The psychologist Naomi Eisenberger describes herself as a mutt of a scientist. Never quite fitting the mould of the fields she studied – psychobiology, health psychology, neuroscience – she took an unusual early interest in what you might call the emotional life of the brain. As a doctoral student at the University of California, Los Angeles (UCLA), Eisenberger found it curious that we often describe being rejected in terms of physical pain: ‘My heart was broken’, ‘I felt crushed’, ‘He hurt my feelings’, ‘It was like a slap in the face’. More than metaphors, these expressions seem to capture something essential about how we feel in a way that we can’t convey directly. And you’ll find similar ones not just in English but in languages all over the world. Eisenberger wondered why. Could there be a deeper connection between physical and emotional pain?
In a landmark experiment in 2003, Eisenberger and her colleagues had test subjects strapped with virtual-reality headsets. Peering through goggles, the participants could see their own hand and a ball, plus two cartoon characters – the avatars of fellow participants in another room. With the press of a button, each player could toss the ball to another player while the researchers measured their brain activity through fMRI scans. In the first round of CyberBall – as the game became known – the ball flew back and forth just as you’d expect, but pretty soon the players in the second room started making passes only to each other, completely ignoring the player in the first room. In reality, there were no other players: just a computer programmed to ‘reject’ each participant so that the scientists could see how exclusion – what they called ‘social pain’ – affects the brain.
Physical pain involves several brain regions, some of which detect its location, while others, such as the anterior insula (AI) and the dorsal anterior cingulate cortex (dACC), process the subjective experience, the unpleasantness, of pain. In fMRI scans of people playing CyberBall, Eisenberger’s team saw both the AI and the dACC light up in participants excluded from the game. Moreover, those who felt the most emotional distress also showed the most pain-related brain activity. In other words, being socially rejected triggered the same neural circuits that process physical injury, and translate it into the experience we call pain.
At the time, this was a radical idea – and it still is. It essentially suggests that the brain makes no distinction between a broken bone and an aching heart. Rejection, it tells us, actually hurts. For Eisenberger, this overlap between physical and social pain transcends scientific interest. ‘It reveals something to people that they probably already knew but maybe were afraid to believe,’ she told Edge magazine in 2014. ‘It’s not just in our head. It is in our head because it’s in our brain.’
Since the original CyberBall experiment, a number of studies have replicated and extended its results. Researchers have found, for example, that social rejection doesn’t have to be explicit to trigger the brain’s pain mechanism: just seeing a picture of your ex-partner or even a video of disapproving faces activates the same neural pathways as physical pain does. At one point, Eisenberger and her team posed a seemingly daft question: if physical and emotional pain are related, could a painkiller relieve heartache? In the study that followed, some participants took two daily doses of Tylenol (a common painkiller) for three weeks while others took a placebo, and each group recorded their day-to-day emotions in a diary. By the end of the experiment, the Tylenol group reported less distress and showed less brain activity in the pain regions after being rejected than the placebo group.
That’s not the end of emotional pain, of course, and you can surely do better than pop a pill each time the world snubs you. Still, the Tylenol study reveals something remarkable about rejection: that it can spill beyond our emotional lives and into our physical selves. In fact, in recent years social rejection has emerged as key to a number of discoveries across psychology, neuroscience, economics, evolutionary biology, epidemiology and genetics, forcing scientists to rethink what makes us sick or healthy, why some people live long while others die early, and how social inequalities affect our brains and bodies.
According to Eisenberger, the significance of social pain goes back to evolution. Throughout history, we depended on other people for survival: they nurtured us, helped to gather food and provide protection against predators and enemy tribes. Social relationships literally kept us alive. Perhaps, then, just like physical pain, the pain of rejection evolved as a signal of threat to our lives. And perhaps nature, taking a clever shortcut, simply ‘borrowed’ the existing mechanism for physical pain instead of creating a new one from scratch, which is how broken bones and broken hearts ended up so intimately interconnected in our brains.
What’s remarkable about this connection is how even trivial slights can ‘get under the skin’, as researchers put it. During CyberBall, being ignored by people you didn’t know and couldn’t even see was enough to trigger an ancient pain response designed to keep you alive. And simply watching videos of disapproving faces produced the same effect. But what about major blows to our need to belong? Intuitively, you’d expect that, the more significant the rejection, the stronger the ensuing pain – but this is not what researchers find. It turns out that something else happens too, when we get rejected – by spouses, bosses, peers, at work, at school, at home – and it can help us understand not only our struggle for acceptance but the often longing desperation that comes with it.
