How Children Succeed: Grit, Curiosity, and the Hidden Power of Character (4 page)

Midway through her second year as principal, Dozier told me that she was beginning to feel that the most important tools at her disposal were ones that didn’t have much to do with classroom instruction. In the wake of Derrion Albert’s murder, Holder and Arne Duncan pledged $500,000 in federal money to set up afterschool programs in anger management and trauma counseling at Fenger, and the school began to refer to counseling not just students but their families as well. Dozier enrolled twenty-five of her most troubled students in an intensive mentoring program. She was looking for any kind of intervention that might address what now seemed to her to be the most pressing crisis at Fenger—not her students’ academic deficits, though those remained acute and distressing, but a deeper set of problems, born out of her students’ troubled and often traumatic home lives, that made it difficult for them to get through each day. “When I came into this job, I discounted questions like ‘What families do kids come from?’ and ‘What effect does poverty have on children?’” Dozier said to me one morning. “But since I started working at Fenger, my thinking has evolved.”

2. Nadine Burke Harris

What effect does poverty have on children?
Halfway across the country, this was the question Nadine Burke Harris was asking as well. But she was a doctor, not an educator, and so she approached the question from the perspective of her patients’ physical health. Since 2007, Burke Harris had been the lead pediatrician of the Bayview Child Health Center in the Bayview–Hunters Point neighborhood of San Francisco, a bleak industrial area tucked away in the city’s southeast corner that is home to some of the city’s biggest and most violent housing projects. When Burke Harris founded the clinic, she was a recent graduate of the Harvard School of Public Health, a fresh young idealist hired by the California Pacific Medical Center, a well-funded private hospital chain, to take on a vaguely defined but noble-sounding mission: to identify and address health disparities in the city of San Francisco. Those disparities were not hard to find, especially in Bayview–Hunters Point: the rate of hospitalization for congestive heart failure there was five times as high as it was in the Marina District, a few miles away. And before Burke Harris’s clinic opened, there was only one pediatrician in private practice in a community with more than ten thousand children.

Burke Harris had studied health disparities at Harvard, and she knew what the public-health playbook said you should do to remediate them: improve access to health care, especially primary care, for low-income families. When the clinic opened its doors, Burke Harris targeted the low-hanging fruit of pediatrics, the health issues where the disparities between rich and poor children were most obvious and best understood: asthma management, nutrition, vaccinations for diphtheria and whooping cough and tetanus. And in just a few months, she made significant headway. “It turned out to be surprisingly easy to get our immunization rates way up and to get our asthma hospitalization rates way down,” she told me when I first visited her clinic. And yet, she explained, “I felt like we weren’t actually addressing the roots of the disparity here. I mean, as far as I know, no child in this community has died of tetanus in a very, very long time.”

Burke Harris found herself in a situation much like Dozier’s. Here she was, in her dream job. She had ample resources, she was well trained, she was working hard—and yet she didn’t seem to be making much of a difference in the lives of the young people she was trying to help. They were still surrounded by violence and chaos, at home and in the streets, that was clearly taking a grave toll on them, both physically and emotionally. Many of the children she saw in the clinic seemed depressed or anxious, and some of them were downright traumatized, and the stress of their daily lives expressed itself in a variety of symptoms, from panic attacks to eating disorders to suicidal behavior. She sometimes felt less like a primary-care pediatrician and more like a battlefield surgeon, patching up her patients and sending them back to war.

Burke Harris went looking for answers, and her quest took her into a new and unfamiliar conversation about poverty and adversity, one that was taking place not in public-policy magazines and at political science symposiums but in medical journals and at neuroscience conferences. Gradually, Burke Harris became convinced of what had at first seemed a radical idea: that in neighborhoods like Bayview–Hunters Point and Roseland, many of the problems we generally think of as social issues—the province of economists and sociologists—are actually best analyzed and addressed on the molecular level, down deep in the realm of human biology.

