Why Zebras Don't Get Ulcers: The Acclaimed Guide to Stress, Stress-Related Diseases, and Coping

by Robert M. Sapolsky

One of the hallmarks of the stress-response is the rapid mobilization of energy from storage sites and the inhibition of further storage. Glucose and the simplest forms of proteins and fats come pouring out of your fat cells, liver, and muscles, all to stoke whichever muscles are struggling to save your neck. If your body has mobilized all that glucose, it also needs to deliver it to the critical muscles as rapidly as possible. Heart rate, blood pressure, and breathing rate increase, all to transport nutrients and oxygen at greater rates. Equally logical is another feature of the stress-response. During an emergency, it makes sense that your body halts long-term, expensive building projects.

but rather, with sufficient activation, that the stress-response can become more damaging than the stressor itself, especially when the stress is purely psychological. This is a critical concept, because it underlies

The half of the autonomic nervous system that is turned on is called the sympathetic nervous system.* Originating in the brain, sympathetic projections exit your spine and branch out to nearly every organ, every blood vessel, and every sweat gland in your body. They even project to the scads of tiny little muscles attached to hairs on your body. If you are truly terrified by something and activate those projections, your hair stands on end; gooseflesh results when the parts of your body are activated where those muscles exist but lack

Naturally, the problem was that it didn’t work. There wasn’t any testosterone in the testicular extracts—patients would be injected with a water-based extract, and testosterone does not go into solution in water. And the smidgens of organs that were transplanted would die almost immediately, with the scar tissue being mistaken for a healthy graft. And even if they didn’t die, they still wouldn’t work—if aging testes are secreting less testosterone, it is not because the testes are failing, but because another organ (stay tuned) is no longer telling them to do so.

So hooray for Guillemin and Schally; the brain turned out to be the master gland. It is now recognized that the base of the brain, the hypothalamus, contains a huge array of those releasing and inhibiting hormones, which instruct the pituitary, which in turn regulates the secretions of the peripheral glands. In some cases, the brain triggers the release of pituitary hormone X through the action of a single releasing hormone. Sometimes it halts the release of pituitary hormone Y by releasing a single inhibiting hormone. In some cases, a pituitary hormone is controlled by the coordination of both a releasing and an inhibiting hormone from the brain—dual control. To make matters worse, in some cases (for example, the miserably confusing system that I study) there is a whole array of hypothalamic hormones that collectively regulate the pituitary, some as releasers, others as inhibitors.

Taylor argues convincingly that the physiology of the stress-response can be quite different in females, built around the fact that in most species, females are typically less aggressive than males, and that having dependent young often precludes the option of flight. Showing that she can match the good old boys at coming up with a snappy sound bite, Taylor suggests that rather than the female stress-response being about fight-or-flight, it’s about “tend and befriend”—taking care of her young and seeking social affiliation. As will be seen in the final chapter of the book, there are some striking gender differences in stress management styles that support Taylor’s view, many of them built around the propensity toward social affiliation.

What good are glucocorticoids if some of their actions occur long after your typical dawn-on-the-savanna stressor is over with? Some glucocorticoid actions do help mediate the stress-response. Others help mediate the recovery from the stress-response. As will be described in chapter 8, this probably has important implications for a number of autoimmune diseases. And some glucocorticoid actions prepare you for the next stressor. As will be discussed in chapter 13, this is critical for understanding the ease with which anticipatory psychological states can trigger glucocorticoid secretion.

has found that the sympathetic nervous system is particularly activated in a socially subordinate rodent that is vigilant and trying to cope with a challenge. In contrast, it is the glucocorticoid system that is relatively more activated in a subordinate rodent that has given up on coping. Studies of humans have shown what may be a human analogue of that dichotomy. Sympathetic arousal is a relative marker of anxiety and vigilance, while heavy secretion of glucocorticoids is more a marker of depression. Furthermore, all stressors do not cause secretion of both epinephrine and norepinephrine, nor of norepinephrine from all branches of the sympathetic system.

