelings of vulnerability, helplessness, mourning, grief, and despair. Following disasters, increased stress can also make people more likely to engage in behavior that has a negative impact on their health (e.g., smoking, risky behavior, and unhealthy eating habits; e.g. Stain et al. (2011) found that people living in a drought-affected area who had also recently experienced some other adverse life event were more likely to express a high degree of worry about the ongoing drought conditions. Although not as dramatic and acute a disaster as a hurricane, drought is associated with psychological distress, and one study found increased rates of suicide among male farmers in Australia during periods of prolonged drought. Several studies have found that many victims of a flood disaster express psychological distress even years after the flood.

Impacts of stress on physical health

High levels of stress and anxiety also appear to be linked to physical health effects.

For example, chronic distress results in a lowered immune system response, leaving people more vulnerable to pathogens in the air and water and at greater risk for a number of physical ailments. Sleep disorders also increase in response to chronic distress. Doppelt (2016) has described potential physiological responses to the stress of climate change, such as increased levels of the stress hormone cortisol, which, if prolonged, can affect digestion, lead to memory loss, and suppress the immune system. The World Heart Federation (2016) lists stress as a serious risk factor in developing cardiovascular disease.

Strains on social relationships

Particularly in home environments, disasters precipitate a set of stressors that can strain interpersonal interactions. A review of research on the impacts of natural disasters identified problems with family and interpersonal relations, as well as social disruption, concerns about the wider community, and feelings of obligation to provide support to others. Families whose homes are damaged by a flood, storm, or wildfire may need to be relocated, sometimes multiple times, before settling permanently. Family relationships may suffer. Separation from one another and from their systems of social support may occur. Children may have to attend a new school or miss school altogether; parents may find themselves less able to be effective caregivers. In addition, even those who are able to remain in their own home may still lose a sense of their home as a safe and secure environment. This has implications for interpersonal connections, as a home provides the context for social relationships. When the physical home is damaged, it changes the dynamic of the social relationships, often negatively. Domestic abuse, for example, including child abuse, often increases among families who have experienced disasters, such as Hurricane Katrina or the Exxon Valdez oil spill.

CHRONIC IMPACTS

Aggression and violence

The psychological impacts of warmer weather on aggression and violence have been extensively studied. Lab-based experiments and field-based surveys have demonstrated a causal relationship between heat and aggression. In other words, as the temperature goes up, so does aggression. This influenced researcher Craig Anderson (2012) to predict a demonstrable increase in violence associated with increased average temperatures. The relationship between heat and violence may be due to the impacts of heat on arousal, which results in decreases in attention and self-regulation, as well as an increase in the availability of negative and hostile thought, effect on cognitive function, which may reduce the ability to resolve a conflict without violence. Although this impact can manifest as an acute impact (e.g., as a result of a heat wave), due to the pervasive warming trends, and the shifting of climate zones, it is listed under chronic impacts.

Mental health emergencies

There is evidence that increases in mean temperature are associated with increased use of emergency mental health services. This is true not only in hot countries, like Israel and Australia, and in parts of the United States but also in relatively cooler countries, such as France and Canada. Higher temperatures have been linked to increased levels of suicide. It appears that the distress of feeling too hot can overwhelm coping ability for people who are already psychologically fragile. Climate emergencies can also exacerbate preexisting symptoms and lead to more serious mental health problems.

Loss of personally important places

Perhaps one of the best ways to characterize the impacts of climate change on perceptions is the sense of loss. Loss of relationship to place is a substantial part of this. As climate change irrevocably changes people‘s lived landscapes, large numbers are likely to experience a feeling that they are losing a place that is important to them, a phenomenon called solastalgia. This psychological phenomenon is characterized by a sense of desolation and loss similar to that experienced by people forced to migrate from their home environment. Solastalgia may have a more gradual beginning due to the slow onset of changes in one’s local environment. Silver and Grek-Martin (2015) described the emotional pain and disorientation associated with changes in the physical environment that were expressed by residents of a town damaged by tornadoes, even by residents who had not experienced personal loss.

Loss of place is not a trivial experience. Many people form a strong attachment to the place where they live, finding it to provide a sense of stability, security, and personal identity. People who are strongly attached to their local communities report greater happiness, life satisfaction, and optimism; whereas work performance, interpersonal relationships, and physical health can all be negatively affected by disruption to place attachment. For instance, Scannell and Gifford (2016) found that people who visualized a place to which they were attached showed improved self-esteem and sense of belonging relative to those who visualized a place to which they were not attached.

Climate change is likely to have a significant effect on human well-being by increasing migration. When people lose their home to rising sea levels, or when a home becomes unsuitable for human habitation due to its inability to support food crops, they must find another place to live. Although it is difficult to identify climate change as the causal factor in a complex sequence of events affecting migration, a common prediction is that 200 million people will be displaced due to climate change by 2050. Migration in and of itself constitutes a health risk. Immigrants are vulnerable to mental health problems, probably due to the accumulated stressors associated with the move, as well as with the condition of being in exile. Adger, Barnett, Brown, Marshall, and O‘Brien (2013) found being forced to leave one‘s home territory can threaten one’s sense of continuity and belonging. Because of the importance of connection to place in personal identity, such displacement can leave people literally alienated, with a diminished sense of self and increased vulnerability to stress. Although empirical research on the psychological impacts of migration is rare, Tschakert, Tutu, and Alcaro (2013) studied the emotional experience among residents of Ghana who were forced to move from the northern region of the country to the capital, Accra, because local conditions no longer supported their farming practices. Also, respondents expressed nostalgia and sadness for the home left behind and helplessness due to changes in their environments, such as deforestation, that were described as sad and scary.

Loss of autonomy and control

Climate change will intensify certain daily life inconveniences, which can have psychological impacts on individuals’ sense of autonomy and control. The desire to be able to accomplish basic tasks independently is a core psychological need, central to human well-being, and basic services may be threatened due to dangerous conditions. This may make mobility a challenge, particularly for the elderly and those with disabilities. Exposure to unwanted change in one’s environment can also reduce one’s sense of control over one’s life, which, in turn, has negative impacts on mental health.

Loss of personal and occupational identity

A more fundamental loss is the loss of personal identity tied to mundane aspects of daily life. Losing treasured objects when a home is damaged or destroyed is one way in which climate change can significantly impair an individual’s sense of self and identity. This is because objects help provide a continuing sense of who we are, particularly objects that represent important moments in life (e.g., journals), relationships (e.g., gifts or photographs), or personal family history (e.g., family heirlooms). Interviewees in a study conducted by Carroll et al. (2009) indicated that flood victims were particularly troubled by the loss of personal possessions, such as things they had made themselves or special things they had spent time and effort to procure or maintain. Although this may seem acute, the losses are permanent; the impacts are persistent and therefore become chronic.

A loss of identity associated with climate change is also sometimes attributable to its effect on place-bound occupations. This is likely due to the close relationship between identity and place-based occupations, like farming and fishing. Because severe storms and high temperatures disrupt economic activity climate change may have an effect on occupational identity in general. Loss of occupation has been associated with increased risk of depression following natural disaster.

Helplessness, depression, fear, fatalism, resignation, and ecoanxiety

Gradual, long-term changes in climate can also surface a number of different emotions, including fear, anger, feelings of powerlessness, or exhaustion. A review by Coyle and Van Susteren (2011) described cases in which fear of extreme weather approaches the level of phobia and the “unrelenting day-by-day despair” that can be experienced during a drought. Watching the slow and seemingly irrevocable impacts of climate change unfold, and worrying about the future for oneself, children, and later generations, may be an additional source of stress. Albrecht (2011) and others have termed this anxiety ecoanxiety. Qualitative research provides evidence that some people are deeply affected by feelings of loss, helplessness, and frustration due to their inability to feel like they are making a difference in stopping climate change. Some writers stress the possible detrimental impact of guilt, as people contemplate the impact of their own behavior on future generations. Although the impacts of climate change are not always visible, they perpetuate a delayed destruction that, like the damage to climate, are incremental and can be just as damaging as acute climate impacts.

IMPACTS ON COMMUNITY AND SOCIETY

In addition to the effects on individual health and wellbeing, climate change affects how individuals interact in communities and relate to each other. For example, natural disasters can have a negative impact on community bonds. A changing climate will likely affect aspects of community wellbeing, including social cohesion, aggression, and social relationships.

SOCIAL COHESION AND COMMUNITY CONTINUITY

Compounded stress from climate change has been observed among various communities. For example, CunsoLo Willox et al. (2013) examined the impacts of climate change on a small Inuit COMMUNITY. Members of the community, who all reported a strong attachment to the land, said they had noticed changes in the local climate and that these changes contributed to negative effects on themselves. As a result of altered interactions with the environment, community members reported food insecurity, sadness, anger, increased family stress, and a belief that their sense of self-worth and community cohesion had decreased. Elders expressed specific concern for the preservation of Inuit language and culture as they directly influence mental wellbeing and social cohesion.

Social cohesion and social capital can protect communities against mental and physical health impacts during a climate related disaster. Regardless of socioeconomic or cultural backgrounds, communities with high levels of social capital and community leadership experience the quickest recoveries after a disaster and the highest satisfaction with community rebuilding.

When locaI conditions become practically uninhabitable, ecomigration, leading to environmental refugees, can result. Such migrations erode social networks, as communities disperse in different directions. Because social networks provide important practical and emotional resources that are associated with health and wellbeing, the loss of such networks places people’s sense of continuity and belonging at risk. The current Syrian conflict, which has resulted in mass migration, may partially stem from climate change driven precipitation changes, rising mean sea levels, and a decrease in soil moisture. These climate impacts were exacerbated during the drought from 2007 to 2010 due to human disruptions within natural systems, leading to crop failure and large-scale conflict, hunger, and desperation. Although such civil unrest cannot be attributed to a single cause, recent evidence suggests climate-change caused drought may have played a significant role in the unraveling of an already vulnerable political and ecological climate.

AGGRESSION

Heightened anxiety and uncertainty about one’s own future can reduce the ability to focus on the needs of others, negatively impacting social relationships with friends and co-workers, as well as attitudes toward other people in general.

Interpersonal violence

High temperatures associated with climate change may increase people‘s aggressive tendencies. Aggression can also be exacerbated by decreased access to stress reducing green spaces and supportive social networks. Rising levels of frustration in society consequently lead to interpersonal aggression (such as domestic violence, assault, and rape). Ranson (2012) calculated that between 2010 and 2099, climate change would cause an estimated additional 30,000 murders, 200,000 cases of rape, and 3.2 million burglaries due to increased average temperatures.

Intergroup aggression

Climate change may increase conflict through several mechanisms. Violence may increase when competition for scarce natural resources increases or when ecomigration brings formerly separate communities into contact and they compete for resources, like jobs and land. In a recent metaanalysis, Hsiang, Burke, and Miguel (2013) found evidence that climate change can contribute to the frequency of intergroup violence (ie. political conflict and war). For example, in Houston, Texas, crime rates increased significantly following Hurricane Katrina, although Katrina migrants have not been definitively sourced as the cause. Meanwhile, restraints on crime weaken when existing social institutions are disrupted, thus increasing the probability of criminal behavior. For example, when government resources are devoted to damaged infrastructure from natural disasters, those resources may be diverted away from criminal justice systems, mental health agencies, and educational institutions, all of which tend to help mitigate crime. Agnew (2012) further pointed out that the effects of climate chanqe are likely to promote crime by “increasing strain, reducing social control, and weakening social support.”

Intergroup attitudes can also be negatively impacted by climate change. In a recent study, survey respondents displayed more negative attitudes toward policies to support minorities and immigrants when temperatures were high. An experimental study showed that people who were thinking about climate change became more hostile to individuals outside their social group (that is, people they consider to be unlike them) and more likely to support the status quo and its accompanying social inequities. Hostility toward individuals outside one’s social group can be a way of affirming one’s own group identity in the face of a perceived threat. In a vicious cycle, lower levels of social cohesion and connectedness, greater social inequalities, lack of trust between community members and for institutions, and other factors that inhibit community members from working together are associated with intergroup aggression.

THE PROBLEM OF INEQUITY

The impacts of climate change are not distributed equally. Some people will experience natural disasters firsthand, some will be affected more gradually over time, and some will experience only indirect impacts. This section describes some of the populations that are more vulnerable to the mental health impacts of climate change, including people who live in risk-prone areas, indigenous communities, low-income groups, certain communities of color, women, children, older adults, and people with disabilities or chronic illnesses. A thorough review of demographic differences in vulnerability to climate change can be found in Dodqen et al. (2016).

RISK-PRONE AREAS

Communities in which people’s livelihoods are directly tied to the natural environment, through agriculture, fishing, or tourism, are at greater risk. Some parts of the world are geologically more vulnerable to storms, rising seas, wildfires, or drought. There are detailed reports of farmers in Australia who have been negatively affected by prolonged periods of drought caused by changing weather patterns. Additionally, communities in low-lying areas, such as coastal Louisiana and islands in the Chesapeake Bay, are losing their land to erosion and rising seas. This past year, residents of Isle de Jean Charles, Louisiana, became the first climate refugees in the United States; a $48 million budget was allocated to relocate residents to a less flood-prone area, inhabitants of indigenous communities often depend on natural resources for their livelihoods and are located in geographically vulnerable regions.

Communities that lack resources, both physical and financial, can experience climate impacts more severely. This can be demonstrated by higher incidents of extreme weather within impoverished communities. In disasters, socioeconomically disadvantaged communities often suffer the most. For example, following Hurricane Sandy, lower income residents reported weak or absent social support networks and had the greatest percentages of severe mental distress and diagnosis of depression or anxiety after the hurricane. Furthermore, 35% of children living in a household that earns less than $20,000 annually experienced feelings of sadness, depression, fear, or nervousness following the hurricane.

INDIGENOUS COMMUNITIES

Indigenous communities are at risk of losing their cultural heritage, as well as their homes. Imperiled indigenous communities are found around the world, including the United States. In Alaska, for example, some native Alaskans have seen their villages literally vanish due to the thawing permafrost, and others are facing a similar outcome in the near future. For indigenous communities, climate change may threaten not oniy their physical home but also their lifestyle, including access to traditional food and culturally meaningful practices. Chief Albert Naquin of a Louisiana tribal community threatened by climate change stated, ”We’re going to lose all our heritage, all our culture”. Cunsolo, Willox et al. (2013) reviewed case studies of several Inuit communities and reported weakening social networks, increased levels of conflict, and significant stress associated with relocation or even thinking about relocation. In evocative language, Inuit community members interviewed by Durkalec et al. (2015) reported that an inability to go out on the sea ice (due to a changing climate) would make them feel like they “have no health” and ”can’t breathe,“ and they would ”be very sad,” “be lost,” or ”go crazy”.

The loss of any community is tragic, but the impact on native communities is particularly notable because it diminishes the cultural heritage and because indigenous communities are often defined by a special connection to the natural environment. This connection includes traditional patterns of behavior and environmental knowledge about the specific local ecosystem, knowledge that is disappearing, and about how to adapt to changing environments that could help us as a broader society as we adapt to the consequences of climate change.

CHILDREN AND INFANTS

Climate change has a big impact on young people. Children are more vulnerable to many of the effects due to their small size, developing organs and nervous systems, and rapid metabolisms. Children are more sensitive to temperature, because their physiological regulatory systems may be less effective (e.g., they sweat less) and because they are more likely to depend on others to help them regulate their behavior. Their small size makes very young children more susceptible to dehydration, and children under age five living in poverty represent 80% of victims of sanitation-related illnesses and diarrheal disease.

Climate impacts may have long-term and even permanent effects, such as changing the developmental potential and trajectory of a child. Currie and Almond (2011) reviewed evidence that even minor disturbances during childhood may have effects on health and earning potential that last into adulthood. Studies have shown that children who experience a flood or a drought during key developmental periods are shorter, on average, as adults. Fetuses are vulnerable to heat waves, with research shows that exposure to heat waves especially during the second and third trimesters of pregnancy leads to a lower average birth weight and possibly a greater incidence of preterm birth. Malnourishment or severe threat to health during the early years is associated with fewer years of schooling and reduced economic activity as adults, as well as with behavioral and motor problems and reduced IQ. Additionally, early exposure to disease provoked by climate change can have a major and permanent impact on neurological development, as can be dramatically seen in children exposed prenatally to the Zika virus.

Children can experience PTSD and depression following traumatic or stressful experiences with more severity and prevalence than adults. After climate events, children typically demonstrate more severe distress than adults. Furthermore, the prevalence of distress is also higher; higher rates of PTSD were found in children two years after a flood. Children’s mental health can also be affected not only by their experiences of stressors, such as natural disasters, extreme weather, and ecomigration, but also by the mental health of their caregivers. Children also have the potential to be emotionally affected if they become separated from their primary caregivers. Similar to physical experiences, traumatic mental experiences can have lifelong effects. Of course, early childhood is critical for brain development. Studies have documented that high levels of stress during childhood can affect the development of neural pathways, in ways that impair memory, executive function, and decision-making in later life.

Children are also at increased risk from disruptions to the educational system. Natural disasters, in particular can damage or destroy schools or make them inaccessible to teachers and students. After Hurricane Katrina, for example, 196,000 public school students had to change schools, and many of them missed a month or more of schooling. In this case, because the hardest-hit school districts were also some of the worst-performing ones, some students benefitted by transferring to better schools. However the effects on school achievement were negative.

Disasters may cause children to lose their social support networks to a greater extent. During adversity, people draw upon all of their personal resources, emotional and material. Although social networks can fill the gaps when individual resources become depleted during extreme trauma, the resources available from a tight-knit community may not go far, especially if the network is small or the community is poor. When disasters hit an area, they affect everyone and put entire neighborhoods in need of help. A study of children impacted by Hurricane Katrina found that those who were hit hardest by the storm also experienced less social support, likely because people in their immediate support network were themselves suffering.

DISADVANTAGED COMMUNITIES

Some communities of color are prone to experience increased impacts. A persistent reality in American culture is the existence of environmental injustice: Some racial and ethnic groups tend to be more exposed to environmental risks and to have fewer financial and political resources to buffer the impact. This is partly, but not completely, explained by economic status. Communities with fewer resources and greater exposure, for example, in Phoenix, Arizona, are likely to experience greater rates of high temperature impacts than majority groups. Lower-income communities are more likely to have outdated infrastructure, such as a lack of extreme weather warning systems, inadequate storm surge preparedness, and clogged or inadequate storm sewer systems, which places these communities at greater risk for the impacts of climate change. Areas with a high number of residents who lack access to health care or health insurance, or already experience poor health are more likely to be affected by climate change. Communities are also less resilient when they are weakened by social stressors, such as racism, economic inequality, and environmental injustices. Many of the communities in New Orleans that were affected by Hurricane Katrina possessed all of these characteristics, and the effects of racial disparities were clearly visible in the aftermath of the storm.

OCCUPATIONAL GROUPS

Certain lines and fields of work are more directly exposed to the impact of climate change. These occupations may include but not be limited to first responders, construction workers, health care workers, farmers, farm workers, fishermen, transportation workers, and utility workers. Inequitable health outcomes may arise directly through workers’ exposure to increased temperatures, air pollution, and extreme weather, and indirectly through vector-borne diseases, increased use of pesticides, and many other elements. According to the US Environmental Protection Agency, outdoor workers will be the first to endure the effects of climate change, as they will be exposed to extreme heat, which can cause heat stroke, exhaustion, and fatigue. As natural disasters occur more frequently, such as wildfires and flooding, firefighters and paramedics face increased safety risks. Agricultural workers face increased vulnerability to allergens, insects carrying diseases, such as West Nile, and pesticide exposure that are increased by changing weather and insect migration patterns.

ADDITIONAL POPULATIONS OF CONCERN

Individuals of all ages with disabilities or chronic mental or physical health issues may experience climate-related impacts at a greater extent. Often, people living with disabilities have disproportionately far lower access to aid during and after climate-related disasters. Those with mental health disorders can also experience exacerbated symptoms due to natural disasters. Degraded infrastructure creates barriers for people with mental illnesses to receive proper medical attention, leading to additional negative mental and physical health outcomes. For instance, following the 2012 Wisconsin heat wave, 52% of all heat-related deaths were among individuals with at least one mental illness. Half of those suffering from mental illness were taking psychotropic medications, which impede one’s ability to regulate one’s body temperature. These medications that treat mental illness are one of the main underlying causes of heat-related deaths. Additionally, those suffering from ongoing asthma and respiratory illnesses, like chronic obstructive pulmonary disease (COPD), are more sensitive to reduced air quality. Moreover, inequalities in the incidence of those who are chronically ill arise as a result of several socioeconomic factors.

Due to increased health and mobility challenges, the elderly are very susceptible to the risks of climate impacts. Higher rates of untreated depression and other physical illnesses reported among seniors contribute to this increased vulnerability. Research suggests the elderly, in particular, experience declines in cognitive ability when exposed to air pollution over the long ter. A study by Dominelii (2013) found that when infrastructure broke down (e.g., roads were impassable) due to floods. heat waves, or freeze-thaw events (all potentially climate-driven), formal care services were not available to vulnerable people, such as the elderly. They could not get to the services, and their normal services could not come through. Heat can have a particuIarly severe impact on the elderly and on people with pre-existing mental health problems; some of the medications associated with mental illness make people more susceptible to the effects of heat. Extreme temperatures or pollution can also make it more difficult for seniors to engage in regular outdoor activities, thus depriving them of the associated physical and mental benefits.

The stress directly related to supporting a child makes women more affected by climate change. Because of a mother’s frequent caregiver role, and because, on average, women have fewer economic resources than men, women may also be more affected, in general, by the stress and trauma of natural disasters. Possible loss of resources, such as food, water, shelter, and energy, may also contribute to personal stress. Epidemiological studies of post-disaster cohorts and the general population, suggest that women are more likely to experience mental health problems as a result of trauma. For example, the prevalence of PTSD in the general population is reported to be approximately twofold greater in women than in men.