3. The ACE Study

Burke Harris’s journey began with a medical-journal article that Whitney Clarke, a psychologist on the clinic’s staff, dropped on her desk one day in 2008: “The Relationship of Adverse Childhood Experiences to Adult Health: Turning Gold into Lead.”
The author was Vincent Felitti, the head of the department of preventive medicine at Kaiser Permanente, the giant health maintenance organization based in California, and the article described the Adverse Childhood Experiences study, commonly called the ACE study, that Felitti had conducted in the 1990s with Robert Anda, an epidemiologist at the Centers for Disease Control in Atlanta. When Burke Harris read the paper, she told me, something clicked: “The clouds parted,” she said with a smile. “Angels sang. It was like that scene at the end of
The Matrix
where Neo can see the whole universe bending and changing.”

Beginning in 1995, patients enrolled in the Kaiser HMO who came in for comprehensive medical exams were mailed questionnaires asking them to relate their personal histories in ten different categories of adverse childhood experiences, including physical and sexual abuse, physical and emotional neglect, and various measures of household dysfunction, such as having divorced or separated parents or family members who were incarcerated or mentally ill or addicted. Over the course of a few years
, more than seventeen thousand patients completed and returned the questionnaires—a response rate of almost 70 percent. As a group, the respondents represented a very mainstream, middle- to upper-middle-class demographic: 75 percent were white; 75 percent had attended college; the average age was fifty-seven.

When Anda and Felitti tabulated the responses, they were surprised, first, by the sheer prevalence of childhood trauma among this generally well-off population. More than a quarter of the patients said they had grown up in a household with an alcoholic or a drug user; about the same fraction had been beaten as children. When the doctors used the data to assign each patient an ACE score, giving them one point for each category of trauma they had experienced, they found that two-thirds of the patients had experienced
at least one ACE, and one in eight had an ACE score of 4 or more.

The second and more significant surprise came when Anda and Felitti compared the ACE scores with the voluminous medical histories that Kaiser had collected on all the patients. The correlations between adverse childhood experiences and negative adult outcomes were so powerful that they “stunned us,”
Anda later wrote. What’s more, those correlations seemed to follow a surprisingly linear dose-response model: the higher the ACE score, the worse the outcome on almost every measure from addictive behavior to chronic disease. Anda and Felitti produced one bar chart after another from the data, and each one traced more or less the same shape. Along the bottom of each chart, the x-axis, the doctors plotted the number of ACEs that patients had experienced. Along the y-axis, they indicated the prevalence of a specific undesirable outcome: obesity, depression, early sexual activity, history of smoking, and so on. On each chart, the bars rose steadily and consistently from left (0 ACEs) to right (more than 7 ACEs). Compared to people with no history of ACEs,
people with ACE scores of 4 or higher were twice as likely to smoke, seven times more likely to be alcoholics, and seven times more likely to have had sex before age fifteen.
They were twice as likely to have been diagnosed with cancer, twice as likely to have heart disease,
twice as likely to have liver disease,
four times as likely to suffer from emphysema or chronic bronchitis. On some charts, the slopes were especially steep: adults with an ACE score above 6 were thirty times more likely to have attempted suicide
than those with an ACE score of 0. And men with an ACE score above 5 were forty-six times more likely to have injected drugs
than men with no history of ACEs.

The behavior outcomes, though surprising in their intensity, at least made some intuitive sense. Psychologists had long believed that traumatic events in childhood could produce feelings of low self-esteem or worthlessness, and it was reasonable to assume that those feelings could lead to addiction, depression, and even suicide. And some of the health effects that turned up in the ACE study, like liver disease and diabetes and lung cancer, were most likely the result, at least in part, of self-destructive behaviors like heavy drinking, overeating, and smoking. But Felitti and Anda found that ACEs had a profound negative effect on adult health even when those behaviors
weren’t
present. When they looked at patients with high ACE scores (7 or more) who didn’t smoke, didn’t drink to excess, and weren’t overweight, they found that their risk of ischemic heart disease
(the single most common cause of death in the United States) was still 360 percent higher than those with an ACE score of 0. The adversity these patients had experienced in childhood was making them sick through a pathway that had nothing to do with behavior.