There’s one final cardiovascular trick in response to stress, involving the kidneys. As that zebra with its belly ripped open, you’ve lost a lot of blood. And you’re going to need that blood to deliver energy to your exercising muscles. Your body needs to conserve water. If blood volume goes down because of dehydration or hemorrhage, it doesn’t matter what your heart and veins are doing; your ability to deliver glucose and oxygen to your muscles will be impaired. What’s the most likely place to be losing water? Urine formation, and the source of the water in urine is the bloodstream. Thus, you decrease blood flow to your kidneys and, in addition, your brain sends a message to the kidneys: stop the process, reabsorb the water into the circulatory system. This is accomplished by the hormone vasopressin (known as antidiuretic hormone for its ability to block diuresis, or urine formation),

For humans, it is a mystery, just a boring storage site. The kidneys, now those are something else. Kidneys are reabsorptive, bidirectional organs, which means you can spend your whole afternoon happily putting water in from the circulation and getting some back and regulating the whole thing with a collection of hormones. But once the urine leaves the kidneys and heads south to the bladder, you can kiss that stuff good-bye; the bladder is unidirectional. When it comes to a stressful emergency, a bladder means a lot of sloshy dead weight to carry in your sprint across the savanna. The answer is obvious: empty that bladder.*

How does stress-induced elevation of blood pressure during chronic psychological stress wind up causing cardiovascular disease, the number one killer in the United States and the developed world? Basically, your heart is just a dumb, simple mechanical pump, and your blood vessels are nothing more exciting than hoses. The cardiovascular stress-response essentially consists of making them work harder for a while, and if you do that on a regular basis, they will wear out, just like any pump or hose you’d buy at Sears. The first step in the road to stress-related disease is developing hypertension, chronically elevated blood pressure.* This one seems obvious: if stress causes your blood pressure to go up, then chronic stress causes your blood pressure to go up chronically. Task accomplished, you’ve got hypertension. It’s a bit messier because a vicious cycle emerges at this point. The little blood vessels distributed throughout your body have the task of regulating blood flow to the local neighborhoods as a means of ensuring adequate local levels of oxygen and nutrients.

The latter takes more muscle. And that’s precisely what happens at these small vessels. They build a thicker muscle layer around them, to better control the increased force of blood flow. But as a result of these thicker muscles, these vessels now have become more rigid, more resistant to the force of blood flow. Which tends to increase blood pressure. Which tends to further increase vascular resistance. Which tends…

“left ventricular hypertrophy,” which means increasing the mass of the left ventricle, the part of the heart in question. Your heart is now lopsided, in a sense, being overdeveloped in one quadrant. This increases the risk of developing an irregular heartbeat. And more bad news: in addition, this thickened wall of ventricular heart muscle may now require more blood than the coronary arteries can supply. It turns out that after controlling for age, having left ventricular hypertrophy is the single best predictor of cardiac risk.

(As a measure of how extraordinarily efficient this repeated bifurcation is in the circulatory system, no cell in your body is more than five cells away from a blood vessel—yet the circulatory system takes up only 3 percent of body mass.)

How can you measure the amount of inflammatory damage? A great marker is turning out to be something called C-reactive protein (CRP). It is made in the liver and is secreted in response to a signal indicating an injury. It migrates to the damaged vessel where it helps amplify the cascade of inflammation that is developing. Among other things, it helps trap bad cholesterol in the inflamed aggregate. CRP is turning out to be a much better predictor of cardiovascular disease risk than cholesterol, even years in advance of disease onset. As a result, CRP has suddenly become quite trendy in medicine, and is fast becoming a standard endpoint to measure in general blood work on patients.

Establish male monkeys in a social group, and over the course of days to months they’ll figure out where they stand with respect to one another. Once a stable dominance hierarchy has emerged, the last place you want to be is on the bottom: not only are you subject to the most physical stressors but, as will be reviewed in chapter 13 on psychological stress, to the most psychological stressors as well. Such subordinate males show a lot of the physiological indices of chronically turning on their stress-responses. And often these animals wind up with atherosclerotic plaques—their arteries are all clogged up. As evidence that the atherosclerosis arises from the overactive sympathetic nervous system component of the stress-response, if Kaplan gave the monkeys at risk drugs that prevent sympathetic activity (beta-blockers), they didn’t form plaques.