In one study, he and his team divided undergraduates into groups of four to six, gave them some time to mingle, then separated them and asked each one to pick two other students as partners on the next task. Some participants were told that everyone had picked them, while others were told that no one had. In the end, when all the students rated their feelings, the rejected group showed no change in emotions: instead of feeling upset, they seemed to have become emotionally numb.
The same thing happened over and over, no matter how the researchers simulated rejection or measured emotion. They thought that perhaps the hurt feelings were there but the students felt too embarrassed to admit them. So in another experiment the participants had to rate how they felt about a fellow student who was in significant pain after a leg injury or a romantic breakup. The researchers reasoned that, even if the students couldn’t face their own emotions, they should still be able to feel for someone else. Once again, though, the socially rejected showed much less empathy, which led to the conclusion that their emotions had indeed shut down.
Baumeister calls this phenomenon ego-shock – an allusion to the physical numbness that can follow injury. Cutting yourself on a tin of tuna, for example, you might feel nothing at first; it’s as if for a brief moment your body shuts down to shield you against the pain. When you get rejected, Baumeister says, your psyche might similarly freeze up to protect you against the onslaught of emotional pain. Rejection, it seems, doesn’t always hurt; sometimes it goes beyond hurt, leaving us unable to feel anything at all.
What is identity but the slow, lifelong accretion of gazes: us looking at ourselves being looked at by others?
In one study, Baumeister asked participants to write about a major blow to their self-worth and describe their immediate reaction. Peer rejection was, by far, most frequently recounted, followed by academic and romantic rejection. Moreover, compared with minor incidents, the aftermath of major threats provoked significantly different responses in the subjects. They were more likely to become disoriented and paralysed, as well as loose their ability to think straight and make decisions. They felt removed from their bodies, as if looking at things from a distance. The world appeared to them unfamiliar and strange. This limbo state doesn’t normally last beyond a few minutes. Eventually, people collect themselves, and remember who and where they are.
However fleeting, such moments of shock, of utter unguardedness, reveal something about rejection and belonging that normally remains hidden. We are more than social animals. We don’t just live with others but also through them and in them. They place us and ground us into the world. When they see us, they identify us. After all, what is identity but the slow, lifelong accretion of gazes: us looking at ourselves being looked at by others? What we see is, largely, what they see, or what we think they see. And when they turn away, when we become unseen, in a way we cease to be.
Rejection doesn’t have to come from family, or even people you know, to do harm. Nor does it have to be particularly overt. In insidious forms, it lurks woven into the very fabric of society. In an interview for Radio Boston in 2012, Jerome Kagan, a psychologist at Harvard University, and a pioneer in child development and personality studies, said: ‘The best predictor today in Europe or North America of who will be depressed is not a gene and it’s not a measure of your brain; it’s whether you’re poor.’ Kagan’s statement echoes something researchers have long known: that poor people have poorer health. It’s an argument that makes intuitive sense. Poverty, after all, entails a host of risk factors – child maltreatment, drug abuse, crime, unemployment, bad nutrition, inadequate health care – that have been linked to various physical and mental illnesses.
But debilitating as it is, poverty doesn’t tell the whole story. In developed countries in particular, as average incomes and living standards have steadily improved, health problems have continued to beset enormous numbers of people – and not just the poor. Consider the Whitehall studies: between 1967 and 1970, the epidemiologist Michael Marmot at University College London Medical School and his team collected data on 18,000 men from the British civil service (based at Whitehall, London). After following them for 10 years, they found that unskilled workers at the bottom of the hierarchy died at about three times the rate of senior administrative staff at the top. Access to healthcare – free then as it is now – could not explain the dramatic difference in mortality between the employment ranks. What’s more, a similar pattern emerged not just at the extremes but at all levels of the pecking order: the lower your status at work, the shorter your life.
Mounting evidence over the past two decades has established low socioeconomic status as a key predictor of early mortality and poor health, including cardiovascular disease, arthritis, diabetes, respiratory illnesses, cervical cancer, schizophrenia, substance abuse and anxiety. And as with the Whitehall studies, the negative health effects extend beyond the poor to everybody on the social ladder. The link between health and social status – whether you measure it by income, education or occupation, or even by where people think they stand in relation to others – has appeared with remarkable consistency in studies of thousands of US adolescents, South Koreans, African Americans, and older adults in the UK. According to Marmot’s data, ‘if everyone in England had the same death rates as the most advantaged, a total of between 1.3 and 2.5 million extra life years would be enjoyed by those dying prematurely each year.’
