As you read this, 13 million American adults are struggling with depression. It looms as a pre-eminent public-health menace for the foreseeable future. The World Health Organization projects that the amount of disability and life lost to depression worldwide will, by 2030, be greater than that from war, accidents, cancer, stroke, or any other health condition besides heart disease.
Suicide, an all-too-common outcome of severe depression, surpasses car accidents as a cause of death, with the suicide rate among Americans ages 35 to 64 having risen by nearly 30 percent in just the last decade. Rates of depression are particularly epidemic among young people. A large nationwide survey, the National Comorbidity Survey Replication, which assessed lifetime depression risk in younger, middle-age, and older age groups, found that 18- to 29-years olds are already more likely to have experienced depression than those 60 and older, even though the younger people have been alive for less than half as long.
If that depressed person isn’t you, it’s surely someone you know—neighbor, teacher, doctor, friend. Walk down any street in America and you’ll need to knock on only five or six doors before finding a resident who bears depression’s burden.
Perhaps the most troubling and ironic thing about the toll of depression is that it has risen while more research and treatment resources have been poured into combating it. In fact, depression represents an $83-billion annual burden to the United States economy in lost productivity and increased medical expenses. Why aren’t we winning this fight?
I have come to believe that we are failing in part because our most fundamental idea about depression—the intuitively tidy notion that it stems from some kind of defect—is misconceived.
There are different versions of the defect model. The cognitive therapist says the deficiency lies in thoughts; the psychoanalyst locates it in childhood; the priest, pastor, or rabbi may search for it in a person’s spirit or moral code; and the psychiatrist says it’s found in a person’s brain. Pre-eminent among the defect models is the notion of the correctible chemical imbalance. We live in a biological age and this comforting idea is popular, embraced by media, patient groups, and mental-health professionals alike. It is a mind-set borne out in prescriptions filled: 27 million Americans take antidepressants.
Yet for all of the searching, in none of the defect models has the deficiency causing depression been found. There remains no biological test for depression, despite the many hundreds of physical assays available. Moreover, current treatments—though often useful—leave much to be desired. For instance, two-thirds of those who are treated with antidepressants continue to be burdened with depressive symptoms. There are 26 antidepressants on the market. But newer antidepressant medications are no more effective than those developed nearly 60 years ago.
Survey data indicate that widespread adoption of the disease model has not lifted the stigma of depression. One reason sufferers avoid getting help is that they are leery of being branded as defective. Others get help and come to internalize what they are repeatedly told—that they are deficient in some important way, an idea that is clinically unhelpful, to say the least.
There are, however, alternatives to the defect model. A new vein of research examines how depression connects to universal aspects of our psychology. More specifically, it considers how depression is a natural outgrowth of our mood system, drawing on mood science, a field that in the past 20 years has developed an increasingly sophisticated set of tools to measure mood and emotion, such as functional brain scans and miniature sensors that monitor the body in everyday circumstances.
Mood is a sensible focus, given that depression’s defining feature is a persistent low mood. The typical depressed person reports moods that are excessively dull, empty, and sad, lacking in joy, excitement, or cheer. The centrality of mood to depression is reflected in its classification as a “mood disorder.”
But where does the capacity for mood come from? Although we may experience moods as random, moods obey a variety of laws. They are an adaptation, an evolutionary legacy, which has shaped not only the physical structures of our bodies but also mental processes, including unpleasant ones like anxiety and pain.
What makes moods so effective as an adaptation is that they flexibly tune behavior to situational requirements. When a situation is favorable, high moods lead to more efficient pursuit of rewards. Reward-seeking behavior is invigorated: Make hay while the sun shines. In an unfavorable situation, low moods focus attention on threats and obstacles, and behavior is restrained: Hunker down until the blizzard ends.
Mood reflects the availability of key resources in the environment, both external (food, allies, potential mates) and internal (fatigue, hormone levels, adequacy of hydration), and ensures that an animal does not waste precious time and energy on fruitless or even dangerous efforts, like doing a mating dance when predators are lurking. Given that resources of every sort—be they time, energy, or money—are finite, expending resources on unreachable goals can be ruinous.