Suppose you keep the dominance system unstable by shifting the monkeys into new groups every month, so that all the animals are perpetually in the tense, uncertain stage of figuring out where they stand with respect to everyone else. Under those circumstances, it is generally the animals precariously holding on to their places at the top of the shifting dominance hierarchy who do the most fighting and show the most behavioral and hormonal indices of stress. And, as it turns out, they have tons of atherosclerosis; some of the monkeys even have heart attacks (abrupt blockages of one or more of the coronary arteries).

In general, the monkeys under the most social stress were most at risk for plaque formation. Kaplan showed that this can even occur with a low-fat diet, which makes sense, since, as will be described in the next chapter, a lot of the fat that forms plaques is being mobilized from stores in the body, rather than coming from the cheeseburger the monkey ate just before the tense con...

Whenever you inhale, you turn on the sympathetic nervous system slightly, minutely speeding up your heart. And when you exhale, the parasympathetic half turns on, activating your vagus nerve in order to slow things down (this is why many forms of meditation are built around extended exhalations). Therefore, the length of time between heartbeats tends to be shorter when you’re inhaling than exhaling. But what if chronic stress has blunted the ability of your parasympathetic nervous system to kick the vagus nerve into action? When you exhale, your heart won’t slow down, won’t increase the time intervals between beats. Cardiologists use sensitive monitors to measure interbeat intervals. Large amounts of variability (that is to say, short interbeat intervals during inhalation, long during exhalation) mean you have strong parasympathetic tone counteracting your sympathetic tone, a good thing. Minimal variability means a parasympathetic component that has trouble putting its foot on the brake. This is the marker of someone who not only turns on the cardiovascular stress-response too often but, by now, has trouble turning it off.

So a big reason why most of us become hyperphagic during stress is our westernized human capacity to have intermittent psychological stressors throughout the day. The type of stressor is a big factor.

Insufficient Amounts of Prostaglandins In this scenario, micro-ulcers begin now and then in your gut, as part of the expected wear and tear on the system. Normally your body can repair the damage by secreting a class of chemicals called prostaglandins, thought to aid the healing process by increasing blood flow through the stomach walls. During stress, however, the synthesis of these prostaglandins is inhibited by the actions of glucocorticoids. In this scenario, stress does not so much cause ulcers to form as impair your body’s ability to catch them early and repair them. It is not yet established how often this is the route for ulcer formation during stress. (Aspirin also inhibits prostaglandin synthesis, which is why aspirin can aggravate a bleeding ulcer.)

What impresses me is how careful and calculating the body has to be during stress in order to coordinate hormonal activities just right. It must perfectly balance the costs and benefits, knowing exactly when to stop secreting the hormone. If the body miscalculates in one direction and growth hormone secretion is blocked too early, there is relatively less mobilization of energy for dealing with the stressor. If it miscalculates in the other direction and growth hormone secretion goes on too long, stress may actually enhance growth. One oft-quoted study suggests that the second type of error occurs during some stressors.

It turns out that in a lot of species, stressors associated with mating season competition or with mating itself not only don’t suppress the reproductive system, but can stimulate it a bit. In some species where this applies, the seeming stressor doesn’t cause secretion of stress hormones; in other cases, the stress hormones are secreted but the reproductive system becomes insensitive to them.

Having established a thread of sympathy for these beasts, let me explain what is really strange about them. Among hyenas, females are socially dominant, which is fairly rare among mammals. They are more muscular and more aggressive, and have more of a male sex hormone (a close relative of testosterone called androstenedione) in their bloodstreams than males. It’s also almost impossible to tell the sex of a hyena by looking at its external genitals.