4. The Firehouse Effect

That initial ACE study led Burke Harris to other research papers, and before long she was immersed, staying up late every night reading articles from medical journals and tracking down footnotes and references on PubMed, the online medical database. The research she compiled during those furious months of study now sits in four fat binders on the shelf of her office at the clinic. The papers within span many scientific disciplines, but most of them are rooted in two fairly obscure medical fields: neuroendocrinology (the study of how hormones interact with the brain) and stress physiology (the study of how stress affects the body). Although Anda and Felitti initially didn’t understand the biological mechanisms at work in their ACE data, scientists have reached a consensus in the past decade that the key channel through which early adversity causes damage to developing bodies and brains is
stress.

Our bodies regulate stress using a system called the HPA axis. HPA stands for “hypothalamic-pituitary-adrenal,” and that tongue-twisting phrase describes the way that chemical signals cascade through the brain and the body in reaction to intense situations. When a potential danger appears,
the first line of defense is the hypothalamus, the region of the brain that controls unconscious biological processes like body temperature, hunger, and thirst. The hypothalamus emits a chemical that triggers receptors in the pituitary gland; the pituitary releases signaling hormones that stimulate the adrenal glands; and the adrenal glands then send out stress hormones called glucocorticoids that switch on a host of specific defensive responses. Some of these responses we can recognize in ourselves as they happen: emotions like fear and anxiety, and physical reactions like increased heart rate, clammy skin, and a dry mouth. But many effects of the HPA axis are less immediately apparent to us, even when we’re the ones experiencing them: neurotransmitters activate, glucose levels rise, the cardiovascular system sends blood to the muscles, and inflammatory proteins surge through the bloodstream.

In his insightful and entertaining book
Why Zebras Don’t Get Ulcers,
the neuroscientist Robert Sapolsky explains that our stress-response system, like that of all mammals, evolved to react to brief and acute stresses. That worked well when humans were out on the savanna running from predators. But modern humans rarely have to contend with lion attacks. Instead, most of our stress today comes from mental processes: from worrying about things. And the HPA axis isn’t designed to handle that kind of stress. We “activate a physiological system that has evolved for responding to acute physical emergencies,” Sapolsky writes, “but we turn it on for months on end, worrying about mortgages, relationships, and promotions.” And over the past fifty years, scientists have discovered that this phenomenon is not merely inefficient but also highly destructive. Overloading the HPA axis, especially in infancy and childhood, produces all kinds of serious and long-lasting negative effects—physical, psychological, and neurological.

The tricky thing about this process, though, is that it’s not actually the stress itself that messes us up. It is the body’s
reaction
to the stress. In the early 1990s, Bruce McEwen, a neuroendocrinologist
at Rockefeller University, proposed a theory of how this works, one that is now broadly accepted in the field. According to McEwen, the process of managing stress, which he labeled
allostasis,
is what creates wear and tear on the body. If the body’s stress-management systems are overworked, they eventually break down under the strain. McEwen called this gradual process allostatic load, and he says that you can observe its destructive effects throughout the body. For example, acute stress raises blood pressure to provide adequate blood flow to the muscles and organs that need to respond to a dangerous situation. That’s good. But repeatedly elevated blood pressure leads to atherosclerotic plaque, which causes heart attacks. That’s not so good.

Although the human stress-response system is highly complex in design, in practice it has all the subtlety of a croquet mallet. Depending on what kind of stress you experience, the ideal response might come from one of any number of defense mechanisms. If you’re about to receive a flesh wound, for instance, then it would be a good idea for your immune system to start producing copious antibodies. If you need to run away from an attacker, you want your heart rate and blood pressure to elevate. But the HPA axis can’t distinguish between different types of threat, so it activates every defense, all at once, in response to any threat. Unfortunately, this means you often experience stress responses that are not at all helpful—like when you need to speak before an audience, and suddenly your mouth goes dry. Your HPA axis, sensing danger, is conserving fluids, preparing to ward off an attack. And you’re standing there looking for a glass of water and swallowing hard.