The distasteful and unattractive aspects of low mood, then, are not at odds with its utility. People in a low mood blame and criticize themselves, turn situations that went wrong over and over in their heads, and are pessimistic about the future. These characteristics, although uncomfortable, are also potentially useful. A keen awareness of what has gone wrong and what can go wrong again can help a person avoid similar stressors in the future. In the psychiatrist Randolph Nesse’s elegant phrase, this processing style “can prevent calamity even while perpetuating misery.”
In humans the value of low mood is put to the fullest test when people face serious situations in which current problems need to be carefully assessed. We might think of the groom who is left at the altar, the loyal employee who is suddenly fired from his job, the death of a child. If we had to find a unifying function for low mood across these diverse situations, it would be that it functions like a cocoon, a place to pause and analyze what has gone wrong. In this mode, we will stop what we are doing, assess the situation, draw in others, and, if necessary, change course.
A variety of experimental data have shown that low mood confers benefits to thinking and decision making. That lends credence to the idea that mood is part of a conservative behavioral guidance system that impels us toward actions that have been successful in the past—meaning, actions that helped our ancestors to reproduce and spread their genes. One way to appreciate why these states have enduring value is to ponder what might happen if we had no capacity for them. Just as animals with no capacity for anxiety were long ago gobbled up by predators, without a capacity for sadness, we and other animals would likely commit rash acts and repeat costly mistakes. Physical pain teaches a child to avoid hot burners; psychic pain teaches us to navigate life’s rocky shoals with due caution.
Mood is part of a behavioral guidance system that impels us toward actions that helped our ancestors to reproduce and spread their genes.
Low mood is useful on average, but like other adaptations, it is not useful in every instance. Think of the spine, which enables upright walking but also exposes us to disabling pain. Many people hold on to the idea of evolution as an inevitable ladder of progress, when, in reality, good design represents a compromise among trade-offs. For instance, a big brain makes for a smarter person but also raises the risk of the mother dying in childbirth.
Once the capacity for low mood evolved, it was inevitable that there would also be at least some severe depression. In these respects, low mood is akin to anxiety, another psychological capacity that is at once an important defense against threats and a lurking vulnerability to paralyzing conditions. As with physical traits like agility, mental traits vary among people, including temperaments that make some people more likely than others to experience prolonged low moods.
But if mood science explains the existence of depression, what explains the current depression epidemic?
Many colleagues and I think it’s due to a perfect storm: an ancient mood system colliding with a highly novel operating environment. While other mammals get depressed, human depression is worsened by our elaborate language, which can magnify wallowing, and by the sometimes self-destructive ways, like substance abuse, with which we regulate mood. Changes in the cultural environment magnify these problems. Triggers include mood-punishing routines—too much work, too much stimulation, and too little sleep—and even changes in our attitudes toward sadness. Ironically, our stratospherically high expectations about happiness have made low moods harder to bear.
We are not prisoners of evolution, of course, and the mood-science approach also contains clues as to how the depression epidemic might be better contained. Epidemiological research demonstrates that nearly all episodes of depression have an endpoint, and that nearly half of all people who have a bout with depression never have another. We carry mood vulnerabilities, but also a natural resilience.
From a treatment standpoint, the best thing about the mood system is that it is open to multiple inputs. That means help may come from many quarters. Mood can be elevated by changing how we think, by changing events around us, by changing our relationships, by changing what is happening in our bodies (by exercising or sleeping better), and by changing our brains through medications or diet. Conventional approaches to depression, by contrast—whether mainstream psychiatry or cognitive-behavioral therapy—often present only a small subset of these available levers as the sole solutions. Mood science, guided by the openness of the mood system, would suggest that sufferers not only take advantage of available treatments but also improvise, to make one’s own path to recovery.
Depression chewed up a self-assured Ivy League grad and spat out a person who spent most days lying in bed.
If this all sounds a bit abstract, it’s not. The tenets of mood science hit close to home. Before depression became my object of study, it also, many years ago, almost took my life.
In embarking on an evolutionary account of the depression epidemic, I promised to deliver a candid treatment of a difficult subject. That would have to include a story I hadn’t told my colleagues and had only hinted at to my own daughter.