Social primates do this all the time. However, among hyenas, an erection is a sign of social subordinance. When a male is menaced by a terrifying female, he gets an erection—“Look, I’m just some poor no-account male; don’t hit me, I was just leaving.” Low-ranking females do the same thing; if a low-ranking female is about to get trounced by a high-ranking one, she gets a conspicuous clitoral erection—“Look, I’m just like one of those males; don’t attack me; you know you’re dominant over me, why bother?” If you’re a hyena, you get an erection when you are stressed. Among male hyenas, the autonomic wiring has got to be completely reversed in order to account for the fact that stress causes erections. This hasn’t yet been demonstrated, but perhaps Berkeley scientists working on this, squandering tax dollars that could otherwise be going to Halliburton and Bechtel, will do it. Thus the hyena stands as the exception to the rule about erectile functions being adversely affected by stress, a broader demonstration of the importance of looking at a zoological oddity as a means of better seeing the context of our own normative physiology, and a friendly word of warning before you date a hyena.

Such reasoning led Munck to predict that if you fail to have phase B, if you don’t coast that activated immune system back down to baseline, you’re more at risk for an autoimmune disease. This idea has been verified in at least three realms. First, artificially lock glucocorticoid levels in the low basal range in rats and then stress them. This produces animals that have phase A (mostly mediated by epinephrine), but there isn’t the rise in glucocorticoids to fully pull off phase B. The rats are now more at risk for autoimmune disease. Second, doctors have to occasionally remove one of the two adrenal glands (the source of glucocorticoids) from a patient, typically because of a tumor. Immediately afterward, circulating glucocorticoid levels are halved for a period, until the remaining adrenal bulks up enough to take on the job of two. During that period of low glucocorticoid levels, people are more likely than normal to flare up with some autoimmune or inflammatory disease—there’s not enough glucocorticoids around to pull off phase B when something stressful occurs. Finally, if you look at strains of rats or, weirdly, chickens, that spontaneously develop autoimmune diseases, they all turn out to have something wrong with the glucocorticoid system so that they have lower than normal levels of the hormone, or have immune and inflammatory cells that are less responsive than normal to glucocorticoids.

Insofar as autoimmune diseases involve over activation of the immune system (to the point of considering a healthy constituent of your body to actually be something invasive), the most time-honored treatment for such diseases is to put people “on steroids”—to give them massive amounts of glucocorticoids. The logic here is obvious: by dramatically suppressing the immune system it can no longer attack your pancreas or nervous system, or whatever is the inappropriate target of its misplaced zeal (and, as an obvious side effect to this approach, your immune system will also not be very effective at defending you against real pathogens). Thus, administration of large amounts of these stress hormones makes autoimmune diseases less damaging. Moreover, prolonged major stressors decrease the symptoms of autoimmune diseases in lab rats.

Acupuncture stimulates the release of large quantities of endogenous opioids, for reasons no one really understands. The best demonstration of this is what is called a subtraction experiment: block the activity of endogenous opioids by using a drug that blocks the opiate receptor (most commonly a drug called naloxone). When such a receptor is blocked, acupuncture no longer effectively dulls the perception of pain.

Neuropsychologists are coming to recognize that there is a specialized subset of long-term memory. Remote memories are ones stretching back to your childhood—the name of your village, your native language, the smell of your grandmother’s baking. They appear to be stored in some sort of archival way in your brain separate from more recent long-term memories.

This shifts us to the next magnification of examining how the brain handles memories and how stress influences the process—what’s going on at the level of clusters of neurons within the cortex and hippocampus? A long-standing belief among many who studied the cortex was that each individual cortical neuron would, in effect, turn out to have a single task, a single fact that it knew. This was prompted by some staggeringly important work done in the 1960s by David Hubel and Torstein Wiesel of Harvard on what was, in retrospect, one of the simpler outposts of the cortex, an area that processed visual information. They found a first part of the visual cortex in which each neuron responded to one thing and one thing only, namely a single dot of light on the retina. Neurons that responded to a sequence of adjacent dots of light would funnel their projections to one neuron in the next layer. And thus, what was this neuron responding to? A straight line. A series of these neurons would project to the next level in a way that each neuron in that cortical level would respond to a particular moving line of light. This led people to believe that there would be a fourth level, where each neuron responded to a particular collection of lines, and a fifth and sixth layer, all the way up until, at the umpteenth layer, there would be a neuron that responded to one thing and one thing only, namely your grandmother’s face at a particular angle (and next to it would be a neuron that recognized...