BUILDING RESILIENCE

Developing plans to adapt and cope is critical in addressing the physical and psychological impacts of climate change. Resilience can be defined as the ability of a person (or a community) to cope with, grow through, and transcend adversity.

Climate change is no longer a distant, unimaginable threat; it is a growing reality for communities across the globe. Recognizing the risk, many local governments in the United States (as well as other places around the world) have created preparation or adaptation plans for shoring up physical infrastructure to withstand new weather and temperature extremes. These plans, while an important step, generally overlook the psycho-social impacts of a changing climate and do little to create or support the soft infrastructure needed for community psychological wellbeing. How can communities prepare themselves to minimize suffering and promote resilience in the face of the challenging impacts of climate change? Resilient communities can create the physical and social infrastructure that makes them less susceptible to negative effects.

On an individual level, resilience is built internally and externally through strategies, such as coping and self-regulation, and community social support networks. Most people come through adversity with positive adjustment and without psychopathology. In fact, some individuals may even experience what is called post-traumatic growth and come through a significant disruption with the feeling of having gained something positive, such as stronger social relationships or spectfic skills.

Even so, much can be done to increase the resilience capacity of individuals and communities, particularly in response to climate change.

Download the full report here.

FEELING TOO MUCH? THE EMPATH’S SURVIVAL GUIDE, the Healing Power of Empathy – Judith Orloff M.D.

The power of empathy & intuition will open your heart and empower your life.

Empathy doesn’t make you a sentimental softy without discernment. It allows you to keep your heart open to foster tolerance and understanding. Empathy is the medicine the world needs right now.

Research suggests that empaths may have a hyperactive mirror neuron system in their brains. These are the cells responsible for compassion. Empaths are people who rank high on the empathic spectrum and actually feel what is happening in others in their own bodies.

Empaths share a highly sensitive person’s love of nature and quiet environments. However, an empath’s capacity for highly developed intuition and their tendency to be an emotional sponge who absorbs the stress of the world sets them apart from someone who is sensitive to excessive sensory stimulation.

Empaths can experience deep compassion for others, but they often get exhausted from feeling “too much”.

Empathy is the game changer. It is the trait that will ultimately save the world.

As a psychiatrist and an empath, I am fascinated by how the phenomenon of empathy works. I feel passionately that empathy is the medicine the world needs right now.

Empathy is when we reach our hearts out to others and put ourselves in their shoes. It also means that we can be happy for others during their times of joy. The Dalai Lama says, “Empathy is the most precious human quality.”

During these stressful times, personally and globally, it’s easy to get overwhelmed. Even so, empathy is the quality that will get us through. It enables us to respect one another, even if we disagree. Empathy doesn’t make you a sentimental softy without discernment. It allows you to keep your heart open to foster tolerance and understanding. Being empathic might not always be effective in getting through to people but I think it’s the best chance we have for peace in our own lives and on the planet.

. . . Psychology Today

Judith Orloff, MD, is an assistant clinical professor of psychiatry at UCLA

“Our innate capacity for empathy is the source of the most precious of all human qualities.” His Holiness the 14th Dalai Lama

The Empath’s Survival Guide. Life Strategies for Sensitive People

Judith Orloff M.D


Chapter 1

ARE YOU AN EMPATH?

Introduction to Empathy

I’m a physician with fourteen years of conventional medical training at USC and UCLA. I am also an empath. In my medical practice of over two decades, I specialize in treating highly sensitive people like myself. Though there is a spectrum of sensitivity that exists in human beings, empaths are emotional sponges who absorb both the stress and joy of the world. We feel everything, often to an extreme, and have little guard up between others and ourselves. As a result, we are often overwhelmed by excessive stimulation and are prone to exhaustion and sensory overload.

I’m so passionate about this topic both professionally and personally because I’ve had to develop specific strategies to manage the challenges of being an empath myself. These allow me to protect my sensitivities so I can maximize their benefits, and there are so many!

I want to share with you how to become a balanced, empowered, and happy empath. To thrive, you must learn ways to avoid taking on the energy, symptoms, and stress of others. I also want to educate your loved ones and peers family, coworkers, bosses, parents, and romantic partners on how best to support and communicate with you. In this book, I will show you how to accomplish these goals.

I offer The Empath’s Survival Guide as a resource for kindred sensitive souls to find understanding and acceptance in a world that is often coarse, heartless, and disdainful of sensitivity. In it, I challenge the status quo and create a new normal for how to view sensitivity, wherever you are on the spectrum.

There is nothing “wrong” with being sensitive. In fact, you are about to discover what’s most “right” about yourself. Through this book, its companion audio program, Essential Tools for Empaths, and my workshops for empaths, I want to create a community of support so that you can find your tribe, be authentic, and shine. I want to support a movement of peopIe who honor their sensitivities. Welcome to a circle of love! My message to you is one of hope and acceptance. I encourage you to embrace your gifts and manifest your full power on the empath journey.

WHAT IS AN EMPATH?

Empaths have an extremely reactive neurological system. We don’t have the same filters that other people do to block out stimulation. As a consequence, we absorb into our own bodies both the positive and stressful energies around us. We are so sensitive that it’s like holding something in a hand that has fifty fingers instead of five. We are truly “super responders.”

Research shows that high sensitivity affects approximately 20 percent of the population, though the degree of one’s sensitivity can vary. Empaths have often been labeled as “overly sensitive” and told to “get a thicker skin.” As children and adults, we are shamed for our sensitivities rather than supported. We may experience chronic exhaustion and want to retreat from the world because it often feels so overwhelming. But at this point in my life, I wouldn’t give up being an empath for anything. It lets me sense the secrets of the universe and know passion beyond my wildest dreams.

However, my empathic abilities haven’t always felt this incredible to me.

GROWING UP AS AN EMPATH

Like many empathic children, I never fit in. In fact, I felt like an alien on earth waiting to be transported to my real home in the stars. I remember sitting in my front yard looking up at the universe and hoping that a spaceship would take me home. I was an only child, so I spent a lot of time by myself. I had no one to relate to who could understand my sensitivities. No one seemed to be like me. My parents, who were both physicians, I come from a family of twenty-five physicians said, “Sweetheart, toughen up and get a thicker skin,” which I didn’t want or even know how to do. I couldn’t go to crowded malls or parties. I’d walk in feeling fine and walk out exhausted, dizzy, anxious, or suffering from some ache or pain I didn’t have before.

What I didn’t know back then was that everyone has a subtle energy field surrounding their body, a subtle radiant light that penetrates and extends beyond it a distance of inches or even feet. These fields communicate information such as emotions and physical wellbeing or distress. When we are in crowded places, the energy fields of others overlap with ours. I picked up all of these intense sensations, but I had absolutely no idea what they were or how to interpret them. I just felt anxious and tired in crowds. And most of all, I wanted to escape.

As a teenager in Los Angeles, I got heavily involved with drugs to block out my sensitivities. (I’m not recommending this to you!) Then, with my sensitivities numbed, I could cope. I was able to attend parties and hang out at shopping malls, just like my friends, and would feel fine. What a relief that was! In my memoir, Second Sight, I wrote about how I turned to drugs to shut off my intuition and empathic abilities. But after a near-tragic car accident, during which I went over a 1,500-foot cliff in Topanga Canyon at three in the morning in an Austin Mini Cooper, my parents were scared to death and sent me to a psychiatrist.

Naturally, I fought my psychiatrist the whole way. But, in fact, this angel in human form was the first person to help me realize that to become whole I had to embrace my sensitivities, not run from them. This was the start of my healing and self-acceptance as an empath. Since I was so frightened by my childhood empathic and intuitive experiences, part of my evolution as a physician and a woman has been to learn to embrace these abilities. They are precious and deserve to be nurtured and supported. That’s why I specialize in helping empaths in my psychiatric practice and workshops.

IF YOU FEEL AS IF YOU DON’T FIT INTO THIS WORLD, IT’S BECAUSE YOU’RE HERE TO CREATE A BETTER ONE. Author Unknown

Yes, we empaths can flourish! Empathy is the medicine the world needs.

THE EMPATH EXPERIENCE

Now let’s explore in more detail the empath experience. See if you relate personally or have a loved one or colleague who qualifies as an empath.

First, what is the difference between ordinary empathy and being an empath? Ordinary empathy means our heart goes out to another person when they are going through a difficult period. It also means that we can be happy for others during their times of joy.

As an empath, however, we actually sense other people’s emotions, energy, and physical symptoms in our bodies, without the usual filters that most people have. We can experience other people’s sorrow and also their joy. We are supersensitive to their tone of voice and body movements. We can hear what they don’t say in words but communicate nonverbally and through silence.

Empaths feel things first, then think, which is the opposite of how most people function in our overintellectualized society. There is no membrane that separates us from the world. This makes us very different from other people who have had their defenses up almost from the time they were born.

Empaths share some or all of the traits of what psychologist Elaine Aron calls Highly Sensitive People, or HSPs. These traits include a low threshold for stimulation, the need for alone time, sensitivity to light, sound, and smell, plus an aversion to large groups. In addition, it takes highly sensitive people longer to wind down after a busy day because their system’s ability to transition from high stimulation to quiet and calm is slower. Empaths also share a highly sensitive person’s love of nature and quiet environments.

Empaths, however, take the experience of the highly sensitive person further. We can sense subtle energy, which is called shakti or prana in Eastern healing traditions, and we absorb this energy into our own bodies. Highly sensitive people don’t typically do that. This capacity allows us to experience the energies around us in extremely deep ways. Since everything is made of subtle energy, including emotions and physical sensations, we energetically internalize the feelings, pain, and various physical sensations of others. We often have trouble distinguishing someone else’s discomfort from our own. Also, some empaths have profound spiritual and intuitive experiences, which aren’t usually associated with highly sensitive people. Some empaths are even able to communicate with animals, nature, and their inner guides. But being a highly sensitive person and an empath are not mutually exclusive: you can be both at the same time.

To determine if you are an empath, see if you relate to one or more of these types.

GENERAL TYPES OF EMPATHS

Physical Empaths. You are especially attuned to other people’s physical symptoms and tend to absorb them into your body. You also can become energized by someone’s sense of wellbeing.

Emotional Empaths. You mainly pick up other people’s emotions and can become a sponge for their feelings, both happy and sad.

Intuitive Empaths. You experience extraordinary perceptions such as heightened intuition, telepathy, messages in dreams, animal and plant communication, as well as contact with the Other Side. The following includes the different types and how they function:

– Telepathic Empaths receive intuitive information about others in present time.

– Precognitive Empaths have premonitions about the future while awake or dreaming.

– Dream Empaths are avid dreamers and can receive intuitive information from dreams that helps others and guides them in their own lives.

– Mediumship Empaths can access spirits on the Other Side.

– Plant Empaths can feel the needs of plants and connect with their essence.

– Earth Empaths are attuned to changes in our planet, our solar system, and the weather.

– Animal Empaths can tune in to animals and communicate with them.

Empaths have diverse and beautifully nuanced sensitivities. You may be one or more of the above types. In future chapters, I’ll also discuss specific kinds of physical and emotional empaths such as food empaths (who are attuned to the energy of foods) and relationship and sexual empaths (who are attuned to their partners’ and friends’ moods, sensuality, and physical health). As you learn to identify your special talents, you will find they can not only enrich your life but also be used for the good of others.

STYLES OF RELATING: INTROVERTED AND EXTROVERTED EMPATHS

Physical, emotional, and intuitive empaths can have different styles of socializing and interacting with the world. Most empaths are introverted, though some are extroverted. Other empaths are a combination of both. Introverted empaths, like me, have a minimal tolerance for socializing and small talk. They tend to be quieter at gatherings and prefer leaving early. Often they arrive in their own cars so they don’t have to feel trapped or dependent on others for a ride.

Many empaths don’t like small talk. It exhausts them.

I love my close circle of friends and mostly stay away from big parties or gatherings. I also don’t like small talk, and I’ve never learned to do it, which is common for the introverted type. I can socialize in groups for usually two to three hours before I feel overstimulated. My friends all know this about me and don’t take it personally when I excuse myself early.

In contrast, extroverted empaths are more verbal and interactive when socializing and enjoy the banter with others more than introverted empaths do. They also can stay longer in social situations without getting exhausted or overstimulated.

HOW DOES SOMEONE BECOME AN EMPATH?

Many factors can contribute. Some babies enter the world with more sensitivity than others, an inborn temperament. You can actually see it when they come out of the womb. They’re much more responsive to light, smells, touch, movement, temperature, and sound. Also, from what I’ve observed with my patients and workshop participants, some sensitivity may be genetically transmitted. Highly sensitive children can come from mothers and fathers with the same traits. In addition, parenting plays a role. Childhood neglect or abuse can also affect sensitivity levels for adults. A portion of empaths I’ve treated have experienced early trauma, such as emotional or physical abuse, or were raised by alcoholic, depressed, or narcissistic parents. This could potentially wear down the usual healthy defenses that a child with nurturing parents develops. As a result of their upbringing, these children typically don’t feel “seen” by their families, and they also feel invisible in the greater world that doesn’t value sensitivity. In all cases, however, empaths haven’t learned to defend against stress in the same way others have. We’re different in this respect. A noxious stimulus, such as an angry person, crowds, noise, or bright light, can agitate us because our threshold for sensory overload is extremely low.

THE SCIENCE OF EMPATHY

There are a number of scientific findings explaining the empath experience that I find fascinating.

The Mirror Neuron System

Researchers have discovered a specialized group of brain cells that are responsible for compassion. These cells enable everyone to mirror emotions, to share another person’s pain, fear, or joy. Because empaths are thought to have hyperresponsive mirror neurons, we deeply resonate with other people’s feelings.

How does this occur? Mirror neurons are triggered by outside events. For example, when our spouse gets hurt, we feel hurt too. When our child is crying, we feel sad as well, and when our friend is happy, we also feel happy. In contrast, psychopaths, sociopaths, and narcissists are thought to have what science calls “empathy deficient disorders”. This means they lack the ability to feel empathy the way other people do, which may be caused by an underactive mirror neuron system. We must beware of these people because they are incapable of unconditional love.

Electromagnetic Fields

The second finding is based on the fact that both the brain and the heart generate electromagnetic fields. According to the HeartMath Institute, these fields transmit information about people’s thoughts and emotions. Empaths may be particularly sensitive to this input and tend to become overwhelmed by it. Similarly, we often have stronger physical and emotional responses to changes in the electromagnetic fields of the earth and the sun. Empaths know well that what happens to the earth and the sun affects our state of mind and energy.

Emotional Contagion

The third finding that enhances our understanding of empaths is the phenomenon of emotional contagion. Research has shown that many people pick up the emotions of those around them. For instance, one crying infant will set off a wave of crying babies in a hospital ward. Or one person loudly expressing anxiety in the workplace can spread it to other workers. People commonly catch other people’s feelings in groups. A recent article in the New York Times stated that this ability to synchronize moods with others is crucial for good relationships. What is the lesson for empaths? To choose positive people in our lives so that we’re not brought down by negativity. And when a friend is going through a hard time, we need to take special precautions to ground and center ourselves. These are important strategies that you will learn in this book.

Increased Dopamine Sensitivity

The fourth finding involves dopamine, a neurotransmitter that increases the activity of neurons and is associated with the pleasure response. Research has shown that introverted empaths tend to have a higher sensitivity to dopamine than extroverts. Basically, introverted empaths need less dopamine to feel happy. That could explain why they are more content with alone time, reading, and meditation and need less external stimulation from parties and other large social gatherings. In contrast, extroverts crave the dopamine rush they get from lively events. In fact, they often can’t get enough of it.

Synesthesia

The fifth finding, which I find particularly compelling, is the extraordinary state called “mirror-touch synesthesia.” Synesthesia is a neurological condition in which two different senses are paired in the brain, for instance, seeing colors when you hear a piece of music or “tasting” words. Famous synesthetics include Isaac Newton, Billy Joel, and Itzhak Perlman. However, with mirror-touch synesthesia, peopIe actually feel the emotions and sensations of others in their own bodies, as if these emotions were their own. This is a wonderful neurological explanation of an empath’s experience.

WHAT AREAS OF LIFE DOES EMPATHY AFFECT?

Empathy can be present in the following areas of daily life:

– Health. Many of the empaths who come to me as patients and in my workshops feel overwhelmed, fatigued, and downright exhausted before they learn practical skills to help them cope with their sensitivities. They have often been diagnosed with agoraphobia, chronic fatigue, fibromyalgia, migraines, chronic pain, allergies, and adrenal fatigue (a form of burnout). On an emotional level, they may experience anxiety, depression, or panic attacks. We will discuss all of these topics in chapter 2.

– Addictions. Some empaths become addicted to alcohol, drugs, food, sex, shopping, or other behaviors in an attempt to numb their sensitivities. Overeating is common since some empaths unwittingly use food to ground themselves. Empaths can easily become overweight because the extra padding provides protection from negative energy. In chapter 3, we’ll look at healthier coping mechanisms.

– Relationships, Love, and Sex. Empaths may unknowingly get involved with toxic partners and become anxious, depressed, or ill. They give their hearts too easily to narcissists and other unavailable people. Empaths are loving and expect others to be that way, which doesn’t always happen. They also absorb their partner’s stress and emotions, such as anger or depression, simply by interacting with them, as well as during lovemaking, a particularly vulnerable time. In chapters 4 and 5, you’ll learn how to have a healthy relationship without getting overloaded, as well as ways to set clear boundaries with toxic people in your life.

– Parenting. Empathic parents often feel especially overwhelmed and exhausted from the intense demands of child-rearing because they tend to absorb their children’s feelings and pain. In chapter 6, empaths who are parents will learn skills to prevent them from doing this. In addition, empathic children can feel overwhelmed by their sensitivities. Their parents need a special education in helping these children to nurture their gifts and to thrive.

– Work. Empaths can feel drained by energy vampires in their workplace yet be at a loss to know how to set boundaries to protect themselves. In chapter 7, empaths will learn to center and replenish themselves in a work environment that may be excessively stimulating or have little privacy.

– Extraordinary Perceptual Abilities. Empaths have high sensitivities that can make them more intuitive, able to sense people’s energy, and open to premonitions, animal communication, and powerful dreams. In chapter 8, we’ll look at how they can become empowered by these abilities in a grounded way.

SELF-ASSESSMENT Are You an Empath?

To find out, take the following empath self-assessment, answering “mostly yes” or “mostly no” to each question.

– Have I ever been labeled overly sensitive, shy, or introverted?

– Do I frequently get overwhelmed or anxious?

– Do arguments and yelling make me ill?

– Do I often feel like I don’t fit in?

– Do crowds drain me, and do I need alone time to revive myself?

– Do noise, odors, or nonstop talkers overwhelm me?

– Do I have chemical sensitivities or a low tolerance for scratchy clothes?

. . .

from

The Empath’s Survival Guide. Life Strategies for Sensitive People

by Judith Orloff M.D

get it at Amazon.com

Hate Is Not a Mental Illness. To prevent mass shootings, focus on gun laws, not mental health – Amy Barnhorst MD.

If we continue to hope that every angry, entitled male with a grudge and an arsenal can be cured by the mental health system, we doom ourselves to watching these tragedies unfold again and again.

This past month, eleven Jewish people were shot at a synagogue by a man who had posted anti-Semitic comments online. Two African-American people were murdered at a grocery store by a gunman who had just tried and failed to enter a black church. Twelve people were shot and killed at a Thousand Oaks nightclub. Like clockwork, public speculation about the presumed mental illness of the shooters unfolded soon thereafter. As the events of each man’s past were slowly unearthed, they started to ring familiar bells: run-ins with the police, domestic violence, involvement with online hate groups, bar fights, brief psychological interventions for threats of suicide or violence. Many of these mass shooters had previous diagnoses of things like depression, autism spectrum disorders, or anxiety. But even if these diagnoses were accurate, did they cause the shootings?

When someone robs a liquor store or assaults their girlfriend, we don’t automatically assume they are mentally ill. Even people who murder neighbors, rivals or family members don’t garner such diagnostic speculation. So why is it different after a mass shooting?

. . . Psychology Today

MINDSIGHT, OUR SEVENTH SENSE, an introduction. Change your brain and your life – Daniel J. Siegel MD.

Mindsight, the brain’s capacity for both insight and empathy.

How can we be receptive to the mind’s riches and not just reactive to its reflexes? How can we direct our thoughts and feelings rather than be driven by them?

And how can we know the minds of others, so that we truly understand “where they are coming from” and can respond more effectively and compassionately?

Mindsight is a kind of focused attention that allows us to see the internal workings of our own minds, making it possible to see what is inside, to accept it, and in the accepting to let it go, and finally, to transform it.

When we develop the skill of mindsight, we actually change the physical structure of our brain. How we focus our attention shapes the structure of the brain.

Mindsight has the potential to free us from patterns of mind that are getting in the way of living our lives to the fullest.

Mindsight, our ability to look within and perceive the mind, to reflect on our experience, is every bit as essential to our wellbeing as our six senses. Mindsight is our seventh sense.

What is Mindsight?

“Mindsight” is a term coined by Dr. Dan Siegel to describe our human capacity to perceive the mind of the self and others. It is a powerful lens through which we can understand our inner lives with more clarity, integrate the brain, and enhance our relationships with others. Mindsight is a kind of focused attention that allows us to see the internal workings of our own minds. It helps us get ourselves off of the autopilot of ingrained behaviors and habitual responses. It lets us “name and tame” the emotions we are experiencing, rather than being overwhelmed by them.

“I am sad” vs. “I feel sad”

Mindsight is the difference between saying “I am sad” and ”I feel sad.” Similar as those two statements may seem, they are profoundly different. “I am sad” is a kind of limited selfdefinition. “I feel sad” suggests the ability to recognize and acknowledge a feeling, without being consumed by it. The focusing skills that are part of mindsight make it possible to see what is inside, to accept it, and in the accepting to let it go, and finally, to transform it.