Not all researchers share Marmot’s view, or his urgency. Some claim that socioeconomic status doesn’t cause ill health, but that ill people, having a harder time in school or at work, simply tend to ‘drift’ to the bottom of the social ladder. The inequality researchers Richard Wilkinson and Kate Pickett in the UK disagree. In their book The Spirit Level (2009), they argue that drift cannot explain the well-documented pattern observed between countries: namely, that more unequal societies, with presumably steeper social hierarchies and bigger status differences, exhibit worse health outcomes. There seems to be something about our social position, they say, that gets under our skin.
But what? How could your social status make you sick? Access to resources – a natural suspect – doesn’t explain the ubiquity of status effects on health. While those at the very bottom might suffer from inadequate hygiene, nutrition and health care, these factors can’t account for the health gaps found across the social ladder. The privileged might seem like a different species at times but neither their doctors nor their food and certainly not their toiletries come infused with magical properties inaccessible to most in the middle. And yet the middle suffers more depression, diabetes and early death than those in the upper echelons of society.
One possible reason, according to Wilkinson and Pickett, is ‘status anxiety’. The core insight here is that social status carries an implicit judgment of one’s value to society. The higher up the ladder you are, the more respect and admiration you command from those around you. By contrast, being lower down the hierarchy implies a failure to live up to society’s standards of success. It is to be judged as lacking and seen as inferior; in other words: to be rejected. The rejection might be implicit but, if anything, that makes it even more pernicious because it goes unquestioned: we often accept social inequality the way we inhale polluted air, or we justify it as a matter of merit. So if you find yourself near the bottom, you can feel worthless, hopeless and helpless.
The harm goes beyond emotions. A growing number of researchers now recognise that threats to our social identity, such as being negatively evaluated by others, can tamper with crucial neurobiological systems. Studies of animals in subordinate rank and people exposed to negative evaluation (for example, after giving a speech to an audience) suggestthat social rejection triggers inflammation – the body’s innate response to injury. Just as with physical threats, social ones can signal mortal danger, setting off a defensive immune attack against microbial intruders. While the process helps to fight infection, according to George Slavich, director of the UCLA Laboratory for Stress Assessment and Research, in cases of social rejection the effect can get out of hand, spiking inflammation to dangerous levels. Chronic inflammation, in turn, has been linked to diabetes, cardiovascular disease, some cancers, Alzheimer’s, arthritis, depression and others. Fuelled by the social rejection that pervades low status, it can also help to explain that elusive link between poor health and social inequalities.
The unsettling thing about social status is that it’s always relative. Where you stand on the social ladder has less to do with your actual circumstances than your comparative position in relation to everyone else on the ladder. Inevitably, this ranking produces more losers than winners, not unlike in sports, where second best is never good enough: there’s only one gold medal in an Olympics game, and everything else feels like a consolation. Here’s how Wilkinson and Pickett put it: ‘Whether people live in a shack with an earth floor and no sanitation or in a three-bedroom house with fridge, washing machine and television, low social status is experienced as overwhelmingly degrading.’
The most unequal countries had twice the levels of mental illness and obesity as the most equal ones
Climbing the ladder doesn’t necessarily solve the problem; it might just raise the bar. Say you jump a few rungs, landing at the top of your peer group. You gaze down from this new perch and think how far you’ve made it. But then you realise that your reference point has now shifted: you’ve moved up to a new social group and the top has been pushed higher. A successful venture capitalist once told me that, despite its outward glamour, Silicon Valley hides a lot of misery. His explanation: no matter how much you achieve, someone is always above you. Status, it seems, is a game you can never win because the target keeps moving, a game in which every success can also be a failure, and every winner – a loser.
Does all this mean we are doomed, bar the lucky few at the top? After all, dominance systems are how we organise social experience, whether we’re talking about bees, chimpanzees or humans. But if we can’t abolish hierarchies, perhaps we can flatten them? Wilkinson and Pickett argue that, apart from lifting the bottom, greater equality will spark a chain of positive changes across society. In one study, the two researchers measured the average income per person in 21 rich nations against an index of each country’s health and social problems, and found no connection between the two. But when they ranked the countries from the most equal (eg, Japan and the Scandinavian nations) to the least (eg, the UK, Portugal and the US), a clear pattern emerged that could not be chalked up to chance: the most unequal countries had twice the levels of mental illness and obesity as the most equal ones; three to five years lower life expectancy; six to 10 times higher teenage birthrates; up to 12 times increased incidence of homicide, and markedly lower literacy.
