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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 suicidethan those with an ACE score of 0. And men with an ACE score above 5 were forty-six times more likely to have injected drugsthan 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.