Mindsight: A Skill that Can Change Your Brain

Mindsight is a learnable skill. It is the basic skill that underlies what we mean when we speak of having emotional and social intelligence. When we develop the skill of mindsight, we actually change the physical structure of the brain. This revelation is based on one of the most exciting scientific discoveries of the last twenty years: How we focus our attention shapes the structure of the brain. Neuroscience has also definitively shown that we can grow these new connections throughout our lives, not just in childhood.

What’s Interpersonal Neurobiology?

Interpersonal neurobiology, a term coined by Dr. Siegel in The Developing Mind, 1999, is an interdisciplinary field which seeks to understand the mind and mental health. This field is based on science but is not constrained by science. What this means is that we attempt to construct a picture of the ”whole elephant” of human reality. We build on the research of different disciplines to reveal the details of individual components, while also assembling these pieces to create a coherent view of the whole.

The Mindsight Institute

Through the Mindsight Institute, Dr. Siegel offers a scientificaliy-based way of understanding human development. The Mindsight Institute serves as the organization from which interpersonal neurobiology first developed and it continues to be a key source for learning in this area. The Mindsight Institute links science, clinical practice, education, the arts, and contemplation, serving as an educational hub from which these various domains of knowing and practice can enrich their individual efforts. Through the Mindsight Institute’s online program, people from six continents participate weekly in our global conversation about the ways to create more health and compassion in the world.

Mindsight Institute

Daniel J. Siegel, MD, is a clinical professor of psychiatry at the UCLA School of Medicine, co-director of the UCLA Mindful Awareness Research Center, and executive director of the Mindsight Institute. A graduate of Harvard Medical School, he is the author of the internationally acclaimed professional texts The Mindful Brain and The Developing Mind, and the co-author of Parenting from the Inside Out.

The groundbreaking bestseller on how your capacity for insight and empathy allows you to make positive changes in your brain and in your life.

Daniel J. Siegel, widely recognised as a pioneer in the field of mental health, coined the term ‘mindsight’ to describe the innovative integration of brain science with the practice of psychotherapy. Combining the latest research findings with case studies from his practice, he demonstrates how mindsight can be applied to alleviate a range of psychological and interpersonal problems from anxiety disorders to ingrained patterns of behaviour.

With warmth and humour, Dr Siegel shows us how to observe the working of our minds, allowing us to understand why we think, feel, and act the way we do; and how, by following the proper steps, we can literally change the wiring and architecture of our brains.

Both practical and profound, Mindsight offers exciting new proof that we have the ability at any stage of our lives to transform our thinking, our wellbeing, and our relationships.

Mindsight, change your brain and your life

Daniel J. Siegel MD

FOREWORD by Daniel Goleman

The great leaps forward in psychology have come from original insights that suddenly clarify our experience from a fresh angle, revealing hidden patterns of connection. Freud’s theory of the unconscious and Darwin’s model of evolution continue to help us understand the findings from current research on human behavior and some of the mysteries of our daily lives. Daniel Siegel’s theory of Mindsight, the brain’s capacity for both insight and empathy, offers a similar “Aha!” He makes sense for us out of the cluttered confusions of our sometimes maddening and messy emotions.

Our ability to know our own minds as well as to sense the inner world of others may be the singular human talent, the key to nurturing healthy minds and hearts. I’ve explored this terrain in my own work on emotional and social intelligence. Self-awareness and empathy are (along with seIf-mastery and social skills) domains of human ability essential for success in life. Excellence in these capacities helps people flourish in relationships, family life, and marriage, as well as in work and leadership.

Of these four key life skills, self-awareness lays the foundation for the rest. If we lack the capacity to monitor our emotions, for example, we will be poorly suited to manage or learn from them. Tuned out of a range of our own experience, we will find it all the harder to attune to that same range in others. Effective interactions depend on the smooth integration of selfawareness, mastery, and empathy. Or so I’ve argued. Dr. Siegel casts the discussion in a fresh light, putting these dynamics in terms of mindsight, and marshals compelling evidence for its crucial role in our lives.

A gifted and sensitive clinician, as well as a master synthesizer of research findings from neuroscience and child development, Dr. Siegel gives us a map forward. Over the years he has continually broken new ground in his writing on the brain, psychotherapy, and childrearing; his seminars for professionals are immensely popular.

The brain, he reminds us, is a social organ. Mindsight is the core concept in “interpersonal neurobiology,” a field Dr. Siegel has pioneered. This two-person view of what goes on in the brain lets us understand how our daily interactions matter neurologically, shaping neural circuits. Every parent helps sculpt the growing brain of a child; the ingredients of a healthy mind include an attuned, empathetic parent, one with mindsight. Such parenting fosters this same crucial ability in a child.

Mindsight plays an integrative role in the triangle connecting relationships, mind, and brain. As energy and information flow among these elements of human experience, patterns emerge that shape all three (and the brain here includes its extensions via the nervous system throughout the body). This vision is holistic in the true sense of the word, inclusive of our whole being. With mindsight we can better know and manage this vital flow of being.

Dr. Siegel’s biographical details are impressive. Harvard-trained and a clinical professor of psychiatry at UCLA and co-director of the Mindful Awareness Research Center there, he also founded and directs the Mindsight Institute. But far more impressive is his actual being, a mindful, attuned, and nurturing presence that is nourishing in itself. Dr. Siegel embodies what he teaches.

For professionals who want to delve into this new science, I recommend Dr. Siegel’s 1999 text on interpersonal neurobiology, The Developing Mind: Toward a Neurobiology of Interpersonal Experience. For parents, his book with Mary Hartzell is invaluable: Parenting from the Inside Out: How a Deeper Self-Understanding Can Help You Raise Children Who Thrive. But for anyone who seeks a more rewarding life, the book you hold in your hands has compelling and practical answers.

Daniel Goleman

INTRODUCTION

Diving into the Sea Inside

Within each of us there is an internal mental world that I have come to think of as the sea inside, that is a wonderfully rich place, filled with thoughts and feelings, memories and dreams, hopes and wishes. Of course it can also be a turbulent place, where we experience the dark side of all those wonderful feelings and thoughts, fears, sorrows, dreads, regrets, nightmares. When this inner sea seems to crash in on us, threatening to drag us down below to the dark depths, it can make us feel as if we are drowning.

Who among us has not at one time or another felt overwhelmed by the sensations from within our own minds? Sometimes these feelings are just a passing thing, a bad day at work, a fight with someone we love, an attack of nerves about a test we have to take or a presentation we have to give, or just an inexplicable case of the blues for a day or two.

But sometimes they seem to be something much more intractable, so much part of the very essence of who we are that it may not even occur to us that we can change them. This is where the skill that I have called “mindsight” comes in, for mindsight, once mastered, is a truly transformational tool. Mindsight has the potential to free us from patterns of mind that are getting in the way of living our lives to the fullest.

WHAT IS MINDSIGHT?

Mindsight is a kind of focused attention that allows us to see the internal workings of our own minds. It helps us to be aware of our mental processes without being swept away by them, enables us to get ourselves off the autopilot of ingrained behaviors and habitual responses, and moves us beyond the reactive emotional loops we all have a tendency to get trapped in. It lets us “name and tame” the emotions we are experiencing, rather than being overwhelmed by them. Consider the difference between saying “I am sad” and “I feel sad.” Similar as those two statements may seem, there is actually a profound difference between them. “I am sad” is a kind of seIf-definition, and a very limiting one. “I feel sad” suggests the ability to recognize and acknowledge a feeling, without being consumed by it. The focusing skills that are part of mindsight make it possible to see what is inside, to accept it, and in the accepting to let it go, and, finally, to transform it.

You can also think of mindsight as a very special lens that gives us the capacity to perceive the mind with greater clarity than ever before. This lens is something that virtually everyone can develop, and once we have it we can dive deeply into the mental sea inside, exploring our own inner lives and those of others. A uniquely human ability, mindsight allows us to examine closely, in detail and in depth, the processes by which we think, feel, and behave. And it allows us to reshape and redirect our inner experiences so that we have more freedom of choice in our everyday actions, more power to create the future, to become the author of our own story. Another way to put it is that mindsight is the basic skill that underlies everything we mean when we speak of having social and emotional intelligence.

Interestingly enough, we now know from the findings of neuroscience that the mental and emotional changes we can create through cultivation of the skill of mindsight are transformational at the very physical level of the brain. By developing the ability to focus our attention on our internal world, we are picking up a “scalpel” we can use to resculpt our neural pathways, stimulating the growth of areas of the brain that are crucial to mental health. I will talk a lot about this in the chapters that follow because I believe that a basic understanding of how the brain works helps people see how much potential there is for change.

But change never just happens. It’s something we have to work at. Though the ability to navigate the inner sea of our minds, to have mindsight, is our birthright, and some of us, for reasons that will become clear later, have a lot more of it than others, it does not come automatically, any more than being born with muscles makes us athletes. The scientific reality is that we need certain experiences to develop this essential human capacity. I like to say that parents and other caregivers offer us our first swimming lessons in that inner sea, and if we’ve been fortunate enough to have nurturing relationships early in life, we’ve developed the basics of mindsight on which we can build. But even if such early support was lacking, there are specific activities and experiences that can nurture mindsight throughout the lifespan. As you will see, mindsight is a form of expertise that can be honed in each of us, whatever our early history.

When I first began to explore the nature of the mind professionally, there was no term in our everyday language that captured the way we perceive our thoughts, feelings, sensations, memories, beliefs, attitudes, hopes, dreams, and fantasies. Of course, these activities of the mind fill our day-to-day lives, we don’t need to learn a skill in order to experience them. But how do we actually develop the ability to perceive a thought, not just have one, and to know it as an activity of our minds so that we are not taken over by it? How can we be receptive to the mind’s riches and not just reactive to its reflexes? How can we direct our thoughts and feelings rather than be driven by them?

And how can we know the minds of others, so that we truly understand “where they are coming from” and can respond more effectively and compassionately? When I was a young psychiatrist, there weren’t many readily accessible scientific or even clinical terms to describe the whole of this ability. To be able to help my patients, I coined the term mindsight so that together we could discuss this important ability that allows us to see and shape the inner workings of our own minds.

Our first five senses allow us to perceive the outside world, to hear a bird’s song or a snake’s warning rattle, to make our way down a busy street or smell the warming earth of spring. What has been called our sixth sense allows us to perceive our internal bodily states, the quickly beating heart that signals fear or excitement, the sensation of butterflies in our stomach, the pain that demands our attention.

Mindsight, our ability to look within and perceive the mind, to reflect on our experience, is every bit as essential to our wellbeing. Mindsight is our seventh sense.

As I hope to show you in this book, this essential skill can help us build social and emotional brainpower, move our lives from disorder to well-being, and create satisfying relationships filled with connection and compassion. Business and government leaders have told me that understanding how the mind functions in groups has helped them be more effective and enabled their organizations to become more productive. Clinicians in medicine and mental health have said that mindsight has changed the way they approach their patients, and that putting the mind at the heart of their healing work has helped them create novel and useful interventions. Teachers introduced to mindsight have learned to “teach with the brain in mind” and are reaching and teaching their students in deeper and more lasting ways.

In our individual lives, mindsight offers us the opportunity to explore the subjective essence of who we are, to create a life of deeper meaning with a richer and more understandable internal world. With mindsight we are better able to balance our emotions, achieving an internal equilibrium that enables us to cope with the small and large stresses of our lives. Through our ability to focus attention, mindsight also helps the body and brain achieve homeostasis, the internal balance, coordination, and adaptiveness that forms the core of health. Finally, mindsight can improve our relationships with our friends, colleagues, spouses, and children, and even the relationship we have with our own selves.

A NEW APPROACH TO WELLBEING

Everything that follows rests on three fundamental principles.

The first is that mindsight can be cultivated through very practical steps. This means that creating wellbeing in our mental life, in our close relationships, and even in our bodies, is a learnable skill. Each chapter of this book explores these skills, from basic to advanced, for navigating the sea inside.

Second, as mentioned above, when we develop the skill of mindsight, we actually change the physical structure of the brain. Developing the lens that enables us to see the mind more clearly stimulates the brain to grow important new connections. This revelation is based on one of the most exciting scientific discoveries of the last twenty years: How we focus our attention shapes the structure of the brain. Neuroscience supports the idea that developing the reflective skills of mindsight activates the very circuits that create resilience and wellbeing and that underlie empathy and compassion as well. Neuroscience has also definitively shown that we can grow these new connections throughout our lives, not just in childhood. The short Minding the Brain sections interspersed throughout part 1 are a traveler’s guide to this new territory.

The third principle is at the heart of my work as a psychotherapist, educator, and scientist. Wellbeing emerges when we create connections in our lives, when we learn to use mindsight to help the brain achieve and maintain integration, a process by which separate elements are linked together into a working whole.

I know this may sound both unfamiliar and abstract at first, but I hope you’ll soon find that it is a natural and useful way of thinking about our lives. For example, integration is at the heart of how we connect to one another in healthy ways, honoring one another’s differences while keeping our lines of communication wide open. Linking separate entities to one another, integration, is also important for releasing the creativity that emerges when the left and right sides of the brain are functioning together.

Integration enables us to be flexible and free; the lack of such connections promotes a life that is either rigid or chaotic, stuck and dull on the one hand or explosive and unpredictable on the other. With the connecting freedom of integration comes a sense of vitality and the ease of wellbeing. Without integration we can become imprisoned in behavioral ruts, anxiety and depression, greed, obsession, and addiction.

By acquiring mindsight skills, we can alter the way the mind functions and move our lives toward integration, away from these extremes of chaos or rigidity. With mindsight we are able to focus our mind in ways that literally integrate the brain and move it toward resilience and health.

MINDSIGHT MISUNDERSTOOD

It’s wonderful to receive an email from an audience member or patient who says, “My whole view of reality has changed.” But not everyone new to mindsight gets it right away. Some people are concerned that it’s just another way to become more self-absorbed, a form of navel-gazing, of becoming preoccupied with “reflection” instead of living fully. Perhaps you’ve also read some of the recent research (or the ancient wisdom) that tells us that happiness depends on “getting out of yourself.” Does mindsight turn us away from this greater good?

While it is true that being selfobsessed decreases happiness, mindsight actually frees you to become less self-absorbed, not more. When we are not taken over by our thoughts and feelings, we can become clearer in our own internal world as well as more receptive to the inner world of another. Scientific studies support this idea, revealing that individuals with more mindsight skills show more interest and empathy toward others. Research has also clearly shown that mindsight supports not only internal and interpersonal wellbeing but also greater effectiveness and achievement in school and work.

Another quite poignant concern about mindsight came up one day when I was talking with a group of teachers. “How can you ask us to have children reflect on their own minds?” one teacher said to me. “Isn’t that opening a Pandora’s box?” Recall that when Pandora’s box was opened, all the troubles of humanity flew out. Is this how we imagine our inner lives or the inner lives of our children? In my own experience, a great transformation begins when we look at our minds with curiosity and respect rather than fear and avoidance. Inviting our thoughts and feelings into awareness allows us to learn from them rather than be driven by them. We can calm them without ignoring them; we can hear their wisdom without being terrified by their screaming voices. And as you will see in some of the stories in this book, even surprisingly young children can develop the ability to pause and make choices about how to act when they are more aware of their impulses.

HOW DO WE CULTIVATE MINDSIGHT?

Mindsight is not an all-or-nothing ability, something you either have or don’t have. As a form of expertise, mindsight can be developed when we put in effort, time, and practice.

Most people come into the world with the brain potential to develop mindsight, but the neural circuits that underlie it need experiences to develop properly. For some, such as those with autism and related neurological conditions, the neural circuits of mindsight may not develop well even with the best caregiving. In most children, however, the ability to see the mind develops through everyday interactions with others, especially through attentive communication with parents and caregivers. When adults are in tune with a child, when they reflect back to the child an accurate picture of his internal world, he comes to sense his own mind with clarity. This is the foundation of mindsight. Neuroscientists are now identifying the circuits of the brain that participate in this intimate dance and exploring how a caregiver’s attunement to the child’s internal world stimulates the development of those neural circuits.

If parents are unresponsive, distant, or confusing in their responses, however, their lack of attunement means that they cannot reflect back to the child an accurate picture of the child’s inner world. In this case, research suggests, the child’s mindsight lens may become cloudy or distorted. The child may then be able to see only part of the sea inside, or see it dimly. Or the child may develop a lens that sees well but is fragile, easily disrupted by stress and intense emotions.

The good news is that whatever our early history, it is never too late to stimulate the growth of the neural fibers that enable mindsight to flourish. You’ll soon meet a ninety-two-year-old man who was able to overcome a painful and twisted childhood to emerge a mindsight maven. Here we see living evidence for another exciting discovery of modern neuroscience: that the brain never stops growing in response to experience. And this is true for people with happy childhoods, too. Even if we had positive relationships with our caregivers and parents early on-and even if we write books on the subject, we can continue as long as we live to keep developing our vital seventh sense and promoting the connections and integration that are at the heart of wellbeing.

We’ll begin our journey in part 1 by exploring situations in which the vital skills of mindsight are absent. These stories reveal how seeing the mind clearly and being able to alter how it functions are essential elements in the path toward wellbeing. Part 1 is the more theoretical section of the book, where I explain the basic concepts, give readers an introduction to brain science, and offer working definitions of the mind and mental health. Since I know that my readers will come from a wide variety of backgrounds and interests, I realize that some of you may want to skim or even skip much of that material in order to move directly to part 2.

In part 2, we’ll dive deeply into stories from my practice that illustrate the steps involved in developing the skills of mindsight. This is the section of the book in which I share the knowledge and practical skills that will help people understand how to shape their own minds toward health. At the very end of the book is an appendix outlining the fundamental concepts and a set of endnotes with the scientific resources supporting these ideas.

Our exploration of mindsight begins with the story of a family that changed my own life and my entire approach to psychotherapy. Looking for ways to help them inspired me to search for new answers to some painful questions about what happens when mindsight is lost. It also led to my search for the techniques that can enable us to reclaim and recreate mindsight in ourselves, our children, and our communities. I hope you’ll join me on this journey into the inner sea. Within those depths awaits a vast world of possibility.

PART I

THE PATH TO WELLBEING: MINDSIGHT ILLUMINATED

1. A BROKEN BRAIN, A LOST SOUL The Triangle of WellBeing

Barbara’s family might never have come for therapy if seven year old Leanne hadn’t stopped talking in school. Leanne was Barbara’s middle child, between Amy, who was fourteen, and Tommy, who was three. They had all taken it hard when their mother was in a near fatal car accident. But it wasn’t until Barbara returned home from the hospital and rehabilitation center that Leanne became “selectively mute.” Now she refused to speak with anyone outside the family, including me.

In our first weekly therapy sessions, we spent our time in silence, playing some games, doing pantomimes with puppets, drawing, and just being together. Leanne wore her dark hair in a single jumbled ponytail, and her sad brown eyes would quickly dart away whenever I looked directly at her. Our sessions felt stuck, her sadness unchanging, the games we played repetitive. But then one day when we were playing catch, the ball rolled to the side of the couch and Leanne discovered my video player and screen. She said nothing, but the sudden alertness of her expression told me her mind had clicked on to something.

The following week Leanne brought in a videotape, walked over to the video machine, and put it into the slot. I turned on the player and her smile lit up the room as we watched her mother gently lift a younger Leanne up into the air, again and again, and then pull her into a huge, enfolding hug, the two of them shaking with laughter from head to toe. Leanne’s father, Ben, had captured on film the dance of communication between parent and child that is the hallmark of love: We connect with each other through a give-and-take of signals that link us from the inside out. This is the joy filled way in which we come to share each other’s minds.

Next the pair swirled around on the lawn, kicking the brilliant yellow and burnt-orange leaves of autumn. The mother-daughter duet approached the camera, pursed lips blowing kisses into the lens, and then burst out in laughter. Five-year-old Leanne shouted, “Happy birthday, Daddy!” at the top of her lungs, and you could see the camera shake as her father laughed along with the ladies in his life. In the background Leanne’s baby brother, Tommy, was napping in his stroller, snuggled under a blanket and surrounded by plush toys. Leanne’s older sister, Amy, was off to the side engrossed in a book.

“That’s how my mom used to be when we lived in Boston,” Leanne said suddenly, the smile dropping from her face. It was the first time she had spoken directly to me, but it felt more like I was overhearing her talk to herself. Why had Leanne stopped talking?

It had been two years since that birthday celebration, eighteen months since the family moved to Los Angeles, and twelve months since Barbara suffered a severe brain injury in her accident, a head-on collision. Barbara had not been wearing her seat belt that evening as she drove their old Mustang to the local store to get some milk for the kids. When the drunk driver plowed into her, her forehead was forced into the steering wheel. She had been in a coma for weeks following the accident.

After she came out of the coma, Barbara had changed in dramatic ways. On the videotape I saw the warm, connected, and caring person that Barbara had been. But now, Ben told me, she “was just not the same Barbara anymore.” Her physical body had come home, but Barbara herself, as they had known her, was gone.

During Leanne’s next visit I asked for some time alone with her parents. It was clear that what had been a close relationship between Barbara and Ben was now profoundly stressed and distant. Ben was patient and kind with Barbara and seemed to care for her deeply, but I could sense his despair. Barbara just stared off as we talked, made little eye contact with either of us, and seemed to lack interest in the conversation. The damage to her forehead had been repaired by plastic surgery, and although she had been left with motor skills that were somewhat slow and clumsy, she actually looked quite similar, in outward appearance, to her image on the videotape. Yet something huge had changed inside.

Wondering how she experienced her new way of being, I asked Barbara what she thought the difference was. I will never forget her reply: “

Well, I guess if you had to put it into words, I suppose I’d say that I’ve lost my soul.”

Ben and I sat there, stunned. After a while, I gathered myself enough to ask Barbara what losing her soul felt like.

“I don’t know if I can say any more than that,” she said flatly. “It feels fine, I guess. No different. I mean, just the way things are. Just empty. Things are fine.”