We take advantage of such convergent networks whenever we are trying to pull out a memory that is almost, almost there. Continuing our art history theme, suppose you’re trying to remember the name of a painter, that guy, what’s his name. He was that short guy with a beard (activating your “short guy” neural network, and your “bearded guy” network). He painted all those Parisian dancers; it wasn’t Degas (two more networks pulled in). My high school art appreciation teacher loved that guy; if I can remember her name, I bet I can remember his…wow, remember that time I was at the museum and there was that really cute person I tried to talk to in front of one of his paintings…oh, what was the stupid pun about that guy’s name, about the train tracks being too loose. With enough of those nets being activated, you finally stumble into the one fact that is at the intersection of all of them: Toulouse-Lautrec, the equivalent of a neuron C.

The second feature is even more important. Under the right conditions, when a synapse has just had a sufficient number of superexcitatory glutamate-driven “aha’s,” something happens. The synapse becomes persistently more excitable, so that next time it takes less of an excitatory signal to get the aha. That synapse just learned something; it was “potentiated,” or strengthened. The most amazing thing is that this strengthening of the synapse can persist for a long time. A huge number of neuroscientists flail away at figuring out how this process of “long-term potentiation” works.

The first point, of course, is that mild to moderate short-term stressors enhance memory. This makes sense, in that this is the sort of optimal stress that we would call “stimulation”—alert and focused. This effect has been shown in laboratory animals and in humans. One particularly elegant study in this realm was carried out by Larry Cahill and James McGaugh at the University of California at Irvine. Read a fairly unexciting story to a group of control subjects: a boy and his mother walk through their town, pass this store and that one, cross the street and enter the hospital where the boy’s father works, are shown the X-ray room…and so on. Meanwhile,

Tested weeks later, the experimental subjects remember their story better than do the controls, but only the middle, exciting part. This fits with the picture of “flashbulb memory,” in which people vividly remember some highly aroused scene, such as a crime they witnessed. Memory for the emotional components is enhanced (although the accuracy isn’t necessarily all that good), whereas memory for the neutral details is not.

The sympathetic nervous system pulls this off by indirectly arousing the hippocampus into a more alert, activated state, facilitating memory consolidation. This involves an area of the brain that is going to become central to understanding anxiety when we get to chapter 15, namely the amygdala. The sympathetic nervous system has a second route for enhancing cognition. Tons of energy are needed for all that explosive, nonlinear, long-term potentiating, that turning on of light-bulbs in your hippocampus with glutamate. The sympathetic nervous system helps those energy needs to be met by mobilizing glucose into the bloodstream and increasing the force with which blood is being pumped up into the brain. These changes are quite adaptive. When a stressor is occuring it is a good time to be at your best in memory retrieval (“How did I get out of this mess last time?”) and memory formation (“If I survive this, I’d better remember just what I did wrong so I don’t get into a mess like this again.”). So stress acutely causes increased delivery of glucose to the brain, making more energy available to neurons, and therefore better memory formation and retrieval.

In a disorder called Cushing’s syndrome, people develop one of a number of types of tumors that result in secretion of tons of glucocorticoids. Understand what goes wrong next in a “Cushingoid” patient and you understand half of this book—high blood pressure, diabetes, immune suppression, reproductive problems, the works. And it’s been known for decades that they get memory problems, specifically explicit memory problems,

As the clearest evidence, just a few days of high doses of synthetic glucocorticoids impairs explicit memory in healthy volunteers. As one problem in interpreting these studies, these synthetic hormones work a bit differently from the real stuff, and the levels administered produce higher circulating glucocorticoid levels than the body normally produces, even during stress. Importantly, stress itself, or infusion of stress levels of the type of glucocorticoid that naturally occurs in humans, disrupts memory as well. As with the nonhuman studies, implicit memory is fine, and it’s the recall, the retrieval of prior information, that is more vulnerable than the consolidation of new memories.