One way to account for the benefits of greater equality might be that it dissolves the boundaries between groups, promoting social mixing and integration. For a long time, researchers have known that socially integrated people enjoy better health and longevity than socially isolated ones, but until recently it wasn’t clear why. Was it that social relationships improved people’s health or that healthy people simply had better social lives? The data was too limited to tell until the mid-1980s, when well-designed longitudinal studies enabled scholars to track thousands of people over several decades. These rich datasets, combined with stronger theoretical frameworks, provide plenty of evidence for the damaging effects of social isolation.
In 2015, the psychologists Julianne Holt-Lunstad and Timothy Smith of Brigham Young University in Utah looked at 70 studies that collectively followed more than 3 million older adults for an average of seven years. The researchers found that social isolation increased a subject’s likelihood of being dead at the end of the study by 29 per cent. This result held true even when the researchers controlled for the participants’ initial health status. Other studies have linked social isolation to coronary heart disease, stroke, dementia and Alzheimer’s – some of the leading causes of death and disability in the world today.
Despite advances in research, it’s still unclear exactly what counts as social isolation. Usually, it’s seen as an objective deprivation, most acutely affecting the elderly as they retire, survive family members, stop driving, fall ill or become too frail to take part in social activities. Pooled data from a number of studies shows that as many as 40-50 per cent of over-80s report social isolation. However grim that figure, the flip side is that half of the very old continue to live well-integrated, healthy lives. Some of these seniors actually expand their social networks as time previously spent on work gets freed up for volunteering and socialising. Crucially, belonging to a social network gives elderly people a sense of purpose, and motivates them to take better care of themselves. By maintaining relationships or forging new ones, seniors benefit from what researchers call social support– whereby other people step up to provide information, help around the house or a shoulder to cry on, making it easier to weather difficult times. Giving rather than receiving social support is another antidote. In a study of 423 married older couples, helping out family, friends and neighbours (emotionally and in practical ways) predicted lower mortality rates five years later.
The quality of these connections counts, too. Some seniors thrive by nurturing fewer but deeper links, while others will find greater enjoyment still in solitude. Of course, none of this is to deny the deleterious effects of social isolation or question the plight of the elderly. But it does suggest a crucial difference between an objective state and subjective experience. The two are doubtless related, but being alone is not the same as feeling alone. According to Louise Hawkley, a research scientist at NORC at the University of Chicago, and the late John Cacioppo, a neuroscientist at the University of Chicago who studied this issue for more than two decades: ‘People can be a social outcast in their own minds even while living among others.’
And it is in our minds, perhaps, that rejection reveals itself at its most insidious – not in the pricks of pain it sends through our skulls, nor in the havoc it wreaks on our bodies. In the mind, rejection can live on, fed by nothing more than our own twisted imaginations. To perceive yourself as isolated means to be rejected over and over, even when in reality no one is slighting you. It is to be, at once, the one rejected and the one who rejects. This is how rejection ultimately hurts us – by making us hurt ourselves, complicit in its cruel act.
The local doctors didn’t know much about these drugs, so they asked Summerfield to explain them. When he finished, they explained that they didn’t need these new chemicals — because they already had antidepressants. Puzzled, Summerfield asked them to explain, expecting that they were going to tell him about some local herbal remedy. Instead, they told him about something quite different.
The doctors told Summerfield a story about a farmer they had treated. He worked in the water-logged rice fields, and one day he stepped on a land mine and his leg was blasted off. He was fitted with an artificial limb, and in time he went back to work. But it’s very painful to work when your artificial limb is underwater, and returning to the scene of his trauma must have made him highly anxious. The farmer became deeply depressed.
So the doctors and his neighbors sat with this man and talked through his life and his troubles. They realized that even with his new artificial limb, his old job — working in the paddies — was just too difficult, that he was constantly stressed and in physical pain, and that these things combined to make him want to just stop living. His interlocutors had an idea.