We moved on to practical issues about care for the children, and the session ended.

A DAMAGED BRAIN

It wasn’t clear yet how much Barbara could or would recover. Given that only a year had passed since the accident, much neural repair was still possible. After an injury, the brain can regain some of its function and even grow new neurons and create new neural connections, but with extensive damage it may be difficult to retrieve the complex abilities and personality traits that were dependent on the now destroyed neural structures.

Neuroplasticity is the term used to describe this capacity for creating new neural connections and growing new neurons in response to experience. Neuroplasticity is not just available to us in youth: We now know that it can occur throughout the lifespan. Efforts at rehabilitation for Barbara would need to harness the power of neuroplasticity to grow the new connections that might be able to reestablish old mental functions. But we’d have to wait awhile for the healing effects of time and rehabilitation to see how much neurological recovery would be possible.

My immediate task was to help Leanne and her family understand how someone could be alive and look the same yet have become so radically different in the way her mind functioned. Ben had told me earlier that he did not know how to help the children deal with how Barbara had changed; he said that he could barely understand it himself. He was on double duty, working, managing the kids’ schedules, and making up for what Barbara could no longer do. This was a mother who had delighted in making homemade Halloween costumes and Valentine’s Day cupcakes. Now she spent most of the day watching TV or wandering around the neighborhood. She could walk to the grocery store, but even with a list she would often come home empty-handed. Amy and Leanne didn’t mind so much that she cooked a few simple meals over and over again. But they were upset when she forgot their special requests, things they’d told her they liked or needed for school. It was as if nothing they said to her really registered.

As our therapy sessions continued, Barbara usually sat quietly, even when she was alone with me, although her speech was intact. Occasionally she’d suddenly become agitated at an innocent comment from Ben, or yell if Tommy fidgeted or Leanne twirled her ponytail around her finger. She might even erupt after a silence, as if some internal process was driving her. But most of the time her expression seemed frozen, more like emptiness than depression, more vacuous than sad. She seemed aloof and unconcerned, and I noticed that she never spontaneously touched either her husband or her children. Once, when three-year-old Tommy climbed onto her lap, she briefly put her hand on his leg as if repeating some earlier pattern of behavior, but the warmth had gone out of the gesture.

When I saw the children without their mother, they let me know how they felt. “She just doesn’t care about us like she used to,” Leanne said. “And she doesn’t ever ask us anything about ourselves,” Amy added with sadness and irritation. “She’s just plain selfish. She doesn’t want to talk to anyone anymore.” Tommy remained silent. He sat close to his father with a drawn look on his face.

Loss of someone we love cannot be adequately expressed with words. Grappling with loss, struggling with disconnection and despair, fills us with a sense of anguish and actual pain. Indeed, the parts of our brain that process physical pain overlap with the neural centers that record social ruptures and rejection. Loss rips us apart.

Grief allows you to let go of something you’ve lost only when you begin to accept what you now have in its place. As our mind clings to the familiar, to our established expectations, we can become trapped in feelings of disappointment, confusion, and anger that create our own internal worlds of suffering. But what were Ben and the kids actually letting go of? Could Barbara regain her connected way of being? How could the family learn to live with a person whose body was still alive, but whose personality and “souI”, at least as they had known her, were gone?

“YOU-MAPS” AND “ME-MAPS”

Nothing in my formal training, whether in medical school, pediatrics, or psychiatry, had prepared me for the situation I now faced in my treatment room. I’d had courses on brain anatomy and on brain and behavior, but when I was seeing Barbara’s family, in the early 1990s, relatively little was known about how to bring our knowledge of such subjects into the clinical practice of psychotherapy. Looking for some way to explain Barbara to her family, I trekked to the medical library and reviewed the recent clinical and scientific literature that dealt with the regions of the brain damaged by her accident.

Scans of Barbara’s brain revealed substantial trauma to the area just behind her forehead; the lesions followed the upper curve of the steering wheel. This area, I discovered, facilitates very important functions of our personality. It also links widely separated brain regions to one another, it is a profoundly integrative region of the brain.

The area behind the forehead is a part of the frontal lobe of the cerebral cortex, the outermost section of the brain. The frontal lobe is associated with most of our complex thinking and planning. Activity in this part of the brain fires neurons in patterns that enable us to form neural representations, “maps” of various aspects of our world. The maps resulting from these clusters of neuronal activity serve to create an image in our minds. For example, when we take in the light reflected from a bird sitting in a tree, our eyes send signals back into our brain, and the neurons there fire in certain patterns that permit us to have the visual picture of the bird.

Somehow, in ways still to be discovered, the physical property of neurons firing helps to create our subjective experience, the thoughts, feelings, and associations evoked by seeing that bird, for example. The sight of the bird may cause us to feel certain emotions, to hear or remember its song, and even to associate that song with ideas such as nature, hope, freedom, and peace. The more abstract and symbolic the representation, the higher in the nervous system it is created, and the more forward in the cortex.

The prefrontal cortex, the most damaged part of the frontal lobe of Barbara’s brain, makes complex representations that permit us to create concepts in the present, think of experiences in the past, and plan and make images about the future. The prefrontal cortex is also responsible for the neural representations that enable us to make images of the mind itself. I call these representations of our mental world “mindsight maps.” And I have identified several kinds of mindsight maps made by our brains.

The brain makes what I call a “me-map” that gives us insight into ourselves, and a “you-map” for insight into others. We also seem to create “we-maps,” representations of our relationships. Without such maps, we are unable to perceive the mind within ourselves or others. Without a me-map, for example, we can become swept up in our thoughts or flooded by our feelings. Without a you-map, we see only others’ behaviors, the physical aspect of reality, without sensing the subjective core, the inner mental sea of others. It is the you-map that permits us to have empathy. In essence, the injury to Barbara’s brain had created a world without mindsight. She had feelings and thoughts, but she could not represent them to herself as activities of her mind. Even when she said she’d “lost her soul,” her statement had a bland, factual quality, more like a scientific observation than a deeply felt expression of personal identity. (I was puzzled by that disconnect between observation and emotion until I learned from later studies that the parts of our brain that create maps of the mind are distinct from those that enable us to observe and comment on self-traits such as shyness or anxiety or, in Barbara’s case, the lack of a quality she called “soul.”)

In the years since I took Barbara’s brain scans to the library, much more has been discovered about the interlinked functions of the prefrontal cortex. For example, the side of this region is crucial for how we pay attention; it enables us to put things in the “front of our mind” and hold them in awareness. The middle portion of the prefrontal area, the part damaged in Barbara, coordinates an astonishing number of essential skills, including regulating the body, attuning to others, balancing emotions, being flexible in our responses, soothing fear, and creating empathy, insight, moral awareness, and intuition. These were the skills Barbara was no longer able to recruit in her interactions with her family.

I will be referring to, and expanding on, this list of nine middle prefrontal functions throughout our discussion of mindsight. But even at first glance, you can see that these functions are essential ingredients for wellbeing, ranging from bodily processes such as regulating our hearts to social functions such as empathy and moral reasoning.

After Barbara emerged from her coma, her impairments had seemed to settle into a new personality. Some of her habits, such as what she liked to eat and how she brushed her teeth, remained the same. There was nothing significantly changed in how her brain mapped out these basic behavioral functions. But the ways in which she thought, felt, behaved, and interacted with others were profoundly altered. This affected every detail of daily life, right down to Leanne’s crooked ponytail. Barbara still had the behavioral moves necessary to fix her daughter’s hair, but she no longer cared enough to get it right.

Above all, Barbara seemed to have lost the very map-making ability that would enable her to honor the reality and importance of her own or others’ subjective inner lives. Her mindsight maps were no longer forming amid the now jumbled middle prefrontal circuitry upon which they depended for their creation. This middle prefrontal trauma had also disrupted the communication between Barbara and her family, she could neither send nor receive the connecting signals enabling her to join minds with the people she had loved most.

Ben summed up the change: “She is gone. The person we live with is just not Barbara.”

A TRIANGLE OF WELLBEING: MIND, BRAIN, AND RELATIONSHIPS

The videotape of Ben’s birthday had revealed a vibrant dance of communication between Barbara and Leanne. But now there was no dance, no music keeping the rhythm of two minds flowing into a sense of a “we.” Such joining happens when we attune to the internal shifts in another person, as they attune to us, and our two worlds become linked as one. Through facial expressions and tones of voice, gestures and postures, some so fleeting they can be captured only on a slowed-down recording, we come to “resonate” with one another. The whole we create together is truly larger than our individual identities. We feel this resonance as a palpable sense of connection and aliveness. This is what happens when our minds meet.

A patient of mine once described this vital connection as “feeling felt” by another person: We sense that our internal world is shared, that our mind is inside the other. But Leanne no longer “felt felt” by her mom.

The way Barbara behaved with her family reminded me of a classic research tool used to study infant-parent communication and attachment. Called the “still-face” experiment, it is painful both to participate in and to watch.

A mother is asked to sit with her four-month-old infant facing her and when signaled, to stop interacting with her child. This “still” phase in which no verbal or nonverbal signals are to be shared with the child is profoundly distressing. For up to three minutes, the child attempts to engage the now nonresponsive parent in a bid for connection. At first the child usually amps up her signals, increasing smiles, coos, eye contact. But after a period of continuing nonresponse, she becomes agitated and distressed, her organized bids for connection melting into signs of anguish and outrage. She may then attempt to soothe herself by placing her hand in her mouth or pulling at her clothes. Sometimes researchers or parents call off the experiment at this time, but sometimes it goes on until the infant withdraws, giving up in a kind of despondent collapse that looks like melancholic depression. These stages of protest, self-soothing, and despair reveal how much the child depends upon the attuned responses of a parent to keep her own internal world in equilibrium.

We come into the world wired to make connections with one another, and the subsequent neural shaping of our brain, the very foundation of our sense of self, is built upon these intimate exchanges between the infant and her caregivers. In the early years this interpersonal regulation is essential for survival, but throughout our lives we continue to need such connections for a sense of vitality and well-being.

. . .

from

Mindsight, change your brain and your life

by Daniel J. Siegel MD

get it at Amazon.com

LOOKING BACK FROM DEATH ROW. A Gunman’s Regret – R. Douglas Fields * Study: Violent aggression predicted by multiple pre-adult environmental hits – Molecular Psychiatry.

Alternative Title: Adverse Childhood Experiences cause Epigenetic changes in the developing young Brain, leading to mental illness, depression, anger management issues, violent crime, incarceration and a multi generational vicious cycle of hopelessness and despair.

With only 5 percent of the world’s population, the United States has 25 percent of the world’s prison population. Why?

This study is the first to provide sound evidence, based on 6 separate cohorts, of a disease independent relationship between accumulation of multifaceted pre-adult environmental hits and violent aggression.

The name “correctional facility” is accurate from society’s perspective, but it is a delusional euphemism from the perspective of most inmates. According to the National Institute of Justice, three quarters of prisoners will be rearrested within five years of their release.

We lock up 7.16 out of 1,000 people in the United States, the highest rate of incarceration in the world.

The explosion of senseless mass violence in places that were once society’s most cherished communal places, schools, concert stadiums, public transportation and even houses of worship, is ripping apart the social fabric of American life.

The roots of violence at the level of brain biology need to be understood so that violence can be prevented.

Researchers have found a high incidence of genetic factors that increase impulsivity and anger in the violent prison population, and also an increased incidence of neurological abnormalities detectable with brain imaging. Studies of twins show that heredity accounts for over 60 percent of the risk for aggression.

The perpetrators of violent crime are almost always male. Humans have evolved through the survival-of-the-fittest struggle in the wild, evolved brain and bodily attributes that equip and predispose them to engage in aggression to provide and protect. This biological drive in males for aggression still exists in modern civilization.

Changes in society and in traditional male roles must be accompanied by new approaches to channel male aggression positively.

This can be reached by a path guided by neuroscience. Males have this biology of aggression for a reason, but it must be adapted to our current environment.

A new study finds that exposure to certain adverse events in early life, while the brain is undergoing maturation, greatly multiplies the odds of being institutionalized as an adult for violent aggression. They include poverty, social rejection from peer groups, cannabis and alcohol abuse, living in an urban environment, traumatic brain injury, immigration, conflict and violence in the home, and physical or sexual abuse.

. . . Scientific American

Molecular Psychiatry: Study

Violent aggression predicted by multiple pre-adult environmental hits.

Early exposure to negative environmental impact shapes individual behavior and potentially contributes to any mental disease. We reported previously that accumulated environmental risk markedly decreases age at schizophrenia onset. Follow up of matched extreme group individuals unexpectedly revealed that high risk subjects had 5 times greater probability of forensic hospitalization.

In line with longstanding sociological theories, we hypothesized that risk accumulation before adulthood induces violent aggression and criminal conduct, independent of mental illness. We determined in 6 independent cohorts (4 schizophrenia and 2 general population samples) pre adult risk exposure, comprising urbanicity, migration, physical and sexual abuse as primary, and cannabis or alcohol as secondary hits. All single hits by themselves were marginally associated with higher violent aggression.

Most strikingly, however, their accumulation strongly predicted violent aggression. An epigenome wide association scan to detect differential methylation of blood-derived DNA of selected extreme group individuals yielded overall negative results. Conversely. detemination in peripheral blood mononuclear cells of histone deacetylasel mRNA as ‘umbrella mediator’ of epigenetic processes revealed an increase in the high risk group, suggesting lasting epigenetic alterations.

Together, we provide sound evidence of a disease independent unfortunate relationship between well defined pre adult environmental hits and violent aggression, calling for more efficient prevention.

Introduction

Early exposure to external risk factors like childhood maltreatment, sexual abuse or head trauma, but also living in urban environment or migration from other countries and cultures, have long been known or suspected to exert adverse effects on individual development and socioeconomic functioning. Moreover, these environmental risk factors seem to contribute to abnormal behavior and to severity and onset of mental illness, even though different risk factors may have different impact, dependent on the particular neuropsychiatric disease in focus. On top of these ‘primary factors‘ that are rather inevitable for the affected, ‘secondary’, avoidable risks add to the negative individual and societal outcome, namely cannabis and alcohol abuse.

Adverse experiences in adulthood, like exposure to violence, traumatic brain injury, or substance intoxication, can act as single triggers to increase the short term risk of violence in mentally ill individuals as much as in control subjects.

However, comprehensive studies, including large numbers of individuals and replication cohorts, on pre-adult accumulation of environmental risk factors and their long term consequences on human behavior do not exist.

In a recent report we showed that accumulation of environmental risks leads to a nearly 10 year earlier schizophrenia onset, demonstrating the substantial impact of the environment on mental disease, which by far outlasted any common genetic effects. To search for epigenetic signatures in blood of carefully matched extreme group subjects of this previous study we had to re-contact them. This reconnect led to the unforeseen observation that high risk subjects had 5 times higher probability to be hospitalized in forensic units compared to low risk subjects.

This finding stimulated the present work: Having the longstanding concepts of sociologists and criminologists in mind, we hypothesized that early accumulation of environmenml risk factors would lead to increased violent aggression and social rule-breaking in affected individuals, independent of any mental illness. To test this hypothesis, we explored environmental risk before the age of 18 years in 4 schizophrenia samples of me GRAS (Göttingen Research Association for Schizophrenia) data collection. Likewise, risk factors were assessed as available in 2 general population samples.

In all cohorts, accumulation of pre-adult environmental hits was highly significantly associated with lifetime conviction for violent acts or high psychopathy and aggression hostility scores as proxies of violent aggression and rule breaking.

As a first small hint of epigenetic alterations in our high risk subjects, histone deacelylasel (HDACI) mRNA was found increased in peripheral blood mono nuclear cells (PBMC).

Fig. 1 Multiple environmental hits before adulthood predict violent aggression in mentally ill subjects as well as in the general population. Results from 6 independent samples.

a – Distribution of forensic hospitalization in the discovery sample (see results) suggested a substantial impact of environmental risk accumulation on violent aggression, a finding replicated in the remaining GRAS sample (GRAS I males and females minus extreme group subjects of the discovery sample). Note the ‘stair pattem’ upon stepwise increase in risk factors; stacked charts illustrate risk factor composition in the respective groups (including all risk factors of each individual in the respective risk group), Each color represents a panicular risk (same legend for dg and jk); b – Brief presentation of the violent aggression severity score, VASS, ranging from no documented aggression to lethal consequences of violent aggression with relative weight given to severity of aggression and number of registered re occurrences. c – Highly significant intercorrelation of violent aggression measures used in the present paper. d – Application of VASS to risk accumulation in the discovery sample; Kmskal Wallis H test (two sided). e-g – Schizophrenia replication cohorts 1: ‘stair pattem‘ of aggression proxy in risk accumulation groups: all 12 test (one sided). h – Comparative presentation of subjects (%) with violent aggression in risk accumulation groups across schizophrenia cohorts. i – Comparative presentation of subjects (%) with violent aggression before (pre morbid, ‘early’) or after schizophrenia onset (‘late‘) vs. individuals without evidence of aggression (‘no’) in risk accumulation groups of the discovery sample. j-k – General population replication cohorts IV and V: ‘stair pattern‘ of aggression proxies, LSRP secondary psy chopathy score (j) and aggression hostility factor of ZKFQ 50 CC (k) in risk accumulation groups; Kruskal Wallis 1 test (one sided). l – HDACI mRNA levels in PBMC of male extreme group subjects as available for analysis; Student‘s t test (one sided).

Discussion

The present work was initiated based on the observation in a schizophrenia cohort that accumulation of environmental risk factors before adulthood promotes the likelihood of later forensic hospitalization, interpreted as indicator of violent aggression. This interpretation and the effect of risk accumulation were consolidated using direct scoring of aggression over lifetime or, as aggression proxies, forensic hospitalization and conviction for battery, sexual assault, manslaughter or murder. or respective psychopathology measures in 4 independent schizophrenia cohorts and 2 general population samples. Importantly, our data support the concept of a disease independent development of violent aggression in subjects exposed to multiple pre adult environmental risk factors.

Whereas a vast amount of literature on single environmental risk factors reports consequences for abnormal behavior and mental illness, publications on pre-adult risk accumulation are scarce and mostly based on closely interrelated social/familial risk factors. Also, risk and consequence are often not clearly defined. Studies including larger, comprehensively characterized datasets and replication samples do not exist.

The present work is the first to provide sound evidence, based on 6 separate cohorts, of a disease independent relationship between accumulation of multifaceted pre-adult environmental hits and violent aggression.

The overall societal damage is enormous, and we note that mentally ill individuals who re-enter the community from prison are even more at risk for unemployment, homelessness, and criminal recidivism. These results should encourage better precautionary measures, including intensified research on protective factors which is still underrepresented.

In the psychosociological literature, the so called externalizing behavior in childhood includes hostile and aggressive physical behavior toward others, impulsivity, hyperactivity, and noncompliance with limit setting. The respective risk factors are all highly plausible, yet often theoretical, and derived from 4 broad domains: child risk factors (e.g., adverse temperament, genetic and gender risk), sociocultural risks (e.g., poverty, stressful life events), parenting and caregiving (e.g., confiict and violence at home, physical abuse), and children’s peer experiences (e.g., instable relationships, social rejection). A full model of the development of conduct problems has been suggested to include at least these 4 domains.

The risk factors analyzed in the present study are perhaps somewhat clearer defined but partially related to and overlapping across these domains. Urbanicity, migration, cannabis and alcohol reflect sociocultural input but also peer experience, and physical or sexual abuse belong to the parenting/caregiver aspect.

Certainly, there are many more, still undiscovered risk and numerous protective factors, potentially explaining why ‘only’ 40-50% of high risk individuals in our schizophrenia samples fulfill criteria of violent aggression.

We note that this study does not include genetic data analysis or correction for any genetic impact. The genetic influence on aggression, however, may be of considerable relevance for the individual, even though highly heterogeneous as for essentially all behavioral traits. Heritability of aggression, estimated from twin studies, reaches >60%. In fact, 50% of individuals with violent aggression upon pre-adult risk accumulation in the present study means another 50% without detectable aggression. This consistent finding across samples likely indicates that genetic predisposition is prerequisite for whichever behavioral consequence. Individuals without genetic predisposition and/or with more protective factors (genetic and environmental) may not react with violent aggression to accumulated environmental risk.

Importantly, the obvious gender effect may be a matter of degree rather than of pattern. In fact, the etiology of externalizing behavior problems is similar for girls and boys, as is the consequence of risk accumulation in the present study for males and females.

The risk factors of the sociological domains seem to be stable predictors over time, to some degree interchangeable, pointing to many pathways leading to the same outcome (principle of equifinality). The interchangeability is highly interesting also with respect to potential biological mechanisms. It appears that any of the here investigated hits alone, independent of its kind, can be compensated for but that higher risk load increases the probability of violent aggression.

Also for that reason, we are weighing risk factors equally in the present study. This could theoretically create some bias. However, to be able to estimate the true effect size of each specific factor separately on violent aggression and subsequently weigh all factors in a more proper way, much larger samples sizes would be needed that are presently not available anywhere in the world.

In contrast to the marginal influence of genome wide association data on mental disease in GRAS, the accumulated environmental impact on development of violent aggression is huge, reflected by odds ratios of >10. When striking at a vulnerable time of brain development, namely around/before puberty, the environmental input may ‘non specifically’ affect any predisposed individual. The hypothetical biological mechanisms underlying this accumulation effect in humans may range from alterations in neuroendocrine and neurotransmitter systems, neuronal/ synaptic plasticity and neurogenesis to changes in the adaptive immune system and interference with developmental myelination, affecting brain connectivity and network function.