Before I became a research psychologist, I was studying to become a historian and living in Baltimore, and I became severely depressed, for a long time. Over four horrific years, depression chewed up a self-assured Ivy League grad and spat out a person who spent most days lying in bed or on the floor and who could barely read a shopping list. Eventually, I would come to call my problem depression, but at the outset I thought I was dying. I had little clue about what depression was, or that it could apply to me.
I received attentive treatment from several mental-health professionals, and the full complement of psychopharmacology. Yet the depression refused to budge. I wound up being admitted to the Johns Hopkins Hospital Henry Phipps Psychiatric Service. Little by little, with more time, a supportive family, and a new career direction, I got back on my feet. I outlasted it.
As I wrote about my struggle and those of others, I had to confront my shame about having had a chronic depression and my rationalizations for why I could not tell others about it. I came clean to my colleagues and to my students. For the first time, I told my 16-year-old daughter the full extent of my travails, which happened mostly before she came into the world. Despite my anxieties about broaching the topic, the conversation was surprisingly natural and matter-of-fact. I told her about being depressed at my own wedding, depressed at her birth, depressed for her first word, her first steps. She listened intently. Toward the end she just asked me, “Are you worried it’s going to come back?” We talked about the odds, which are clearly greater than zero. She is used to me being scientific about such matters. Yet after going so many years without a recurrence, I could look her in the eye and say, “I think I’m going to be one of the lucky ones.”
Nearly two decades after my hospitalization, I reconnected with my psychiatrist. While I saw several, there was one who was special. I saw him for a few years. He really cared. He really listened. He wrote prescriptions that he really thought would help. The only problem was that nothing changed. Every week, the hollowed-out me would go to his office and try to use my words to communicate that I was still swallowed by a monster. I wanted to be a good patient. I wanted to be better. But nothing—no new drug, no change in dosage, no kind remark, no insight—made any perceptible difference. I was desperately depressed, and I felt guilty that I could not be a success for the doctor. I felt even guiltier because, despite the fact that he could not make me better, I liked him a good deal. And I thought the real me would as well.
So this past fall I reintroduced myself. I composed an email, which began: “It’s been almost 20 years since I was your patient at JHU, with a depression that would respond to nothing.” It ended: “I am writing to achieve some greater closure on what happened. You don’t need to write me back. I know you did your best with me. It was just a nasty depression that nothing could touch.”
He wrote me back. We had a phone call. I told him about how I made it out of the depression alive, that the depression closed the door on a career in history but opened one into psychology, and that I had written a book about depression. I sent him the book and he has read it. We are colleagues now.
My disclosures have been therapeutic for me personally, but I have come to believe that talking honestly about depression serves a larger social goal. Stigma has taught us not to speak of depression. It’s an impolite topic. But as a nation, we can no longer afford to be silent. The only way we can have a frank conversation that is worthy of the scientific, political, and human challenges posed by the depression epidemic is to speak freely, even if the conversation is sometimes awkward.
Too often, our scientific and public dialogue about depression has lacked imagination; we’re often asked to choose among the defect models. Much recent dialogue could be condensed to the question, “To Prozac, or not to Prozac?” From Peter Kramer to Robert Whitaker, the heated talk about the promise and peril of antidepressants has sucked the oxygen out of the room.
We have been taught to listen to Prozac, but not to depression itself. The defect models tell us there is little value in listening, that the symptoms of depression are largely noise—the static of neurotransmitters run amok.
To achieve a livelier, more open-minded conversation about depression, we need to set those models aside and share our experiences with depression. Let’s reject the defect model and its view that the legions of the depressed are a broken people, an ever-afflicted group that will likely need repeated assistance throughout their lives. If we bring depression out of the dark, maybe they won’t. Continued shame and whispers will only worsen their odds—and someday maybe yours.
Jonathan Rottenberg is an associate professor of psychology at the University of South Florida, where he is director of the Mood and Emotion Laboratory. He is the author of The Depths: The Evolutionary Origins of the Depression Epidemic, new from Basic Books. In 2013 he started the Come Out of the Dark campaign.