They suggested that he work as a dairy farmer, a job that would place less painful stress on his false leg and produce fewer disturbing memories. They believed he was perfectly capable of making the switch. So they bought him a cow. In the months and years that followed, his life changed. His depression, once profound, lifted. The Cambodian doctors told Summerfield: “You see, doctor, the cow was an analgesic, and antidepressant.”
In time, I came to believe that this little scene in Southeast Asia, which at first sounds just idiosyncratic, deeply “foreign,” in fact represents in a distilled form a shift in perspective that many of us need to make if we are going to make progress in tackling the epidemic of depression, anxiety, and despair spreading like a thick tar across our culture.
It’s not just about brain chemistry
For more than 30 years, we have collectively told one primary story about depression and anxiety. When I was a teenager and I went to my doctor and explained I felt distress was pouring out of me uncontrollably, like a foul smell, he told me a story.
The doctor said that depression is caused by the spontaneous lack of a chemical in the brain called serotonin, and I simply needed to take some drugs to get my serotonin levels up to a normal level. A few days before I wrote this piece, a young friend of one of my nephews, who was not much older than I was when I was first diagnosed, went to his doctor and asked for help with his depression. His doctor told him he had a problem with dopamine in his brain. In 20 years, all that has shifted is the name of the chemical.
I believed and preached versions of this story for more than a decade. But when I began to research the causes of depression and anxiety for my new book, Lost Connections, I was startled to find leading scientific organizations saying this approach was based on a misreading of the science. There are real biological factors that contribute to depression, but they are very far from being the whole story.
The World Health Organization, the leading medical body in the world, explained in 2011: “Mental health is produced socially: The presence or absence of mental health is above all a social indicator and therefore requires social, as well as individual, solutions.” The United Nations’ special rapporteur on the right to health, Dr. Dainius Pūras — one of the leading experts in the world on mental health — explained last April that “the dominant biomedical narrative of depression” is based on “biased and selective use of research outcomes.”
“Regrettably, recent decades have been marked with excessive medicalization of mental health and the overuse of biomedical interventions, including in the treatment of depression and suicide prevention,” he said. While there is a role for medications, he added, we need to stop using them “to address issues which are closely related to social problems.”
I was initially bemused by statements like this: They were contrary to everything I had been told. So I spent three years interviewing the leading scientists in the world on these questions, to try to understand what is really going on in places where despair in our culture is worst, from Cleveland to Sao Paulo, and where the incidence of despair is lowest, including Amish communities. I traveled 40,000 miles and drilled into the deepest causes of our collective depression.
I learned there is broad agreement among scientists that there are three kinds of causes of depression and anxiety, and all three play out, to differing degrees, in all depressed and anxious people. The causes are: biological (like your genes), psychological (how you think about yourself), and social (the wider ways in which we live together). Very few people dispute this. But when it comes to communicating with the public, and offering help, psychological solutions have been increasingly neglected, and environmental solutions have been almost totally ignored.
The hotly contested studies of chemical antidepressants
Instead, we focus on the biology. We offer, and are offered, drugs as the first, and often last, recourse. This approach is only having modest results. When I took chemical antidepressants, after a brief burst of relief, I remained depressed, and I thought there was something wrong with me.I learned in my research that many researchers have examined the data on antidepressants and come to very different conclusions about their effectiveness. But it’s hard not to conclude, looking at the evidence as a whole, that they are at best a partial solution.
Depression is often measured by something called the Hamilton Depression Rating Scale, a 17-item test administered by clinicians, where a score of zero means you show no symptoms of the disorder and a score of 52 would indicate an absolutely debilitating episode.
The studies that most strongly support chemical antidepressants found that some 37 percent of people taking them experience a significant shift in their Hamilton scores amounting to a full remission in their symptoms. When therapy and other interventions were added in addition to or in place of these drugs — in treatment-resistant cases — remission rates went higher.
Yet other scholars, looking at the exact same data set, noticed that over the long term, fewer than 10 percent of the patients in the study — who were, incidentally, receiving more support than the average depressed American would receive from their doctor — experienced complete remission that lasted as long as a year. When I read this, I noticed to my surprise that it fit very closely with my own experience: I had a big initial boost, but eventually the depression came back. I thought I was weird for sinking back into depression despite taking these drugs, but it turns out I was quite normal.