Our approach to detect methylation changes in blood using an epigenome wide association scan was unsuccessful despite matched extreme group comparison, likely due to the small sample size, and perhaps the etiological/pathogenetic complexity of accumulated risks. Changes in brain, not accessible here for analysis, can certainly not be excluded. Interestingly, however, HDAC1 mRNA levels in PBMC of male extreme group subjects were increased in the high risk compared to the low risk group. This finding confirms peripheral HDAC1 mRNA levels as a more robust readout of epigenetic alterations in relatively small sample sizes, as compared to specific methylation sites in epigenome wide association scans or even in candidate genes. To gain further mechanistic insight and thereby develop in addition to prevention measures novel individualized treatment concepts, animal studies modeling risk accumulation seem unavoidable.

To conclude, this study should motivate sociopolitical actions, aiming at identifying individuals at risk and improving precautionary measures. Effective violence prevention strategies start early and include family focused and school based programs. Additional risk factors, interchangeable in their long term consequences, like urbanicity, migration, and substance abuse, should be increasingly considered. Health care providers are essential for all of these prevention concepts. More research on protective factors and resilience should be launched. Animal studies need to be supported that model risk accumulation for mechanistic insight into brain alterations leading to aggression, and for developing new treatment approaches, also those targeting reversal of epigenetic alterations. As a novel concept, scientific efforts on ‘phenaryptyping of the environment’, should be promoted to achieve more fundamental risk estimation and more effective prevention in the future.

*

Read the complete study here: Violent aggression predicted by multiple pre-adult environmental hits

Can Treatment Resistant Depression Be Successfully Treated? – Robert J. Hedaya.

If you or a loved one suffers from depression that doesn’t seem to get better no matter what medication you take or psychotherapy you receive, read this article.

Between one-half to two-thirds of people with depression do not have a full recovery from their depression.
More than 1/3 fail to improve with the standard of care approach, which is medication and therapy.
The most common cause of treatment-resistant depression is a failure to identify and treat the underlying biological causes of depression.
A strong Functional Medicine program can effectively resolve treatment-resistant depression.
So addressing the cause or causes of inflammatory signaling, rather than just prescribing a drug to boost serotonin levels, is an example of a functional medicine approach to treating depression. In fact, it is highly unlikely that a drug will work in such a situation for the simple reason that the SSRI medications require enough serotonin to be present to work on. But with inflammation, by definition, brain serotonin levels are deficient.

Basic science has now enlightened us as to the underlying biological causes of depression, and this information takes us way, way beyond the outdated and inadequate neurotransmitter, neuro-centric model of depression.

. . . Psychology Today

The Book of Human Emotions. An Encyclopedia of Feeling, from Anger to Wanderlust – Tiffany Watt Smith.

“Our emotions are evolved physical responses, and they are affected by the play of our unconscious minds.”

As early as the 1830s, Charles Darwin was treating emotions as a topic worthy of serious scientific attention.

Is your heart fluttering in anticipation? is your stomach tight with nerves? Are you falling in love? Feeling a bit miffed? Are you curious, perhaps about this book? Do you have the heebie-jeebies?

Some emotions wash the world in a single colour, like the terror felt as the car skids, or the euphoria of falling in love. Others, like clouds, are harder to grasp.

A surge of joy or a nervous tremble is the work of the delicate lattice of our nervous system, at the centre of which is a single organ: the brain.

In the 1880s William James argued that our bodily responses ARE the emotion, and our subjective feeling just follows. While ‘common sense says we meet a bear, are frightened, and run,’ he wrote, it is more rational to say that we feel ‘afraid because we tremble’. The physical response comes first, the subjective quality, the ‘feeling’, a byproduct, he called it an ‘epiphenomenon’, a split second later.

Sigmund Freud later said one had also to consider the far more elusive and complex influence of the mind, or ‘psyche’. He spoke of emotions poetically, as ‘feeling-tones’.

The idea that our emotions take circuitous routes through our minds as well as our bodies has been of profound therapeutic importance and left traces on today’s emotional language.

These Victorians are responsible for two of the most influential ideas about our feelings today: Our emotions are evolved physical responses, and they are affected by the play of our unconscious minds.

The Book of Human Emotions is a gleeful, thoughtful collection of 156 feelings, both rare and familiar. Each has its own story, and reveals the strange forces which shape our rich and varied internal worlds. In reading it, you’ll discover feelings you never knew you had (like basorexia, the sudden urge to kiss someone), uncover the secret histories of boredom and confidence, and gain unexpected insights into why we feel the way we do.

Tiffany Watt Smith is a research fellow at the Centre for the History of the Emotions, Queen Mary University of London, and was also a 2014 BBC New Generation Thinker. Before beginning her academic career she worked as a theatre director, including as an Associate Director at the Arcola Theatre and International Associate at the Royal Court. She lives in London.

“And how delightful other people’s emotions were! much more delightful than their ideas, it seemed to him.” Oscar Wilde, The Picture of Dorian Gray

Look up. Look up at the clouds. Are they grey and solemn in a windless sky? Or wisps floating carelessly on a breeze? Is the horizon drenched in a hot red sunset, angry with desire?

To the painter John Constable, the sky was full of emotion. He called it, in a letter written in 1821, the ‘key note’ and ‘chief organ of sentiment in painting’. it is for this reason that he dedicated much of his time to collecting and classifying the clouds. Walking out from his house in Hampstead, at that time a village near London with a bundle of papers, and a pocket full of brushes, he would sit for hours on the heath rapidly painting the changing shapes above him, the wind rustling his papers, rain drops pooling the colours. Once home, he arranged his sketches according to the latest meteorological classifications, noting the date, time and weather conditions.

Constable wanted to master the language of the sky and when you look at his paintings, it’s clear that he did. But he also lived in an age obsessed with the desire to label and put into categories, a passion for taxonomy that would always sit uneasily with the melting, drifting skies. Clouds are so hard to fix. Arranging them into groups, as the art critic John Ruskin discovered forty years later, was always a matter ‘more of convenience than true description’. The clouds fold into one another and drift away. They switch allegiances until it’s hard to tell them apart.

Look at the clouds, and you might see an emotion colour everything for an instant but then the skies will rearrange themselves and it’ll be gone.

Recognising and naming our emotional weather can be just as peculiar a task. Try to describe exactly how you feel right now. Is your heart fluttering excitedly for the person who’ll be waiting when you step off the train? Or your stomach tight at the thought of tomorrow’s deadline? Perhaps it was curiosity which nudged you towards this book. Or reluctance, studded with giddy defiance, that is making you linger over its pages in the shop rather than returning home. Are you feeling hopeful? Surprised? (Are you bored?)

Some emotions really do wash the world in a single colour, like the terror felt as the car skids, or the euphoria of falling in love. Others, like clouds, are harder to grasp. Plan a surprise for a loved one and you might feel anticipation crinkled with glee and creased at the edges with a faint terror what if they hate it? Storm off during an argument and it might be hard to tell the precise moment at which your indignation ends and your clammy selfloathing begins.

There are some emotions which are so quiet that they slip past before we’ve even had a chance to spot them, like that momentary sense of comfort which makes your hand reach out for a familiar brand at the supermarket. And then there are those that brood on the horizon, the ones we hurry away from, fearing they will burst upon us: the jealousy which makes our fingers itch to search a loved one’s pockets, or the shame that can goad us into self-destruction.

Sometimes it feels more like we belong to our emotions, than they to us.

But perhaps it’s only by paying attention to our feelings, by trying to capture them as Constable did the clouds, that we can truly understand ourselves.

What is an emotion?

Deep inside each of our temporal lobes is a tearshaped structure called the amygdala. Neuroscientists call this the ‘command centre’ of our emotions. It assesses stimuli from the outside world, deciding whether to avoid or approach. It triggers a clatter of responses, raising the heartbeat, instructing the glands to secrete hormones, contracting the limbs or making an eyelid twitch. Recall a sad story or look at a picture of your newborn baby while lying in a brain scanner and the amygdala will be one of the areas that will appear to ‘light up’ on the resulting computer generated image.

With their glowing tapestries of magenta and emerald, studies of the brain can be seductive. They can even seem like the final word on how and why we feel the way we do. But to think of our emotions purely as biochemical fireworks in the brain is, in the words of the writer Siri Hustvedt, ‘rather like saying that Vermeer’s Girl Pouring Milk is a canvas with paint on it or that Alice herself is words on a page. These are facts, but they don’t explain my subjective experience of either of them or what the two girls mean to me.’

More than that, I think, approaching emotions as first and foremost biological facts misrepresents what an emotion actually is.

The invention of emotions

No one really felt emotions before about 1830. Instead, they felt other things ‘passions’, ‘accidents of the soul’, ‘moral sentiments’ and explained them very differently from how we understand emotions today.

Some ancient Greeks believed a defiant rage was carried on an ill wind. Desert dwelling early Christians thought boredom could be implanted in the soul by malignant demons. In the fifteenth and sixteenth centuries, passions were not exclusive to humans, but could work their strange effects on other bodies too, so that palm trees could fall in love and yearn for one another, and cats become melancholic.

But alongside this intangible realm of souls and supernatural forces, doctors also developed a complex approach to understanding the body’s influence on the passions. Their insights were based on a theory of humoral medicine from the ancient Greek physician Hippocrates, which spread via the physicians of the medieval Islamic world, and flourished ultimately in the writings of the court doctors of the European Renaissance. The theory held that each person had a balance of four elemental substances in their bodies blood, yellow bile, black bile and phlegm. These humours were thought to shape personality and mood: those with more blood in their veins were quick tempered, but also brave, while a dominance of phlegm made one peaceful but lugubrious.

Physicians believed strong passions disrupted this delicate ecosystem by moving heat around the body and rousing the humours in turn. Rage sent blood rushing from the heart to the limbs, readying a person to launch an attack. Once black bile was heated, by contrast, it sent poisonous vapours curling up to the brain and crowded it with terrifying visions.

Traces of these ideas still linger: it’s why we speak of people being phlegmatic or in an iII-humour, or say their blood is boiling.

The origin of our modern concept of emotion can be traced to the birth of empirical science in the mid-seventeenth century. Thomas Willis, a London anatomist who dissected hanged criminals, proposed that a surge of joy or a nervous tremble was not the work of strange liquids and fumes, but of the delicate lattice of the nervous system at the centre of which was a single organ: the brain. A hundred or so years later, physiologists studying reflex responses in animals went further and claimed that bodies recoiled in fright or twitched in delight because of purely mechanical processes no immaterial soul substance was necessary at all.

In a draughty Edinburgh lecture hall in the early nineteenth century, the philosopher Thomas Brown suggested this new way of understanding the body required a new vocabulary, and proposed using the word ‘emotion’. Though already in use in English (from the French émotion), the term was imprecise, describing any movements of bodies and objects, from the swaying of a tree to a hot blush spreading across the cheeks. The coinage indicated a novel approach to the life of feelings, one which used experiments and anatomical investigations to focus on observable phenomena: clenched teeth; rolling tears; shudders; wide eyes.

This provoked a flurry of interest among Victorian men of science in understanding how the body’s smiles and frowns expressed and even stimulated internal emotions. One man in particular stands out: Charles Darwin. As early as the 1830s, Darwin was treating emotions as a topic worthy of serious scientific attention. He sent out questionnaires to missionaries and explorers across the globe asking how grief or excitement was expressed by the indigenous people they encountered. He experimented on himself, trying to isolate the muscles used when he shuddered or smiled. He even studied his infant son, William, meticulously charting his responses: ‘at his 8th day he frowned much when little under five weeks old, smiled’.

In 1872 Darwin published his findings in The Expression of the Emotions in Man and Animals, and made the audacious claim that our emotions were not fixed responses, but the result of millions of years of evolutionary processes which were still ongoing. As basic and important as breathing or digestion, as much animal as human, our emotions were there because they had helped us survive, preventing us from ingesting poisons, as in disgust, or helping us form bonds and cooperate, like love or compassion.

By the 1880s, the view that emotions were inherited reflexes was so established among scientists that the philosopher William James could argue that the bodily responses were the emotion, and the subjective feeling just followed. While ‘common sense says we meet a bear, are frightened, and run,’ he wrote, it was more rational to say that we feel ‘afraid because we tremble’. He thought the physical response came first, the subjective quality, a byproduct he called it an ‘epiphenomenon’ a split second later.

What is an Emotion? William James, 1884

Not everyone approached emotions in this way. The year after Darwin published his theories on the evolution of emotional expressions, Sigmund Freud began his medical training in Vienna. By the early 1890s however, Freud had abandoned his career as a neurologist, believing that it wasn’t enough to talk about prolonged sorrow or excessive suspicion in terms only of the brain and body: ‘it is not easy to treat feelings scientifically,’ he wrote.

One had also to consider the far more elusive and complex influence of the mind, or psyche.

Although he never set out a comprehensive theory of what he considered emotions to be, he spoke of them, poetically, as ‘feeling-tones’ Freud’s work added depth and complexity to the vision of emotions as biological twitches and jerks. It’s through his work that many of us have come to think of emotions as things which either can be repressed, or else build up and require venting. And that some particularly those urgent terrors and furious desires of childhood can sink down and hide in the deepest recesses of our minds only to emerge years later in dreams, or compulsions, or even physical symptoms like an aching head or cramping stomach.

It’s also from Freud that we have inherited the idea that we might not even recognise some of our emotions, but that our anger or jealousy might be ‘subconscious’, springing up like a jack-in-the-box accidentally (‘Freudian slips’), or in the jokes we tell, or in habits such as persistent unpunctuality.

Although many of the technical details of Freud’s theories have long since been discredited, the idea that our emotions take circuitous routes through our minds as well as our bodies has been of profound therapeutic importance and left traces on today’s emotional language.

In this way, the Victorians are responsible for two of the most influential ideas about our feelings today: that our emotions are evolved physical responses, and that they are affected by the play of our unconscious minds.

Emotional cultures

In fact, the answer to the question ‘what is an emotion?’ lies not only in our biology or private psychological histories. The way we feel is also enmeshed in the expectations and ideas of the cultures in which we live. Hate, anger or desire can seem to come from the most untamed, animal parts of ourselves. Yet they can also be aroused by those things which make us distinctly human: our language and the concepts we use to understand our bodies; our religious convictions and moral judgements; the fashions, even the politics and economics, of the times we live in.

The seventeenth century nobleman Francois de La Rochefoucauld recognised that even our most ardent urges can be conjured by the need to keep up with conventions: ‘Some people,’ he quipped, ‘would never fall in love if they hadn’t heard love talked about.’ And just as talking, watching and reading can incite emotions in our bodies, they can quieten our feelings too. The Baining people of Papua New Guinea leave a bowl of water out overnight to absorb awumbuk, the gloom and inertia which descend when a much-loved guest departs. The ritual is reported to work every time.

The influence of our ideas can be so powerful that they can sometimes shape those biological responses we think of as the most natural. How else is it possible that in the eleventh century, knights could faint in dismay or yawn for love? Or that 400 years ago people could die of nostalgia?

The idea that emotions might be shaped by our cultures, as well as by our bodies and minds, was enthusiastically taken up in the 1960s and 703. Western anthropologists living in remote communities became interested in the emotional vocabulary of different languages. For instance song, the outrage felt on receiving a less than fair share, is held in high esteem in the cooperative culture of the Pacific islanders of Ifaluk.

It became clear that some cultures take very seriously certain feelings which in English speaking cultures might seem petty. What’s more, some emotions seemed to be so significant that people were fluent in its many subtle tastes and textures, like the fifteen distinct sorts of fear the Pintupi of Western Australia are able to feel. Other emotions which might seem fundamental to English speakers were missing in some languages: there is, for instance, no word which precisely captures the meaning of ‘worry’ among the Machiguenga of Peru.

This interest in emotional languages was intriguing: if different people have different ways of conceptualising their emotions, might they feel them differently too?

Historians had long suspected the importance of passions to understanding the mindsets of the past. However, a decade or so after these initial anthropological studies, they began excavating long-dead emotional cultures in earnest. Of course, they couldn’t interview Roman slaves or medieval lovers about their feelings. But they could uncover the ways people of the past had understood their passions or sentiments by looking at diaries and letters, conduct manuals and medical regimens, even legal documents and political speeches.

They began to ask the questions which have become so familiar to those who work in this field today. Was boredom invented by the Victorians? What made American presidents start smiling in their official portraits? Why did self-help authors in the sixteenth century encourage people to be sad, where today they’d exhort us to be happy? Why, in the eighteenth century, did artists want to broadcast the fact that they’d felt shocked? How could some emotions disappear such as the combination of listlessness and despair the early Christians called ‘acedia’ and others like ‘ringxiety’ suddenly pop into existence? To study the emotions of the past wasn’t only to understand how rituals of love and grief had changed over time, or why in different historical periods some emotions could be publicly expressed, while others were hidden, or restrained through penance or prayer. The new field of study asked how these cultural values imprinted themselves on our private experiences. It asked whether our emotions were entirely our own.

Even accounts of those emotions which are sometimes thought to be ‘basic’ or ‘universal’, such as fear or disgust, vary across times and places. The idea that some emotions are more fundamental than others is a very old one. The Li Chi, a Confucian collection of precepts and rituals which can be dated back to at least the first century BCE, identifies seven inherent feelings (joy, anger, sadness, fear, love, dislike and fondness). The philosopher René Descartes thought there were six ‘primitive passions’ (wonder, love, hatred, desire, joy and sadness). In our own time, some evolutionary psychologists argue that between six and eight ‘basic’ emotions are expressed in the same way by all people. The list usually includes disgust, fear, surprise, anger, happiness and sadness though not ‘love’, whose displays we expect to be tangled up in the rituals of different cultures.

These ‘basic’ emotional expressions are thought to be evolved responses to universal predicaments: a disgusted grimace ejects poisons from our mouths when we stick out our tongues; the rush of energy which comes when we are enraged may help us fight off a rival. But does it really follow that these emotions must feel the same way to all people in all places? Imagine a New York trader on the stock-exchange floor with sweating palms, a thumping heart and a prickling scalp. Then think of the same sensations experienced by a thirteenth-century Christian kneeling in a cold chapel in prayer, or by a Pintupi in Australia on waking in the dead of night with a stomach pain.

The trader might call those feelings ‘an adrenaline rush’ or ‘good fear’ (or, on a bad day, ‘stress’). The second might view them as ‘wondrous fear’, an awestruck terror alerting them to the presence of God. The third might feel ngulu, a particular sort of dread the Pintupi experience when they suspect another person is seeking revenge. The meanings we charge an emotion with change our experience of it. They determine whether we greet a feeling with delight or trepidation, whether we savour it or feel ashamed. Ignore these differences and we’ll lose most of what makes our emotional experiences what they are.

It comes down to what you think an emotion is. When we talk about emotions, I think we need what the American anthropologist Clifford Geertz in the 1970s called ‘thick description’. Geertz asked an elegant question: what is the difference between a blink and a wink? If we answer in purely physiological terms and speak of a chain of muscular contractions of the eyelids then a blink and a wink are more or less the same. But you need to understand the cultural context to appreciate what a wink is. You need to understand playing and jokes, and teasing and sex, and learnt conventions like irony and camp. Love, hate, desire, fear, anger and the rest are like this too.

Without context, you only get a ‘thin description’ of what’s going on, not the whole story and it’s this whole story which is what an emotion is.

This book is about these stories, and how they change. It’s about the different ways emotions have been perceived and performed from the weeping jurors in Greek courts to the brave, bearded women of the Renaissance; from the vibrating heartstrings of eighteenth-century doctors to Darwin’s selfexperiments at London Zoo; from the shell-shocked soldiers of the First World War to our own culture of neuroscience and brain imaging. It’s about the different ways our sorrowful, frowning, wincing, joyous bodies inhabit the world. And how the human world, with its moral values and political hierarchies, its assumptions about gender, sexuality, race and class, its philosophical views and scientific theories, inhabits us in return.

Emotion-spotting: a field guide

Today, emotional health, and the necessity of recognising and understanding our feelings to achieve it, is a stated goal of public policy in many countries, from Bhutan to the UK. Turn on a TV or open a newspaper, and there’ll be, somewhere, tips on how to achieve lasting happiness, or why crying can be good for us. The idea that it’s important to pay attention to our emotions is not new. The Stoics of ancient Greece taught that noticing the first stirrings of a passion gave you the best chance of controlling it. Catch the precise moment the hairs on the nape of your neck began to tingle, they thought, and you could remind yourself not to let blind panic set in.

In the seventeenth century the scholar and great anatomist of melancholy Robert Burton also found noticing his emotions helped him, though his approach was rather different. He became curious about his feelings of despair and worry, and tried to understand them in conversation with other writers and philosophers, particularly those of the past. Eventually, his melancholy, which had once seemed so senseless, became filled with meaning and started to loosen its grip.

Today’s enthusiasm for taking our emotions seriously can largely be traced back to psychological research first popularised in the mid 1990s under the catchy heading of emotional intelligence, aka emotional quotient or EQ. Its proponents argued that being able to identify your own and other people’s emotions, and to use them as a guide to making decisions, was as important in determining success as the traditional measure of IQ. Awareness of emotions has been shown to be strongly correlated with greater resilience in times of stress, with improved performance at work, with better management and negotiation skills and with more stable relationships at home. Today EQ, or some version of it, is a concept familiar to educators, business leaders and policy makers alike.

Whether you greet this excitement about emotions with a wide smile or a raised eyebrow, I hope you will agree that there are intriguing connections between our feelings and the words we use to describe them. Some emotions can fade into a smile when you know what to call them, such as ‘umpty’ (the feeling that everything is ‘all wrong’) or matutolypea (a sadness which only strikes in the morning). Some reveal themselves to be a greater part of our experience once we learn their name, such as basorexia (a sudden desire to kiss someone) or gezelligheid (the cosy feeling which comes from being inside with friends on a cold night).

And sometimes, identifying and reading about other people’s emotions can make our own seem less peculiar and isolating. In the course of writing this, many of the stories I encountered offered the consolations of shared experiences. Others resonated for different reasons, helping me to see some of my more wayward feelings from new perspectives. Most of us avoid thinking about some emotion or other. Perhaps you’re ashamed of your resentfulness or scared about your apathy, or struggle with your embarrassment. But given half a chance to think about where our attitudes towards these feelings come from, we might discover they’re not always the bogeymen we’re sometimes led to believe. I hope some of these stories resonate with you too.