Steve Ilardi, a professor of psychology at the University of Kansas, summarizes the research on chemical antidepressants this way, via email: “Only about 50 percent of depressed individuals experience an initial positive response to antidepressants (and only about 30 percent achieve full remission). Of all of those depressed individuals who take an antidepressant, only a small subset — estimated between 5 and 20 percent — will experience complete and enduring remission.” In other words: The drugs give some relief, and therefore have real value, but for a big majority, they aren’t enough.
Irving Kirsch, a professor of psychology who now teaches at Harvard Medical School, was initially a supporter of chemical antidepressants – but then he began to analyze this data, especially the data the drug companies had tried to keep hidden from the public. His research concluded that chemical antidepressants give you a boost, above the placebo effect, of 1.8 points on average on the Hamilton scale. This is less than a third of the boost that you get, by some estimates, from improving your sleep patterns.
(Kirsch points out that a study recently released in The Lancet, to much media coverage, confirmed what we already knew and everyone already agreed on: that chemical antidepressants have more effect than a placebo. The more important questions are: by how much, for how long?)
And even people less skeptical than Kirsch point to this inconvenient fact: Although antidepressant prescriptions have increased 500 percent since the 1980s, there has been no discernible decrease in society-wide depression rates.There’s clearly something very significant missing from the picture we have been offered.
After studying all this, I felt startled, and it took me time to fully absorb it. Kirsch regards the 1.8-point gain he finds as clinically meaningless and not justifying the benefits of these drugs. I found his studies persuasive, but I disagree a little with this takeaway. There are people I know for whom this small but real benefit outweighs the side effects, and for them, my advice is to carry on taking the drugs.
But it is clear, once you explore this science, that drugs are far from being enough. We have to be able to have a nuanced and honest discussion that acknowledges an indisputable fact: that for huge numbers of people, antidepressants only provide either no relief or a small and temporary amount, and we need to radically expand the menu of options to help those people.
Our focus on biology has led us to think of depression and anxiety as malfunctions in the individual’s brain or genes — a pathology that must be removed. But the scientists who study the social and psychological causes of these problems tend to see them differently. Far from being a malfunction, they see depression as partly or even largely a function, a necessary signal that our needs are not being met.
Everyone knows that human beings have innate physical needs — for food, water, shelter, clean air. There is equally clear evidence that human beings have innate psychological needs: to belong, to have meaning and purpose in our lives, to feel we are valued, to feel we have a secure future. Our culture is getting less good at meeting those underlying needs for a large number of people — and this is one of the key drivers of the current epidemic of despair.
I interviewed in great depth scientists who have conclusively demonstrated that many factors in our lives can cause depression (not just unhappiness: full depression). Loneliness, being forced to work in a job you find meaningless, facing a future of financial insecurity — these are all circumstances where an underlying psychological need is not being met.
The strange case of the “grief exception” — and its profound implications
The difficulty that some parts of psychiatry have had in responding to these insights can be seen in a debate that has been playing out since the 1970s. In that decade, the American Psychiatric Association decided, for the first time, to standardize how depression (specifically, “major depressive disorder”) was diagnosed across the United States. By committee, they settled on a list of nine symptoms — persistent low mood, for instance, and loss of interest or pleasure — and told doctors across the country that if patients showed more than five of these symptoms for more than a couple of weeks, they should be diagnosed as mentally ill.
But as these instructions were acted on across the country, some doctors reported a slightly awkward problem. Using these guidelines, every person who has lost a loved one — every grieving person — should be classed as mentally ill. The symptoms of depression and the symptoms of grief were identical.
Embarrassed, the psychiatric authorities came up with an awkward solution. They created something called “the grief exception.” They told doctors to keep using the checklist unless somebody the patient loved had recently died, in which case it didn’t count. But this led to a debate that they didn’t know how to respond to. Doctors were supposed to tell their patients that depression was a brain disease to be identified on a checklist — but now there was, uniquely, one life situation where that explanation didn’t hold.
Why, some doctors began to ask, should grief be the only situation in which deep despair is not a sign of a mental disorder that should be treated with drugs? What if you have lost your job? Your house? Your community? Once you entertain the idea that depression might be a reasonable response to some life circumstances — as Joanne Cacciatore, an associate professor in the school of social work at Arizona State University, told me — our theories about depression require “an entire system overhaul.”
Rather than do this, the psychiatric authorities simply got rid of the grief exception.
Now grieving people can be diagnosed as mentally ill at once. Cacciatore’s research has found that about a third percent of parents who lose a child are drugged with antidepressants or sedatives in the first 48 hours after the death.
Once you understand that psychological and social context is crucial to understanding depression, it suggests we should be responding to this crisis differently from how we now do. To those doctors in Cambodia, the concept of an “antidepressant” didn’t entail changing your brain chemistry, an idea alien to their culture. It was about the community empowering the depressed person to change his life.
All over the world, I interviewed a growing group of scientists and doctors who are trying to integrate these insights into their work. For them, anything that reduces depression should be regarded as an antidepressant.
To know what to fight, we need to think harder about causes of mental malaise. I was able to identify nine causes of depression and anxiety for which there is scientific evidence. Seven are forms of disconnection: from other people, from meaningful work, from meaningful values, from the natural world, from a safe and secure childhood, from status, and from a future that makes sense to you. Two are biological: your genes, and real brain changes.
(It is too crude to describe these as a “chemical imbalance,” the typical shorthand today; Marc Lewis, a neuroscientist at the University of Toronto, told me it makes more sense to think of them as “synaptic pruning” — your brain sheds synapses you don’t use, and if you are pushed into a pained response for too long, your brain can shed synapses, making it harder to navigate away from dark thoughts.)
These scientists were asking: What would antidepressants that dealt with these causes, rather than only their symptoms, look like?
“Social prescribing”: a new kind of treatment
In a poor part of East London in the 1990s, Dr. Sam Everington was experiencing something uncomfortable. Patients were coming to him with depression and anxiety. “When we went to medical school,” he told me, “everything was biomedical, so what you described as depression was [due to] neurotransmitters.” The solution, then, was drugs. But that didn’t seem to match the reality of what he was seeing.
If Everington sat and talked with his patients and really listened, he felt that their pain made sense — they were often profoundly lonely, or financially insecure. He wasn’t against chemical antidepressants. But he felt that they were not responding to the underlying reasons his patients were depressed in the first place. So he tried a different approach — and ended up pioneering a fresh approach to fighting depression.
A patient named Lisa Cunningham came to Everington’s surgery clinic one day. She’d been basically shut away in her home, crippled with depression and anxiety, for seven years. She was told by staffers at the clinic that they would continue prescribing drugs to her if she wanted, but they were also going to prescribe a group therapy session of sorts. There was a patch of land behind the clinic, backing onto a public park, that was just scrubland. Lisa joined a group of around 20 other depressed people, two times a week for a full afternoon, to turn it into something beautiful.
On her first day there, Lisa felt physically sick with anxiety. It was awkward to converse with the others. Still, for the first time in a long time, she had something to talk about that wasn’t how depressed and anxious she was.
As the weeks and months — and eventually years — passed, Everington’s patients taught themselves gardening. They put their fingers in the soil. They figured out how to make things grow. They started to talk about their problems. Lisa was outraged to learn that one of the other people in the group was sleeping on a public bus — so she started to pressure the local authorities to house him. She succeeded. It was the first thing she had done for somebody else in a long time.
As Lisa put it to me: As the garden began to bloom, the people in it began to bloom too. Everington’s project has been widely influential in England but not rigorously analyzed by statisticians, who tend to focus on drug-centered treatment. But a study in Norway of a similar program found it was more than twice as effective as chemical antidepressants — part of a modest but growing body of research suggesting approaches like this can yield striking results.
This fits with a much wider body of evidence about depression: We know that social contact reduces depression, we know that distraction from rumination (to which depressives are highly prone) has a similar effect, and there is some evidence that exposure to the natural world, and anything that increases exposure to sunlight, also has antidepressant effects.
Everington calls this approach “social prescribing,” and he believes it works because it deals with some (but not all) of the deeper social and environmental causes of depression.
Economic stress can lead to depression
I searched out other radical experiments with different kinds of social and psychological antidepressants, often in unexpected places. (Some of these were not designed as antidepressants but ended up serving that purpose.) In the 1970s, the Canadian government embarked on an experiment in a rural town called Dauphin, in Manitoba. They told the population there: From now on, we are going to give you, in monthly installments, a guaranteed basic income. You don’t have to do anything for it — you’re getting this because you are a citizen of our country — and nothing you do can mean we will take this away from you. It added up to roughly $17,000 in today’s US dollars (if they had no income from other sources).
Many things happened as a result of this three-year experiment, but one of the most striking is a big fall in hospitalizations — 8.5 percent in three years, according to Evelyn Forget, a professor in the department of community health services at the University of Manitoba and the leading expert on this experiment. Visits for mental health reasons accounted for a significant part of that drop, Forget says, and visits to doctors for mental health reasons also decreased.