But this book is not really about helping yourself become a happier, or more successful (or even a richer!) individual. Though they are full of intriguing curiosities, understanding the cultural stories of our emotions above all helps us uncover the tacit beliefs about what ‘natural’ (or, worse, ‘normal’) emotional responses might be. If our emotions are so important to us today, if they are measured by governments, subject to increasing pharmaceutical intervention by doctors, taught in our schools and monitored by our employers, then we had better understand where the assumptions we have about them come from and whether we really want to keep signing up.

*

from

The Book of Human Emotions. An Encyclopedia of Feeling, from Anger to Wanderlust

by Tiffany Watt Smith

get it at Amazon.com

The Neuroscience of Emotion: A New Synthesis – Ralph Adolphs and David J. Anderson.

Emotions, while ubiquitous across species and one of the most common topics of conversation, are still, it seems, misunderstood.

We know a lot less than we think we know. This is good news for scientists: there is work to be done, interesting and important work.

We aim to provide a fresh look at emotion from the perspective of biology, a perspective that can provide a foundation for the field from which to move forward in a productive, cross-disciplinary fashion.

We believe that emotions are states of the brain, and that the mechanisms that generate emotions can be investigated with neurobiology.

We believe it is critical to distinguish between emotions as internal functional states, and conscious experiences of emotions, often called “feelings”. Emotions and feelings are not the same thing, although they are of course closely related. Most of this book is about emotions, not about feelings.

A science of emotion needs to examine most of our initial intuitions about emotions, sharpen vague questions so that they can be experimentally investigated, and confront both empirical and conceptual problems.

Emotions, while ubiquitous across species and one of the most common topics of conversation, are still, it seems, misunderstood.

Do emotions have biological roots and, if so, where? And how do physiological factors influence how emotions are felt, expressed, and understood?

For Ralph Adolphs and David J. Anderson, developing a comprehensive science of emotions began with trying to create a framework that is scientifically rigorous, inclusive, cumulative, and yet provides clear operationalization of the relevant concepts of emotions.

Their new book, The Neuroscience of Emotion: A New Synthesis, offers a new way to understand emotions, one that will leave you thinking differently about how emotions work and why they are so important.

“If you are most people, you feel convinced that, because you have emotions, you know a lot about what emotions are, and how they work. We believe you are almost certainly wrong,” write Adolphs and Anderson.

We wrongly assume many things about emotion, and gaining insight into emotion means moving past these assumptions. For one thing, there are many more than four primary emotions, and they are not irreducible.

The authors address this, saying, “There is scant evidence that “joy”, “fear”, or “anger” are irreducible and do not share component parts. Equally plausible is an alternative view in which each of these emotions is made up of a collections of components, or building blocks, some of which are shared by other emotions.”

What neuroscience offers is a way to understand what underlying mechanisms generate emotions, and further, to explain them through their underlying mechanisms.

One example is the feeling of disgust, which the authors explain evolved to help animals avoid poisonous or contaminated food.

Emotions, however, go much further than the reflex-like reaction to a noxious food. Often overlapping with other states, such as motivation, arousal, and drive, emotions serve as adaptive functional states that lie somewhere between reflexes, volitional, and deliberate action.

One way to understand emotions more clearly is to separate them into two classes: building blocks of emotions and features of emotions.

“All emotion states have most of the building blocks, and we can find precursors to emotions states in simpler organisms that already show many of the properties of building blocks. Features, on the other hand, are more elaborated, derived, and variable properties of emotions, and not all emotions have them,” write Adolph and A Anderson.

Emotion states can also be related to one another and integrate information from multiple sources over time. One example is what is known as the “drift-diffusion” model, which describes how we reach a decision threshold depending on how rapidly sensory information is accumulated.

Emotions, however, are not generalizable. The authors write, “Given the highly varied and multimodal sensory inputs that can carry information relevant to a particular emotion (for example, predictors of a threat that could induce a state of fear) there is no simple formula that determines which stimuli cause an emotion, let alone which stimuli cause one type of emotion rather than another.”

Similarly, studying emotions means distinguishing between emotion states, called internal brain states, and feelings, the conscious and subjective experience of those emotions.

While we might not agree on whether animals have feelings, we can study their emotion states to help us better understand the function of our own emotions.

The authors write, “Darwin believed, and we agree, that emotional expression (whether produced in the face, the body, or both) was an evolutionary conserved function, and that its particular manifestations in different species provide insights to how emotions evolved.”

Asking questions like: Do flies engage in sex because it is rewarding or reinforcing to them, or simply because they are genetically programmed to do it?, will help us better understand the internal states of motivation, arousal, and drive, as well as our own subjective feelings of love, lust, anger, and rage.

Separating emotion states from the conscious experience of feelings also helps us understand how sensory stimuli can go undetected and still induce an emotion. One example the authors give is fear conditioning in humans, where conditioned autonomic responses emerge which is a form of emotional learning.

Shedding light on the often misunderstood topic of emotions, The Neuroscience of Emotion: A New Synthesis offers a truly scientific approach to understanding emotions, one that is as thought provoking as it is comprehensive.

Claire Nana, Psych Central

The Neuroscience of Emotion: A New Synthesis

Ralph Adolphs and David J. Anderson.

PREFACE

Emotions are one of the most apparent and important aspects of our lives, yet have remained one of the most enigmatic to explain scientifically. On the one hand, nothing seems more obvious than that we and many other animals have emotions: we talk about emotions all the time, and they feature prominently in our literature, films, and other arts. On the other hand, the scientihc study of emotions is a piecemeal and confused discipline, with some views advocating that we get rid of the word emotion altogether.

If you ask scientists, even those in the field, what they mean by an emotion, you will either get no explanation at all or else several quite discrepant ones that seem to be referring to quite different phenomena. We aim to provide a fresh look at emotion from the perspective of biology, a perspective that can provide a foundation for the field from which to move forward in a productive, cross-disciplinary fashion.

Emotions and feelings have been the topic of countless books, some of them detailed technical books (often a collection of chapters from many different authors), and most of them popular books focused on the psychology of emotion. Ours is none of these. It is not intended as a textbook, a popular book, or a monograph of any sort. Instead, our aim in writing this book was to take stock of the field, from a fairly high level perspective, to provide a survey of the neurobiology of emotion, and, most importantly, to provide both a conceptual framework and ideas for approaches that could be used by a neuroscience of emotion going forward.

Our intended audience is any educated reader, but our core audience is students and researchers who are contemplating going into the field of affective neuroscience, or who are already in the field and wondering what path their research should take. We also hope that at least a good part of the book would be accessible and interesting to readers who do not have a strong scientific background. Indeed, it is entirely possible to glean most of the conceptual framework just from reading chapters 1-4 and chapter 11, and skipping some of the more detailed chapters in the middle.

We decided to eschew detailed citations of the papers behind every point and study that we describe, instead choosing to give a more broadly accessible treatment that only cites the most important key papers or reviews (which, in turn, will provide interested readers with a longer list of further references).

Our book differs from most other books on emotion in scope and organization. One of us (Adolphs) investigates emotion in humans; the other (Anderson) investigates emotion in mice and flies. This breadth of different backgrounds, and the presentation of the different species studied, is a critical ingredient of this book, since it forced us to abstract from many details in order to uncover fundamental principles that would cut across different approaches and different species. It also meant that neither one of us is in fact the authority for all of the book: notwithstanding extensive discussions, comments, and cowriting, there are parts of the book that have only one of us as the principal author and expert. Indeed, there are parts of the book on which we continue to disagree!

We do not intend to provide a comprehensive new theory of emotion. Indeed, we don’t feel that we provide any kind of theory of emotion at all. Instead, we describe ways that scientists should think about emotion, and ways that they should use the word emotion consistently in their science, in order to forge a neuroscience of emotion with the maximal long-lasting impact. Our intent was to provide a framework for investigating emotions that would be applicable to those working in animal models; those working with human subjects; those using functional magnetic resonance imaging (fMRI), electrophysiology, optogenetics, or clinical populations. We even hope that what we have written here would be useful to engineers who are trying to figure out how to build robots that have emotions. In our view, a science of emotion needs to meet two criteria: it should be comprehensive and it should be cumulative.

Forging a comprehensive science means that the encapsulation often evident in papers, journals, and meetings on emotion needs to be overcome. Scientists studying emotion in rats and in humans need to be able to speak to one another, rather than build walls that isolate their research enterprise from the rest. A comprehensive science of emotion also needs to connect with all domains of science that are relevant to emotion: it needs to connect with psychology and with neurobiology. Doing this requires a consistent terminology that makes principled distinctions, and that allows clear operationalization of the different concepts that a science of emotion will use.

We spend some time in the first three chapters articulating such distinctions and outlining the features of emotion that a scientist would look for, whether she is studying emotion in humans, rodents, or flies. This approach necessitates some terminological commitments, and we explain these in the early chapters. We also return to them when we compare our view to some of the many other theories of emotion out there, in chapter 10.

A high-quality science of emotion requires not only clear terminology and operationalization of concepts, it also requires sensitive measures, statistically robust analysis tools, and creative hypotheses. The later chapters take up these issues in the context of a survey of ongoing neuroscience studies. Taken together, these ingredients would enable a cumulative science of emotion, a science in which current studies can build on prior work, and in which the accumulation of many studies over time allows comparisons and contrasts, as well as syntheses and formal meta-analyses. We are currently a long way from having achieved this. Indeed, most meta-analyses of emotion are either extremely narrow, or else hopelessly inconclusive because they mix studies with very different standards or terms.

There is no question in our minds that emotions are real phenomena that need to be explained. We believe that, in addition to humans, many other animals have emotions, both of the authors of this book have cats as pets, and we are convinced that they have emotions. However, intuition and belief are not the same as scientific knowledge, and an important goal of the book is to suggest objective criteria to apply in searching for cases of emotional expression in animals.

Finally, we also believe that emotions are states of the brain, and that the mechanisms that generate emotions can be investigated with neurobiology. Our book is based on these underlying assumptions; we summarize them again in the very last chapter.

CHAPTER 1

What Don’t We Know about Emotions?

“The greatest enemy of knowledge is not ignorance, it is the illusion of knowledge.” Ralph J. Boorstin

If you are like most people, you feel convinced that, because you have emotions, you know a lot about what emotions are, and how they work. We believe you are almost certainly wrong. In the Field of emotion, as in most fields, familiarity is not the same as expertise. After all, you have a heart, but that doesn’t make you an expert on hearts. You leave that to your cardiologist.

Yet the science of emotion is fraught with this problem: everyone seems to think they know what an emotion is. This is because we all have strong, and typically unjustified, intuitive beliefs about emotions. For instance, some people are absolutely certain that animals have emotions; others are absolutely certain that animals could not have emotions. Neither camp can usually give you convincing reasons for their beliefs, but they stick to them nonetheless.

We cannot emphasize enough the pervasive grip that our commonsense view of emotions has on how we (that is, researchers in the field) frame our scientific questions. We need to free ourselves of our commonsense assumptions, or at least question all of them, if we want to ask the right questions in the first place. This chapter introduces the topics of this book through this important premise and concludes by listing what we ideally would want from a mature science of emotion, and what entries in this list we will tackle in this book.

We wrote this book for two overarching aims. The first aim is to motivate the topic of emotion, to note that it is of great interest not only to laypeople but also to many scientific fields of study, and that it is a very important topic as well. At the same time, we emphasize that we currently know remarkably little about it yet, in particular, we know a lot less than we think we know. This is good news for scientists: there is work to be done, interesting and important work.

The second aim is to provide a summary of what we do know and to sketch a framework within which to understand those empirical findings and within which to formulate new questions for the future. This process is in practice very piecemeal: we need to have a little bit of data even to begin thinking about what emotions are, but then we discover problems with the way prior experiments were done and interpreted.

In the dialectic of actual scientific investigation, both conceptual framework and empirical discovery are continuously revised, and inform each other. However, we have not written our book this way. Instead, we begin with some of the foundations for a science of emotion (chapter 2), what kinds of ontological and epistemological commitments it requires, what kind of structure an explanation takes, and then work our way toward a list of features or properties of emotions (chapter 3), which then finally are the things we look for, and discover, through empirical research (chapters 4-9). We return to the foundations and the questions again in chapters 10 and 11 by contrasting our views with those of others, and by suggesting some experiments for the future.

Emotions According to Inside Out

What is it about emotions that we would like to understand? And what do we think we understand, but in fact don’t (or are mistaken about)? Because emotions are ubiquitous in our lives, and integral to our experience of the world, it is dangerously easy to come up with simplistic views that do not stand up to closer scrutiny, and instead impede scientific progress because they create “the illusion of knowledge.”

The film Inside Out, which won the 2016 Academy Award for Best Animated Feature, as well as a Golden Globe, provides a good example of many common but incorrect assumptions about emotion. As you watch the film, you get a fanciful view of how emotions are supposed to work inside a twelve year old girl, how those emotions are supposed to be integrated with memory and personality, and how they are supposed to be expressed as behavior.

If Inside Out’s view of emotion were right, you would be tempted to conclude that we understand an enormous amount about how emotions work, and, more generally, about how the mind and brain work. But Inside Out’s view of how emotions work is wrong. In examining what, exactly, is wrong with it, we can highlight some of the gaps in our current understanding of emotion. If you’ve seen the film and you already find the view of emotion portrayed by Inside Out silly, you are ahead of the game, but bear with us as we use it as an example for uncovering problematic beliefs about emotion.

Inside Out’s view of emotion takes as its starting premise the idea that all our emotions boil down to a few primary ones: in the film, they are joy, anger, fear, sadness, and disgust. These five emotions are animated as different characters, charming little homunculi that live in the brain of the little girl and fight with each other for control of her behavior and mental state. These homunculi sit at a control panel and watch the outside world on a screen. They react to the outside world, and in response they manipulate levers and switches that control the little girl’s behavior. They are also affected by memories that are symbolized by transparent marbles; moreover, a series of theme parks provide a mental landscape symbolizing different aspects of the girl’s personality. The five emotion characters fight over access to the memory marbles and struggle to keep the girl’s theme park attractions open for business.

From the film’s point of view, the five emotions are the dominant force controlling the little girl’s thoughts, memories, personality, and behavior; thinking, reasoning, and other cognitive activities are relegated to a sideshow. Truly, the little girl is an entirely emotional being. These details of the movie may not represent the way you think about emotions, but they characterize how many people do.

So what’s wrong with the film’s creative, engaging metaphor? Let’s unpack a few of the key ideas about emotions that Inside Out showcases, highlight the errors in their underlying assumptions, and try to articulate the scientiiic questions that they raise. Although science may not yet have the answers, the exercise will help us frame the issues.

Idea 1. There are a few primary emotions. The prevailing view, enshrined in many psychology textbooks, is that there is a small set of “primary” or “basic” emotions: as we already mentioned, these are joy, anger, fear, sadness, and disgust, according to Inside Out.

Different scientific emotion theories offer a big range in the number of basic emotions, anywhere from two to eleven! A second type of emotion is often called “social” or “moral” emotion and typically includes shame, embarrassment, pride, and others. These social emotions are thought to be more essentially tied to social communication than the basic emotions are. But although there are multiple schemes, many classic emotion theories tend to share the idea of a fixed, and relatively small, set of emotions that correspond to the words we have for emotions in English.

The idea of a small set of basic emotions was most notably introduced by the psychologist Paul Ekman, based largely on data from his studies of emotional facial expressions in humans. Ekman argued that facial expressions of basic emotions can be recognized across all human cultures (Ekman 1994); he studied them even among tribes in New Guinea. Ekman’s set of basic emotions includes happiness, surprise, fear, anger, disgust, and sadness (although contempt is also sometimes included).

The neurobiologist Jaak Panksepp similarly proposed a set of basic emotions, derived from his observations of animal behavior: seeking, rage, fear, lust, care, panic, and play (Panksepp 1998).

These emotion theories have much to recommend them and stimulated entire lines of important research. But they also suggest two questionable background assumptions (which Ekman and Panksepp themselves may or may not have held).

Questionable assumption 1: Emotions (at least the “primary” ones) are irreducible. A presumption that often accompanies the idea of a small set of primary emotions is that they are irreducible units. According to this assumption, emotions like “fear” or “anger” cannot be broken down into further components that are still emotional. The psychologist Lisa Feldman Barrett has argued strongly against this assumption, pointing out that it requires belief in some kind of mysterious “essences” of emotions, the belief that there is something irreducible that makes each primary emotion the emotion that it is (Feldman Barrett 2017a). This central assumption underlies the representation of each of the primary emotions in Inside Out as a distinct character.

“Joy” and “fear” do not merge with each other; they are each unique individuals. They have stable, fixed identities and functions, and do not share components (for example, in the movie’s metaphorical language, they do not share internal organs, limbs, and such).

Yet there is scant scientific evidence that “joy,” “fear,” or “anger” are irreducible and do not share component parts. Equally plausible is an alternative view in which each of these emotions is made up of a collection of components, or building blocks, some of which are shared by other emotions. Initial doubts such as these lead to the following set of scientific questions that can serve as a starting point for further investigation:

“Are different emotion states composed of features or dimensions that are shared, to variable extents, across multiple emotions? Are some emotions composed of, or based on, combinations of other more basic emotions?”

Questionable assumption 2: the primary emotions correspond to those for which we have names in English.

Related to questionable assumption 1 is the idea that words like anger,” and so forth in fact pick out scientifically principled categories of emotion. It is easy to see why this is unlikely to be the case. For one, we had these words for emotions long before there was any science of emotion, so why would one expect them to align well with scientific emotion categories? For another, different cultures have different words for emotions, and many of these turn out to be extraordinarily difficult to translate. In German, the word “Schadenfreude” denotes the emotion we feel when we feel happy about somebody else’s misfortune. Should that be a primary emotion, just because there’s a common word for it in German? There are many more such examples, entertainingly cataloged in Tiffany Watt Smith’s book, The Book of Human Emotions (Smith 2016). This poses some important scientific questions:

“How should we taxonomize emotions? How many emotions are there, and what names should we give to them? Are there different emotions in different cultures? Are there different emotions in different species? Can we use a word like ‘fear’ to refer to the same type of emotion state in a person, a dog, and a cat? How and when in evolution did emotions first arise, and how did they diversify?”

Given how little we yet know about these questions, and given that there are good reasons to believe our current emotion categories (“happiness,” “sadness,” and such) will need to be revised, we will say little in this book about specific emotions. We will refer to some emotions (notably “fear”) by way of example. And we will sketch how a future science of emotion might give us better categories or dimensions by which to taxonomize emotions. But this book is primarily about emotions in general, not about specific emotion categories.

Idea 2. Emotions are rigidly triggered by specific external stimuli. In the film Inside Out, all five emotion characters sit lazily around the control panel watching a screen that projects the outside world into the little girl’s mind, and are aroused into action only when an appropriate stimulus or circumstance appears. In the film, some stimuli do not activate a given emotion at all (for example, the “anger” character often sits dozing in his chair and does not react unless something maddening happens to the girl), while other stimuli activate multiple emotions. If the depiction from the film were accurate, we could easily figure out the emotion states of other people (and presumably other animals) by a straightforward list of rules that link specific stimuli to specific emotions in a characteristic and inflexible manner. This picture assumes that emotions are far simpler and more automatic than we in fact now know them to be. According to Idea 2, emotions would be just like reflexes. Some things will make you happy, others will make you sad, and some will trigger a specific mix of emotions, according to a set of rules.

Questionable assumption 3. Emotions are like reflexes. The movie gets it right that emotions are often triggered by stimuli in our surroundings. But what determines which emotions are triggered by which stimuli and under which circumstances? Why would seeing a dog trigger only a minimal emotional response in some people, and strong fear or happiness (emotional responses of opposite valence) in others? What accounts for the extraordinary flexibility with which many different stimuli, depending on the context and depending on the person, can elicit emotions? One can pose the following scientific questions:

“What determines whether an external stimulus will evoke an emotion or not, and what determines the kind of emotion evoked? What role do development and learning play in determining an organism’s response to a given stimulus? How does this process differ from simpler stimulus-response mappings, such as a reflex?”

Idea 3. Emotions control our behavior. The film portrays the emotion characters as controlling the little girl’s behavior by operating joysticks on the control panel. The little girl is but a hapless puppet, with emotions determining her behavior. This central visual metaphor encapsulates the title of the movie: our behavior is controlled, from the “inside out,” by our emotions. This feature is the counterpart to 2 above, with respect to the behavioral output rather than the stimulus input.

Questionable assumption 4. Specific emotions cause fixed and specific behaviors. Our subjective experience of emotion leads to the intuition that our emotions cause our behavior: I cry because I feel sad. Yet not all emotion theorists agree with this assumption. Indeed, the nineteenth-century American psychologist William James argued, counterintuitively, that emotions are a consequence, not a cause, of behavior: I feel afraid because I run from the bear, I do not run because I feel afraid (James 1884). Yet James already had doubts that just observing bodily reactions was sufficient to identify specific emotion categories. If it were true that specific emotions cause fixed and specific behaviors, we could infallibly deduce a person’s emotions just from watching their behavior. If so, then taken together with questionable assumption 3, we wouldn’t need emotions at all to explain behavior, there would simply be a set of rules linking stimuli to behavior.

That was the view that behaviorism advocated in the earlier twentieth century. One reason for the demise of behaviorism was that people realized that mappings from stimuli to behavior were far too complicated, and too dependent on context, inference, and learning, to be formulated as rules.

Emotions, in our view, are internal states that afford a flexible mapping to behavior, as we will detail throughout this book.

This leads to the following scientific questions: “Do internal emotion states cause behavior, or are they merely an accompaniment to behavior? Or might emotions actually be a consequence of behavior? What exactly are the causal links between stimuli, emotions, and behavior? How could we identify emotions in the absence of behavior? After all, we can be angry without punching somebody or showing any other easily detectable behavior.”

Idea 4. Different emotions are located in different, discrete brain regions. The beguiling picture of emotions as walking, talking cartoon characters in Inside Out is closely aligned with the belief that different emotions must correspond to anatomically distinct modules in the brain. Is there a place in the brain for fear, for example? This is a question that has received a lot of attention, including serious scientific investigation!

Questionable assumption 5. Specific emotions occur in specific brain structures. The era of functional neuroimaging with fMRI, as well as the study of patients with focal brain lesions, has led to the idea that emotions are generated in localized brain structures. For example, findings on the amygdala (a brain region studied in both of our laboratories to which we will return in some detail in later chapters) have led to the popular view that “fear is in the amygdala.” Yet more recent work clearly shows that this view cannot be right; indeed, that it does not even make sense, and that emotions depend on a much more distributed set of brain regions. This leads to the following scientific questions:

“How is the processing of emotion carried out across the brain? Are there identifiable functional neural substrates that organize or implement specific emotion states? Or is any given emotion state produced in such a highly distributed manner that it is impossible to assign a function in emotion to any brain region or neuronal cell population? Would it ever be possible to predict what emotion an individual is experiencing purely by examining activity in his/her brain ?”

As we will explain later, modern neuroscience approaches have given us a view of brain function that reconciles a dichotomy inherent in these questions. It will turn out that there are no macroscopic brain structures dedicated specifically to emotions (fear is not “in the amygdala”), but that there is specificity nonetheless. The specificity is at the level of circuits and cell populations, a level of organization that requires modern neuroscience tools to visualize. We spend some time in chapters 4 and 5 explaining these neuroscience tools, since their logic is required to reformulate the questions about emotion.

Idea 5. Emotions are conscious homunculi. The movie illustrates beautifully the idea that the brain is a machine with a little person (or persons) inside, who views the outside world, reacts to it, and then transfers those reactions to us. In other words, our subjective experience of emotion is created and embodied by the subjective experience of a miniature version of ourselves in our brain, a so-called homunculus. (As an aside, it is also interesting that this view, of little emotion homunculi within ourselves, to some extent relieves us of full responsibility for our emotional behavior, as when we say, “my anger made me do it.”)

Questionable assumption 6. Emotions are purely subjective experiences. How the brain creates an internal representation of the external world, and translates that representation into thoughts, feelings, and action, is a central open question in neuroscience. We know for sure that there is no little person sitting inside the brain looking at a screen and pulling on joysticks. The only things that have access to the patterns of neuronal activity in the brain are other neurons in the brain. How neurons “decode” the information represented by other groups of neurons and pass that information on to yet further groups of neurons so as to organize and express thoughts, emotions, and actions, is a deep mystery that we are far from solving.

This leads to the following scientific questions:

“How exactly do emotions arise in the brain? Can we separate the subjective, conscious experience of emotions from the existence of emotion states per se? Do emotions always have to be conscious? If so, how should we study them in animals, who may or may not be conscious and, in any case, cannot tell us how they feel?”

As we elaborate in the next section, we believe it is critical to distinguish between emotions as internal functional states, and conscious experiences of emotions (often called “feelings”). Emotions and feelings are not the same thing, although they are of course closely related. Most of this book is about emotions, not about feelings. We review some of the work on feelings near the end of this book.

The fallacy of the homunculus.

A homunculus, literally “little person,” refers to the idea that inside your brain there is a separate observer, something that can watch and interpret the activity of all the other brain regions in the same way that an external scientist might be able to record from your brain and make sense of its processing.

The idea of a homunculus has a long history in psychology and the philosophy of mind. It fundamentally arises from a confusion between different levels of description. On the one hand, we know that humans and animals have emotions (and many other mental states). On the other hand, we know that these mental states are produced by the brain. It is therefore tempting to conclude that emotions must literally be found in the brain if we only look with sufficiently microscopic tools.

But producing emotions is not the same as having an emotion. By analogy, there are many places in the brain that participate in producing vision, from the retina to the thalamus, to the cortex. But you cannot find vision in any one of these regions, nor does any of them have the experience of seeing. Or to take one more example: you can drive a car. So who or what does the driving? You can no more be driving by yourself (without a car) than a car can drive by itself (unless perhaps it’s a self-driving car). And you can’t take apart the car to look for where the “driving” really is located. Driving, vision, and emotion are system properties: they are not properties of any of the constituent parts, but all the parts work together to generate the property.

The most common aspect of emotion where a homunculus fallacy often arises is with respect to the conscious experience of emotion (or, for that matter, the conscious experience of anything else). Unlike the little characters that Inside Out put inside the mind of a girl, there are no homunculi in the brain for experiencing your emotions. There are brain systems that make you have a conscious experience of emotion. But the conscious experience of the emotion is a global property of a person (or animal), and the mechanisms whereby it is produced do not themselves have that property.

Toward a Science of Emotion

Without further reflection, it might seem that it should be straightforward to investigate emotions, and to discover how emotions work in the brain. But the assumptions and questions sketched in the first part of this chapter show us that a science of emotion faces some difficult challenges looming ahead. A science of emotion needs to examine most of our initial intuitions about emotions, sharpen vague questions so that they can be experimentally investigated, and confront both empirical and conceptual problems.

Let’s take a closer look at one of the major sources of conceptual confusion in emotion science. There is an assumption that different words, concepts, or types of data must refer to distinct things. We will argue instead that one and the same thing can be described with very different words and measured with very different types of data. Consider the thought provoking image on the next page (figure 1.1), produced by neuroscientist Rebecca Saxe at MIT and published in Smithsonian Magazine (December 2015).

Saxe got a mother and her infant child to go into an MRI scanner and obtained these images showing their brains. Saxe writes:

“While they lie there, the scanner builds up a picture of what’s inside their skulls. Often MRimages are made for physicians, to find a tumor or a blocked blood vessel. Scientists also make the images, to study brain function and development. In my lab, at MIT, we use MRI to watch blood flow through the brains of children; we read them stories and observe how their brain activity changes in reaction to the plot. By doing so, we’re investigating how children think about other people’s thoughts.

To some people, this image was a disturbing reminder of the fragility of human beings. Others were drawn to the way that the two figures, with their clothes and hair and faces invisible, became universal, and could be any human mother and child, at any time or place in history. Still others were simply captivated by how the baby’s brain is different from his mother’s; it’s smaller, smoother and darker, literally, because there’s less white matter. Here is a depiction of one of the hardest problems in neuroscience: How will changes in that specific little organ accomplish the unfolding of a whole human mind?

As for me, I saw a very old image made new. The Mother and Child is a powerful symbol of love and innocence, beauty and fertility. Although these maternal values, and the women who embody them, may be venerated, they are usually viewed in opposition to other values: inquiry and intellect, progress and power. But I am a neuroscientist, and I worked to create this image; and I am also the mother in it, curled up inside the tube with my infant son.”

As you were reading the above quote, you probably felt a tension between the colder, internal glimpse of two physical bodies shown in the MRI scan and your realization that these are two real people engaged in an affectionate emotional behavior. The MRI scan shows only tissue contrast, revealing bones, fluid, muscle, and brain. At the same time, we know that this is a mother and child, they are people, with thoughts and emotions. Both our everyday view of people and the view made possible with the MRI are of the same thing.

This is perhaps the most critical realization for a science of emotion (indeed, for a science of the mind in general). You can feel emotions. You can infer that other people are having emotions from their behavior. And you can image and record traces of emotions in the brain. These are very different types of data, very different sources of evidence about an emotion. And indeed, they need to be kept separate if one is studying them in their own right, as we shall see, feeling an emotion, having an emotion state, and attributing emotions to another person engage distinct processes in your brain. Nonetheless, your experience of your own emotion, your attribution of an emotion to another person you might see laughing or crying, and the neuroscientist’s investigation of an emotion from neurobiological data are not about three different things. They are ultimately all about one and the same thing, an emotion state. You can infer the emotion state in another person from observing their behavior, you can investigate the neural mechanisms of the emotion state through neuroscience experiments, and the emotion state may cause you yourself to have a conscious experience of the emotion. The behavioral observation, neurobiological measurement, and personal experience each can provide evidence for one and the same thing: an emotion state.

To flesh this out a little further, let’s view emotion from four different perspectives: the perspective of the behavioral biologist who might be carefully watching the behavior of an animal in the wild or the laboratory (or, for that matter, watching the behavior of a human being); the psychologist concerned with having people talk about and rate their conscious emotional experiences; the psychologist measuring emotional responses in the body, such as changes in heart rate or facial expression (common approaches in the psychology of emotion); and the neurobiologist who is studying (or even manipulating) the function of neurons in the brain (figure 1.2). All four perspectives can be perfectly objective and have an established and agreed upon methodology, but they are rather different data and often do not use the same language to describe the concepts and methods that relate their data to emotions. Yet all four investigate emotion.

Of those four perspectives, it is especially neuroscience that can show you things you could never get from your everyday knowledge of emotions. What kind of drug will work best for curing depression? Why do some people fear dogs whereas others love them? And, first and foremost, what are the underlying mechanisms that generate emotions, how do neurobiological events in the brain cause tears to run down our face when we are in a state of sadness, and how does this emotion state change much of the rest of our behavior, our attention, our memory, our decision-making?

FIGURE 1.2. Emotions can be inferred from severalkinds of data. We regularly attribute them to ourselves based on our subiective experience; psychologists might attribute them to us based on our verbal reports of that experience. We also attribute them to other people on the basis of their overt behavior; ethologists might do the same when they observe animal behavior. We might also use additional tools, such as measures of heart rate orblood pressure in the laboratory, to infer that a person is in an emotional state, even when they do not show it in overt behavior. Finally, as neurobiologists, we might look directly into the brain in order to draw conclusions about emotions. All of these measures are parts of a science of emotion.

These and many other questions like them are important for treating psychiatric illnesses, for understanding everyday human cognition and behavior, and for understanding the cognition and behavior of other animals. You cannot get at them by just thinking about your feelings. The aim of a neuroscience of emotion should be to make transparent how and why specific emotions have the features that they do: to explain them through their underlying mechanisms (this is a topic we discuss in detail in chapter 4).

But although this book will focus on neuroscience, our hope is that our broad and functionally based approach will contribute to an integrated science of emotion, a science that investigates emotions through behavior, psychology, and neurobiology. Such a science of emotion should also aim to investigate emotions across species, from worms and insects, to mollusks and fish, to birds and reptiles, to mice and dogs, to monkeys and to people. It would identify specific instances of emotions . . .

*

from

The Neuroscience of Emotion: A New Synthesis

by Ralph Adolphs and David J. Anderson

get it at Amazon.com

The Vagus Nerve, State and Story. The Polyvagal Theory in Therapy and the Autonomic Nervous System – Deb Dana * Stimulating the pathway connecting body and brain can change patients’ lives – Zoe Fisher and Andrew H Kemp.

“The mind narrates what the nervous system knows. Story follows state.”

“Our Autonomic Nervous System fires muscular tensions, triggered by feedback signals from the external & internal world at millisecond speeds below conscious awareness. These muscles tensions fire our Thoughts.”

In her new book, The Polyvagal Theory in Therapy: Engaging the Rhythm of Regulation, Deb Dana offers a window into the inner life of a traumatized person and a way out of trauma and back to finding joy, connection, and safety through enlightening theory, rich experiential practice, and practical steps.

Developing present moment awareness and the ability to detect autonomic nervous system states opens the door for clients to experience state and story as separate experiences and ultimately reshape their nervous system.

The explanatory power of the Polyvagal Theory provides therapists with a language to help their clients reframe reactions to traumatic events. With the theory, clients are able to understand the adaptive functions of their reactions.

The hope polyvagal theory offers is that, in time, clients feel attuned to their autonomic nervous systems, develop a sense of self-compassion that allows them to see their responses as attempts at survival and not simply clinical diagnoses, and honor the innate wisdom of the autonomic nervous system to find their way back to safety, connection, and the rhythm of regulation.

In each of our relationships, the autonomic nervous system is “learning” about the world and being toned toward habits of connection or protection. Hopefulness lies in knowing that while early experiences shape the nervous system, ongoing experiences can reshape it.

The theory transforms the clients narrative from a documentary to a pragmatic quest for safety with an implicit bodily drive to survive. Through the lens of Polyvagal Theory, we see the role of the autonomic nervous system as it shapes clients’ experiences of safety and affects their ability for connection.

Polyvagal Theory demonstrates that even before the brain makes meaning of an incident, the autonomic nervous system has assessed the environment and initiated an adaptive survival response. Neuroception precedes perception. Story follows state.

The clues to a client’s present-time suffering can be found in their autonomic response history.

“The autonomic nervous system,” Deb writes, “responds to challenges in daily life by telling us not what we are or who we are, but how we are.”

Informing, guiding, and regulating our experiences, the autonomic nervous system tells us when we are safe and can proceed forward and when we are under threat and should retreat.

However, when trauma disrupts our experience, it also disrupts the autonomic nervous system, and the result is dysregulation, the interruption of the ability to feel safe.

“Trauma compromises our ability to engage with others by replacing patterns of connection with patterns of protection,” Dana explains.

Because our lived experience relies on our autonomic nervous system’s ability to detect safety, a term known as neuroception, when the autonomic nervous system becomes disrupted, it affects everything about how we move through the world, interact with those around us, and attune to ourselves and the world around us.

Yet trauma survivors are often judged by their actions. Dana writes, ”We still too often blame the victim if they didn’t fight or try to escape but instead collapsed into submission. We make a judgement about what someone did that leads to a belief about who they are.”

The polyvagal theory, however, sees every response as an action in service of survival. In trauma, safety has been threatened, and the system that helps to regain a sense of safety is no longer able to regulate, detect safety, or restore connection.

Dana writes, “If we think of trauma as Robert Macy (president of the International Trauma Center) defined it, ”an overwhelming demand placed upon the physiological human system,” then we immediately consider the autonomic nervous system.”

And because the autonomic nervous system is shaped over time through the experiences we have, we develop a habitual pattern known as a personal neural profile that then guides our actions and responses.

“We live a story that originates in our autonomic state, is sent through autonomic pathways from the body to the brain, and is then translated by the brain into the beliefs that guide our daily living. The mind narrates what the nervous system knows. Story follows state,” writes Dana.

A Polyvagal theory describes the neural experience as well as the expectations for reciprocal connection it holds. When those connections are violated, the result is what is known as “biological rudeness” and an immediate feeling of threat.

The work of the therapist using polyvagal theory is to interrupt the traumatized client’s neural expectations in positive ways.

Dana writes, “Repeatedly violating neural expectations in this way within the therapist-client dyad influences a client’s autonomic assumptions. As a client’s nervous system begins to anticipate in different ways, the old story will no longer fIt and a new story can be explored.”

Humans are social animals dependent on connection and coregulation for a sense of safety. Yet trauma makes connection dangerous and interrupts the process of coregulatory development.

While trauma can make clients feel as if they no longer need or want connection, their autonomic nervous system relies on connection, and it suffers.

“Chronic loneliness sends a persistent message of danger, and our autonomic nervous system remains locked in survival mode,” writes Dana.

Through mapping their autonomic states, clients begin to understand what triggers move them into a state of sympathetic activation and perception of danger, and what glimmers help restore them to a state of safety, hope and growth.

Developing present moment awareness and the ability to detect autonomic nervous system states opens the door for clients to experience state and story as separate experiences and ultimately reshape their nervous system.

The nervous system is relational in nature and Dana describes how therapists can help clients build their capacity for connection, reciprocity and repair: “When a rupture in the therapeutic relationship occurs, look for the moment when the work became too big of an autonomic challenge, name it for your clients, and take responsibility for the misattunement.”

Ruptures, much like trauma itself, can be opportunities for change, growth, and a deeper understanding. While the experience can feel uncertain and the path unknown, the ability to intertwine states and disrupt the all-or-nothing responses so common in trauma is crucial to experiencing play, intimacy, awe, and elevation.

The hope polyvagal theory offers is that, in time, clients feel attuned to their autonomic nervous systems, develop a sense of self-compassion that allows them to see their responses as attempts at survival and not simply clinical diagnoses, and honor the innate wisdom of the autonomic nervous system to find their way back to safety, connection, and the rhythm of regulation.

Psych Central

A BEGINNER’S GUIDE TO POLYVAGAL THEORY

Deb Dana

We come into the world wired to connect. With our first breath, we embark on a lifelong quest to feel safe in our bodies, in our environments, and in our relationships with others. The autonomic nervous system is our personal surveillance system, always on guard, asking the question “Is this safe?” Its goal is to protect us by sensing safety and risk, listening moment by moment to what is happening in and around our bodies and in the connections we have to others.

This listening happens far below awareness and far away from our conscious control. Dr. Porges, understanding that this is not awareness that comes with perception, coined the term neuroception to describe the way our autonomic nervous system scans for cues of safety, danger, and life-threat without involving the thinking parts of our brain.

Because we humans are meaningmaking beings, what begins as the wordless experiencing of neuroception drives the creation of a story that shapes our daily living.

The Autonomic Nervous System

The autonomic nervous system is made up of two main branches, the sympathetic and the parasympathetic, and responds to signals and sensations via three pathways, each with a characteristic pattern of response. Through each of these pathways, we react “in service of survival.”

The sympathetic branch is found in the middle part of the spinal cord and represents the pathway that prepares us for action. It responds to cues of danger and triggers the release of adrenaline, which fuels the fight-or-flight response.

In the parasympathetic branch, Polyvagal Theory focuses on two pathways traveling within a nerve called the vagus. Vagus, meaning “wanderer,” is aptly named. From the brain stem at the base of the skull, the vagus travels in two directions: downward through the lungs, heart, diaphragm, and stomach and upward to connect with nerves in the neck, throat, eyes, and ears.

The vagus is divided into two parts: the ventral vagal pathway and the dorsal vagal pathway. The ventral vagal pathway responds to cues of safety and supports feelings of being safely engaged and socially connected. In contrast, the dorsal vagal pathway responds to cues of extreme danger. It takes us out of connection, out of awareness, and into a protective state of collapse. When we feel frozen, numb, or “not here,” the dorsal vagus has taken control.

Dr. Porges identified a hierarchy of response built into our autonomic nervous system and anchored in the evolutionary development of our species. The origin of the dorsal vagal pathway of the parasympathetic branch and its immobilization response lies with our ancient vertebrate ancestors and is the oldest pathway. The sympathetic branch and its pattern of mobilization, was next to develop. The most recent addition, the ventral vagal pathway of the parasympathetic branch brings patterns of social engagement that are unique to mammals.

When we are firmly grounded in our ventral vagal pathway, we feel safe and connected, calm and social. A sense (neuroception) of danger can trigger us out of this state and backwards on the evolutionary timeline into the sympathetic branch. Here we are mobilized to respond and take action. Taking action can help us return to the safe and sociaI state. It is when we feel as though we are trapped and can’t escape the danger that the dorsal vagal pathway pulls us all the way back to our evolutionary beginnings. In this state we are immobilized. We shut down to survive. From here, it is a long way back to feeling safe and social and a painful path to follow.

The Autonomic Ladder

Let’s translate our basic knowledge of the autonomic nervous system into everyday understanding by imagining the autonomic nervous system as a ladder. How do our experiences change as we move up and down the ladder?

The Top of the Ladder

What would it feel like to be safe and warm? Arms strong but gentle. Snuggled close, joined by tears and laughter. Free to share, to stay, to leave . . .

Safety and connection are guided by the evolutionarily newest part of the autonomic nervous system. Our social engagement system is active in the ventral vagal pathway of the parasympathetic branch. In this state, our heart rate is regulated, our breath is full, we take in the faces of friends, and we can tune in to conversations and tune out distracting noises.

We see the “big picture” and connect to the world and the people in it. I might describe myself as happy, active, interested and the world as safe, fun, and peaceful. From this ventral vagal place at the top of the autonomic ladder, I am connected to my experiences and can reach out to others. Some of the daily living experiences of this state include being organized, following through with plans, taking care of myself, taking time to play, doing things with others, feeling productive at work, and having a general feeling of regulation and a sense of management. Health benefits include a healthy heart, regulated blood pressure, a healthy immune system decreasing my vulnerability to illness, good digestion, quality sleep, and an overall sense of well-being.

Moving Down the Ladder

Fear is whispering to me and I feel the power of its message. Move, take action, escape. No one can be trusted. No place is safe . . .

The sympathetic branch of the autonomic nervous system activates when we feel a stirring of unease, when something triggers a neuroception of danger. We go into action. Fight or flight happens here. In this state, our heart rate speeds up, our breath is short and shallow, we scan our environment looking for danger, we are “on the move.” I might describe myself as anxious or angry and feel the rush of adrenaline that makes it hard for me to be still. I am listening for sounds of danger and don’t hear the sounds of friendly voices. The world may feel dangerous, chaotic, and unfriendly.

From this place of sympathetic mobilization, a step down the autonomic ladder and backward on the evolutionary timeline, I may believe, “The world is a dangerous place and I need to protect myself from harm.”

Some of the daily living problems can be anxiety, panic attacks, anger, inability to focus or follow through, and distress in relationships. Health consequences can include heart disease; high blood pressure; high cholesterol; sleep problems; weight gain; memory impairment; headache; chronic neck, shoulder, and back tension; stomach problems; and increased vulnerability to illness.

The Bottom of the Ladder

I’m far away in a dark and forbidding place. I make no sound. I am small and silent and barely breathing. Alone where no one will ever find me . . .

Our oldest pathway of response, the dorsal vagal pathway of the parasympathetic branch, is the path of last resort. When all else fails, when we are trapped and action taking doesn’t work, the “primitive vagus” takes us into shutdown, collapse, and dissociation.

Here at the very bottom of the autonomic ladder, I am alone with my despair and escape into not knowing, not feeling, almost a sense of not being. I might describe myself as hopeless, abandoned, foggy, too tired to think or act and the world as empty, dead, and dark.