“It just removed the stress — or reduced the stress — that people dealt with in their everyday lives,” she says. There is evidence that if you have no control at work, you are significantly more likely to become depressed (and to die of a stress-related heart attack). A guaranteed income “makes you less of a hostage to the job you have, and some of the jobs that people work just in order to survive are terrible, demeaning jobs.”
The scientists I spoke with wanted to keep chemical antidepressants on the menu, but also to radically expand the options available to depressed and anxious people. Some interventions are things individuals can do by themselves. One is taking part in groups dedicated to rediscovering meaning in life (anything from a choir to a campaign group). Another is practicing a form of mindfulness called “loving-kindness meditation” (an ancient technique for overcoming envy in which you train yourself to feel joy not just for your friends but also for strangers and even for people you dislike).
But many of the most effective social antidepressants require us to come together to fight for big social changes that will reduce depression, like changing our workplaces to reduce the amount of control and humiliation that happens there.
As a 39-year-old gay man, I have seen how people can band together to fight for seemingly impossible goals — and win, radically reducing the amount of unhappiness gay people face. I have also seen how, in one sense, the struggle is the solution: The act of banding together, identifying that you are being mistreated, and fighting for something better restores dignity to people who felt they had been defeated.
Is there a type of depression utterly unconnected to life circumstances?
As I absorbed all this evidence over three years, a persistent question kept coming to me. Yes, there are these deep causes of depression, but what about people who have nothing to be unhappy about, yet still feel this deep despair descend on them?
There is a debate among scientists about whether there is something called “endogenous depression” — a form of despair that is triggered purely by biology. The most detailed research into this, by George Brown of the Institute of psychiatry at the University of London and his colleague Tirril Harris, in the 1970s, found that people diagnosed with this problem in fact had just as many life challenges as people whose depression was supposed to be a response to life events. (They had spent years studying how long-term stress can radically increase depression.)
This could mean that endogenous depression does not exist — or it could mean that scientists were not good at spotting the difference back then. The scientists I spoke to agreed on one thing: If the condition does exist, it affects a tiny minority of depressed and anxious people.
But I only really felt I made a breakthrough in my own thinking — in understanding the mystery of why some people seem to become depressed “for no good reason” — when, by coincidence, I started reading some feminist texts from the 1960s.
At that time, it was common for women to go to their doctors and say something like: “Doctor, there must be something wrong with my nerves. I have everything a woman could want. I have a husband who doesn’t beat me, two kids, a house, a car, a washing machine — but I still feel terrible.” Doctors would agree that they had a problem and would prescribe them drugs like Valium. (The locus of the problem only migrated from the “nerves” to the brain in the 1990s.)
Now if we could go back in time and talk to those women, we would say, “Yes, you have everything you could possibly want by the standards of the culture.”But the standards of the culture are simply wrong: You need much more than this.
In the same way, today, when people tell me they must be biologically broken because they have “everything they could want” yet they are still depressed, I say: Tell me what you have. They talk about having money, or status, or expensive consumer goods. But these are not what people need to have meaningful lives.
If I start to ask about the social and environmental factors of depression and anxiety I’ve mentioned, I have yet to find a depressed person for whom at least some are not playing out. Perhaps some of us are simply biologically broke, but the idea that a purely biological story describes the vast majority of depressed and anxious people is by now, it is fair to say, discredited.
The lesson the psychiatrist took back from Cambodia
After he had completed his work in Cambodia, and after he had heard the story about the farmer who was given a cow as an antidepressant, Summerfield returned to London, where he worked as a psychiatrist, and he realized something he had never quite seen so clearly before. He thought about when he had most helped his depressed and anxious patients. Most often, it occurred to him, it was when he helped them to get secure housing, or to fix their immigration status, or to find a job. “When I make a difference, it’s when I’m addressing their social situation, not what’s between their ears,” he told me.
Yet we have, as a society, built our responses to depression and anxiety almost entirely around changing brains, rather than changing lives. Every year we have done this, our depression and anxiety crisis has got worse. When, I began to wonder, will we learn the lesson that those Cambodian doctors understood intuitively, and that the World Health Organization has been trying to explain to us: Our pain makes sense.
Johann Hari’s latest book is Lost Connections: Uncovering the Real Causes of Depression — and the Unexpected Solutions.