From this earliest place on the evolutionary timeline, where my mind and body have moved into conservation mode, I may believe, “I am lost and no one will ever find me.”

Some of the daily living problems can be dissociation, problems with memory, depression, isolation, and no energy for the tasks of daily living. Health consequences of this state can include chronic fatigue, fibromyalgia, stomach problems, low blood pressure, type 2 diabetes, and weight gain.

The Polyvagal Theory in Therapy: Engaging the Rhythm of Regulation

The polyvagal theory presented in client friendly language.

Deb Dana

This book offers therapists an integrated approach to adding a polyvagal foundation to their work with clients. With clear explanations of the organizing principles of Polyvagal Theory, this complex theory is translated into clinician and client-friendly language. Using a unique autonomic mapping process along with worksheets designed to effectively track autonomic response patterns, this book presents practical ways to work with clients’ experiences of connection. Through exercises that have been specifically created to engage the regulating capacities of the ventral vagal system, therapists are given tools to help clients reshape their autonomic nervous systems.

Adding a polyvagal perspective to clinical practice draws the autonomic nervous system directly into the work of therapy, helping clients re-pattern their nervous systems, build capacities for regulation, and create autonomic pathways of safety and connection. With chapters that build confidence in understanding Polyvagal Theory, chapters that introduce worksheets for mapping, tracking, and practices for repatterning, as well as a series of autonomic meditations, this book offers therapists a guide to practicing polyvagal-informed therapy.

The Polyvagal Theory in Therapy is essential reading for therapists who work with trauma and those who seek an easy and accessible way of understanding the significance that Polyvagal Theory has to clinical work.

FOREWORD

By Stephen W. Porges

Since Polyvagal Theory emerged in 1994, I have been on a personal journey expanding the clinical applications of the theory. The journey has moved Polyvagal concepts and constructs from the constraints of the laboratory to the clinic where therapists apply innovative interventions to enhance and optimize human experiences.

Initially, the explanatory power of the theory provided therapists with a language to help their clients reframe reactions to traumatic events. With the theory, clients were able to understand the adaptive functions of their reactions.

As insightful and compassionate therapists conveyed the elements of the theory to their clients, survivors of trauma began to reframe their experiences and their personal narratives shifted to feeling heroic and not victimized.

The theory had its foundation in laboratory science, moved into applied research to decipher the neurobiological mechanisms of psychiatric disorders, and now through the insights of Deb Dana and other therapists is informing clinical treatment.

The journey from laboratory to clinic started on October 8, 1994 in Atlanta, when Polyvagal Theory was unveiled to the scientific community in my presidential address to the Society for Psychophysiological Research. A few months later the theory was disseminated as a publication in the society’s journal, Psychophysiology (Porges, 1995). The article was titled “Orienting in a Defensive World: Mammalian Modifications of Our Evolutionary Heritage. A Polyvagal Theory.” The title, crafted to crypticaIIy encode several features of the theory, was intended to emphasize that mammals had evolved in a hostile environment in which survival was dependent on their ability to down regulate states of defense with states of safety and trust, states that supported cooperative behavior and health.

In 1994 I was totally unaware that clinicians would embrace the theory. I did not anticipate its importance in understanding trauma-related experiences. Being a scientist, and not a clinician, my interests were focused on understanding how the autonomic nervous system influenced mental, behavioral, and physiological processes. My clinical interests were limited to obstetrics and neonatology with a focus on monitoring health risk during delivery and the first days of life. Consistent with the demands and rewards of being an academic researcher, my interests were directed at mechanisms.

In my most optimistic dreams of application, I thought my work might evolve into novel assessments of autonomic function. In the early 1990’s I was not interested in emotion, social behavior, and the importance of social interactions on health and the regulation of the autonomic nervous system; I seldom thought of my research leading to strategies of intervention.

After the publication of the Polyvagal Theory, I became curious about the features of individuals with several psychiatric diagnoses. I noticed that research was reliably demonstrating depressed cardiac vagal tone (i.e., respiratory sinus arrhythmia and other measures of heart rate variability) and atypical vagal regulation of the heart in response to challenges. I also noticed that many psychiatric disorders seem to share symptoms that could be explained as a depressed or dysfunctional Social Engagement System with features expressed in auditory hypersensitivities, auditory processing difficulties, flat facial affect, poor gaze, and a lack of prosody.

This curiosity led to an expanded research program in which I conducted studies evaluating clinical groups (e.g., autism, selective mutism, HIV, PTSD, Fragile X syndrome, borderline personality disorder, women with abuse histories, children who stutter, preterm infants). In these studies Polyvagal Theory was used to explain the findings and confirm that many psychiatric disorders were manifest in a dysfunction of the ‘ventral’ vagal complex, which included lower cardiac vagal tone and the associated depressed function of the striated muscles of the face and head resulting in flat facial affect and lack of prosody.

In 2011 the studies investigating clinical populations were summarized in a book published by Norton, The Polyvagal Theory: Neurophysiological Foundations of Emotions, Attachment, Communication, and Self-Regulation.

The publication enabled Polyvagal Theory to become accessible to clinicians; the theory was no longer limited to the digital libraries linked to universities and research institutes. The publication of the book stimulated great interest within the clinical community and especially with traumatologists. I had not anticipated that the main impact of the theory would be to provide plausible neurophysiological explanations for experiences described by individuals who had experienced trauma. For these individuals, the theory provided an understanding of how, after experiencing life threat, their neural reactions were retuned towards a defensive bias and they lost the resilience to return to a state of safety.

This prompted invitations to talk at clinically oriented meetings and to conduct workshops on Polyvagal Theory for clinicians. During the past few years, there has been an expanding awareness of Polyvagal Theory across several clinical areas. This welcoming by the clinical community identified limitations in my knowledge. Although I could talk to clinicians and deconstruct their presentations of clinical cases into constructs described by the theory, I was not a clinician. I was limited in how I related the theory to clinical diagnosis, treatment, and outcome.

During this period, I met Deb Dana. Deb is a talented therapist with astute insights into trauma and a desire to integrate Polyvagal Theory into clinical treatment. For Deb, Polyvagal Theory provided a language of the body that paralleled her feelings and intuitive connectedness with her clients. The theory provided a syntax to label her and her client’s experiences, which were substantiated by documented neural mechanisms.

Functionally, the theory became a lens or a perspective in how she supported her clients and how she reacted to her clients.

The theory transformed the client’s narrative from a documentary to a pragmatic quest for safety with an implicit bodily drive to survive.

As the theory infused her clinical model, she began to develop a methodology to train other therapists. The product of this transition is the current book. In The Polyvagal Theory in Therapy, Deb Dana brilliantly transforms a neurobiologically based theory into clinical practice and Polyvagal Theory comes alive.

INTRODUCTION

Deb Dana

When I teach Polyvagal Theory to colleagues and clients, I tell them they are learning about the science of safety, the science of feeling safe enough to fall in love with life and take the risks of living. Polyvagal Theory provides a physiological and psychological understanding of how and why clients move through a continual cycle of mobilization, disconnection, and engagement.

Through the lens of Polyvagal Theory, we see the role of the autonomic nervous system as it shapes clients’ experiences of safety and affects their ability for connection.

The autonomic nervous system responds to the challenges of daily life by telling us not what we are or who we are but how we are. The autonomic nervous system manages risk and creates patterns of connection by changing our physiological state. These shifts are slight for many people, and, in the moments when large state changes happen, their system is resilient enough to help them return to a regulated state.

Trauma interrupts the process of building the autonomic circuitry of safe connection and sidetracks the development of regulation and resilience.

Clients with trauma histories often experience more intense, extreme autonomic responses, which affects their ability to regulate and feel safe in relationships. Polyvagal Theory helps therapists understand that the behaviors of their clients are autonomic actions in service of survival, adaptive responses ingrained in a survival story that is entered into automatically.

Trauma compromises our ability to engage with others by replacing patterns of connection with patterns of protection. If unresolved, these early adaptive survival responses become habitual autonomic patterns. Therapy through a polyvagal lens, supports clients in repatterning the ways their autonomic nervous systems operate when the drive to survive competes with the longing to connect with others.

This book is designed to help you bring Poiyvagal Theory into your therapy practice. It provides a comprehensive approach to intervention by presenting ways to map autonomic response and shape the autonomic nervous system for safety. With this book, you will learn Poiyvagal Theory and use worksheets and experiential exercises to apply that knowledge to the nuts and bolts of practice.

Section I, “Befriending the Nervous System,” introduces the science of connection and creates basic fluency in the language of Poiyvagal Theory. These chapters present the essential elements of Poiyvagal Theory, building a solid foundation of knowledge and setting the stage for work with the clinical applications presented in the remainder of the book.

Section II, “Mapping the Nervous System,” focuses on learning to recognize patterns of response. The worksheets presented in these chapters create the ability to predictably identify individual placement along the autonomic hierarchy.

Section III, “Navigating the Nervous System,” builds on the newly gained expertise in identifying autonomic states and adds the next steps in the process: learning to track response patterns, recognize triggers, and identify regulating resources. A variety of “attending” practices are presented to support a new way of attuning to patterns of action, disconnection, and engagement.

Section IV, “Shaping the Nervous System,” explores the use of passive and active pathways to tone the autonomic nervous system and reshape it toward increased flexibility of response. These chapters offer ways to engage the regulating capacities of the ventral vagal system through both in-the-moment interventions and practices that begin to shift the system toward finding safety in connection.

Through the ideas presented in this book, you will discover how using Polyvagal Theory in therapy will increase the effectiveness of your clinical work with trauma survivors. In this process, not only will your therapy practice change, but also your way of seeing and being in the world will change.

My personal experience, and my experience teaching Polyvagal Theory to therapists and clients, is that there is a “before-and-after” quality to learning this theory. Once you understand the role of the autonomic nervous system in shaping our lives, you can never again not see the world through that lens.

SECTION I

BEFRIENDING THE NERVOUS SYSTEM

“The greatest thing then, in all education, is to make our nervous system our ally as opposed to our enemy.” WILLIAM JAMES

If you do a Google search for “Polyvagal Theory,” more than 500,000 results pop up, and if you search for “Stephen Porges,” more than 150,000 results appear. Polyvagal Theory has made a remarkable journey from a relatively unknown and controversial theory to its wide acceptance today in the field of psychotherapy.

Polyvagal Theory traces its origins to 1969 and Dr. Porges’s early work with heart rate variability and his “vision that monitoring physiological state would be a helpful guide to the therapist during the clinical interaction”

(Porges, 2011a, p. 2). As Dr. Porges wrote, at that time he “looked forward to new discoveries applying these technologies to clinical populations. I had no intention of developing a theory” (p. 5). Polyvagal Theory was born out of the question how one nerve, the vagus nerve, and its tone, which Dr. Porges was measuring, could be both a marker of resilience and a risk factor for newborns. Through solving this puzzle, now known as the vagal paradox, Dr. Porges created the Polyvagal Theory.

Three organizing principles are at the heart of Polyvagal Theory.

Hierarchy: The autonomic nervous system responds to sensations in the body and signals from the environment through three pathways of response. These pathways work in a specified order and respond to challenges in predictable ways. The three pathways (and their patterns of response), in evolutionary order from oldest to newest, are the dorsal vagus (immobilization), the sympathetic nervous system (mobilization), and the ventral vagus (social engagement and connection).

Neuroception: This is the term coined by Dr. Porges to describe the ways our autonomic nervous system responds to cues of safety, danger, and life-threat from within our bodies, in the world around us, and in our connections to others. Different from perception, this is “detection without awareness” (Porges, n.d.), a subcortical experience happening far below the realm of conscious thought.

Co-regulation: Polyvagal Theory identifies co-regulation as a biological imperative: a need that must be met to sustain life. It is through reciprocal regulation of our autonomic states that we feel safe to move into connection and create trusting relationships.

We can think of the autonomic nervous system as the foundation upon which our lived experience is built. This biological resource (Kok et al., 2013) is the neural platform that is beneath every experience. How we move through the world-turning toward, backing away, sometimes connecting and other times isolating, is guided by the autonomic nervous system. Supported by co-regulating relationships, we become resilient. ln relationships awash in experiences of misattunement, we become masters of survival. In each of our relationships, the autonomic nervous system is “learning” about the world and being toned toward habits of connection or protection.

Hopefulness lies in knowing that while early experiences shape the nervous system, ongoing experiences can reshape it. Just as the brain is continually changing in response to experiences and the environment, our autonomic nervous system is likewise engaged and can be intentionally influenced.

As individual nervous systems reach out for contact and co-regulation, incidents of resonance and misattunement are experienced as moments of connection or moments of protection. The signals conveyed, the cues of safety or danger sent from one autonomic nervous system to another, invite regulation or increase reactivity. In work with couples, it is easy to observe the increased reactivity that occurs when a disagreement quickly escalates and cues of danger communicated between the two nervous systems trigger each partner’s need for protection. In contrast, the attunement of the therapist-client relationship relays signals of safety and an autonomic invitation for connection.

Humans are driven to want to understand the “why” of behaviors. We attribute motivation and intent and assign blame. Society judges trauma survivors by their actions in times of crisis.

We still too often blame the victim if they didn’t fight or try to escape but instead collapsed into submission. We make a judgment about what someone did that leads to a belief about who they are. Trauma survivors themselves often think “It’s my fault” and have a harsh inner critic who mirrors society’s response.

In our daily interactions with family, friends, colleagues, and even the casual exchanges with strangers that define our days, we evaluate others by the ways they engage with us.

Polyvagal Theory gives therapists a neurophysiologioal framework to consider the reasons why people act in the ways they do. Through a polyvagal lens, we understand that actions are automatic and adaptive, generated by the autonomic nervous system well below the level of conscious awareness. This is not the brain making a cognitive choice. These are autonomic energies moving in patterns of protection. And with this new awareness, the door opens to compassion.

A working principle of the autonomic nervous system is “every response is an action in service of survival.” No matter how incongruous an action may look from the outside, from an autonomic perspective it is always an adaptive survival response. The autonomic nervous system doesn’t make a judgment about good and bad; it simply acts to manage risk and seek safety. Helping clients appreciate the protective intent of their autonomic responses begins to reduce the shame and self-blame that trauma survivors so often feel. When offered the lens of Polyvagal Theory, clients become curious about the cues of safety and danger their nervous systems are sensing and begin to understand their responses as courageous survival responses that can be held with compassion.

Trauma-trained therapists are taught that a foundation of effective work is understanding “perception is more important than reality.” Personal perception, not the actual facts of an experience, creates posttraumatic consequences.

Polyvagal Theory demonstrates that even before the brain makes meaning of an incident, the autonomic nervous system has assessed the environment and initiated an adaptive survival response. Neuroception precedes perception. Story follows state.

Through a polyvagal framework, the important question “What happened?” is explored not to document the details of an event but to learn about the autonomic response. The clues to a client’s present-time suffering can be found in their autonomic response history.

The goal of therapy is to engage the resources of the ventral vagus to recruit the circuits that support the prosocial behaviors of the Social Engagement System (Porges, 2009a, 2015a). The Social Engagement System is our “face-heart” connection, created from the linking of the ventral vagus (heart) and the striated muscles in our face and head that control how we look (facial expressions), how we listen (auditory), and how we speak (vocalization) (Porges, 2017a). In our interactions it is through the Social Engagement System that we send and search for cues of safety. In both the therapy setting and the therapy session, creating the conditions for a physiological state that supports an active Social Engagement System is a necessary element. “If we are not safe, we are chronically in a state of evaluation and defensiveness” (Porges, 2011b, p. 14). It is a ventral vagal state and a neuroception of safety that bring the possibility for connection, curiosity, and change. A polyvagal approach to therapy follows the four R’s:

– Recognize the autonomic state.

– Respect the adaptive survival response.

– Regulate or co-regulate into a ventral vagal state.

– Re-story.

. . .

*

from

The Polyvagal Theory in Therapy. Engaging the Rhythm of Regulation

by Deb Dana

get it at Amazon.com

See also:

The Vagus Nerve. Stimulating the pathway connecting body and brain can change patients’ lives – Zoe Fisher and Andrew H Kemp.

BEING DEAD BUT YET ALIVE. The psychological secrets of suicide – Britt Mann * A Very Human Ending: How Suicide Haunts Our Species – Jesse Bering.

There’s a tipping point where the agony of living becomes worse than the pain of dying. Many of us would rather go to our graves keeping up appearances than reveal we’re secretly coming undone. We are the only species on earth that deliberately ends its own life. Depression is a secret tomb that no one sees but you, being dead but yet alive.

Statistically we’re far more likely to perish intentionally by our own hand than to die of causes that are more obviously outside of our control. In fact, historically, suicide has accounted for more deaths than all wars and homicides combined.

“Never kill yourself while you are suicidal.” Edwin Shneidman, suicideologist

The suicidal mind is cognitively distorted, and unreliable when it comes to intelligent decision making. As such, waiting out a dark night of the soul, especially if you’re a teenager, a demographic more likely to kill themselves impulsively, can yield a brighter tomorrow.
Even if the act of killing oneself could be considered rational, the “tremendous urge” to do so rarely lasts longer than 24 hours.

Understanding suicidal urges, from a scientific perspective, can keep many people alive, at least in the short term. My hope is that knowing how it all works will help us to short-circuit the powerful impetus to die when things look calamitous.

It’s that everyday person dealing with suicidal thoughts, the suicidal person in all of us, who is the main subject of this book.

American writer and research psychologist Jesse Bering was considering taking his own life before he was offered a job in New Zealand.

Bering found himself fantasising about a tree near his house in upstate New York, which had a particular bough “crooked as an elbow” that seemed a perfect place from which to hang himself.
So goes the opening anecdote in his latest book, A Very Human Ending: How Suicide Haunts Our Species.

In New Zealand, his desire to die has subsided, but the spectre of suicide still emits a “low hum” in his life. His new book explores why people decide to kill themselves, born from a need to understand his own psyche, and prompt those on the edge to think twice before stepping off.

“The best predictor of future behaviour is past behaviour, and unfortunately that’s the case with suicidal thinking and especially suicide attempts. The likelihood of me being in that state again is pretty high… I think of the book as this is me having a conversation with my future self, to talk me out of this.”

The suicidal mind is cognitively distorted, and unreliable when it comes to intelligent decision making. As such, waiting out a dark night of the soul, especially if you’re a teenager, a demographic more likely to kill themselves impulsively, can yield a brighter tomorrow.
Even if the act of killing oneself could be considered rational, the “tremendous urge” to do so rarely lasts longer than 24 hours.

Stuff.co.nz

A Very Human Ending: How Suicide Haunts Our Species

Jesse Bering

‘This book touches on some deep questions relevant to us all… A fascinating, thoughtful, unflinching meditation on one of the most intriguing and curious aspects of the human condition.‘ Dr Frank Tallis

Why do people want to kill themselves? Despite the prevalence of suicide in the developed world, it’s a question most of us fail to ask. On hearing news of a suicide we are devastated, but overwhelmingly we feel disbelief.

In A Very Human Ending, research psychologist Jesse Bering lifts the lid on this taboo subject, examining the suicidal mindset from the inside out to reveal the subtle tricks the mind can play when we’re easy emotional prey. In raising challenging questions Bering tests our contradictory superstitions about the act itself.

Combining cutting-edge research with investigative journalism and first-person testimony, Bering also addresses the history of suicide and its evolutionary inheritance to offer a personal, accessible, yet scientifically sound examination of why we are the only species on earth that deliberately ends its own life.

This penetrating analysis aims to demystify a subject that knows no cultural or demographic boundaries.

FOR THE SUICIDAL PERSON IN ALL OF US

And so far forth death’s terror doth affright,

He makes away himself, and hates the light

To make an end of fear and grief of heart,

He voluntarily dies to ease his smart.

Robert Burton, The Anatomy of Melancholy (1621)

Given the sensitive nature of the material in this book, I have not used any real names (unless otherwise stated), and I have changed physical descriptions, locations, and other features to ensure that no one is identifiable and their story is protected. This is because this is not a book about the individuals I have described, but about what we can learn from them and how they shape our lives.

1

the call to oblivion

“Just as life had been strange a few minutes before, so death was now as strange. The moth having righted himself now lay most decently and uncomplainingly composed. O yes, he seemed to say, death is stronger than I am.” Virginia Woolf, “The Death of the Moth” (1942)

Just behind my former home in upstate New York, in a small, dense pocket of woods, stood an imposing lichen-covered oak tree built by a century of sun and dampness and frost, its hardened veins crisscrossing on the forest floor. It was just one of many such specimens in this copse of dappled shadows, birds, and well-worn deer tracks, but this particular tree held out a single giant limb crooked as an elbow, a branch so deliberately poised that whenever I’d stroll past it while out with the dogs on our morning walks, it beckoned me.

It was the perfect place, I thought, to hang myself.

I’d had fleeting suicidal feelings since my late teenage years. But now I was being haunted day and night by what was, in fact, a not altogether displeasing image of my corpse spinning ever so slowly from a rope tied around this creaking, pain-relieving branch. It’s an absurd thought, that I could have observed my own dead body as if I’d casually stumbled upon it. And what good would my death serve if it meant having to view it through the eyes of the very same head that I so desperately wanted to escape from in the first place?

Nonetheless, I couldn’t help but fixate on this hypothetical scene of the lifeless, pirouetting dummy, this discarded sad sack whose long-suffering owner had been liberated from a world in which he didn’t truly belong.

Globally, a million people a year kill themselves, and many times that number try to do so. That’s probably a hugely conservative estimate, too; for reasons such as stigma and prohibitive insurance claims, suicides and attempts are notoriously underreported when it comes to the official statistics. Roughly, though, these figures translate to the fact that someone takes their own life every forty seconds. Between now and the time you finish reading the next paragraph, someone, somewhere, will decide that death is a more welcoming prospect than breathing another breath in this world and will permanently remove themselves from the popu