Second, neural networks get disconnected. If you look back at the diagram on the “Impressionism neuron”, you’ll see that there are symbols indicating how one neuron talks to another, “projects” to it. As mentioned a few paragraphs after that, those projections are quite literal—long multibranched cables coming out of neurons that form synapses with the multibranched cables of other neurons. These cables (known as axons and dendrites) are obviously at the heart of neuronal communication and neuronal networks. Bruce McEwen has shown that, in a rat, after as little as a few weeks of stress or of exposure to excessive glucocorticoids, those cables begin to shrivel, to atrophy and retract a bit. Moreover, the same can occur in the primate brain. When that happens, synaptic connections get pulled apart and the complexity of your neural networks declines. Fortunately, it appears that at the end of the stressful period, the neurons can dust themselves off and regrow those connections. This transient atrophy of neuronal processes probably explains a characteristic feature of memory problems during chronic stress. Destroy vast acres of neurons in the hippocampus after a massive stroke or late terminal stage Alzheimer’s disease, and memory is profoundly impaired. Memories can be completely lost, and never again will these people remember, for example, something as vital as the names of their spouses. “Weaken” a neural network during a period of chronic stress by retracting some of th...

Third, the birth of new neurons is inhibited. If you learned your introductory neurobiology any time in the last thousand years, one fact that would be hammered in repeatedly is that the adult brain doesn’t make new neurons. In the last decade, it has become clear that this is utterly wrong.* As a result, the study of “adult neurogenesis” is now, arguably, the hottest topic in neuroscience. Two features about

The bizarre thing is that this sequence of events not only occurs in five species of salmon, but also among a dozen species of Australian marsupial mice. All the male mice of these species die shortly after seasonal mating; cut out their adrenal glands, however, and they too keep living. Pacific salmon and marsupial mice are not close relatives. At least twice in evolutionary history, completely independently, two very different sets of species have come up with the identical trick: if you want to degenerate very fast, secrete a ton of glucocorticoids.

A variant of Weiss’s experiment uncovers a special feature of the outlet-for-frustration reaction. This time, when the rat gets the identical series of electric shocks and is upset, it can run across the cage, sit next to another rat and…bite the hell out of it. Stress-induced displacement of aggression: the practice works wonders at minimizing the stressfulness of a stressor. It’s a real primate specialty as well. A male baboon loses a fight. Frustrated, he spins around and attacks a subordinate male who was minding his own business. An extremely high percentage of primate aggression represents frustration displaced onto innocent bystanders. Humans are pretty good at it, too, and we have a technical way of describing the phenomenon in the context of stress-related disease: “He’s one of those guys who doesn’t get ulcers, he gives them.” Taking it out on someone else—

considerably more encouraging for the future of our planet than is displacement aggression. Rats only occasionally use it, but primates are great at it. Put a primate through something unpleasant: it gets a stress-response. Put it through the same stressor while in a room full of other primates and…it depends. If those primates are strangers, the stress-response gets worse. But if they are friends, the stress-response is decreased. Social support networks—it helps to have a shoulder to cry on, a hand to hold, an ear to listen to you, someone to cradle you and to tell you it will be okay.

In each case, social support translated into less of a cardiovascular stress-response. Profound and persistent differences in degrees of social support can influence human physiology as well: within the same family, there are significantly higher glucocorticoid levels among stepchildren than among biological children. Or, as another example, among women with metastatic breast cancer, the more social support, the lower the resting cortisol levels.

in the aftermath of this stressor, there was no notable increase in risk of diseases or mortality, except among those who were already divorced or widowed. Some additional examples concern the cardiovascular system. People who are socially isolated have overly active sympathetic nervous systems. Given the likelihood that this will lead to higher blood pressure and more platelet aggregation in their blood vessels (remember that from chapter 3?), they are more likely to have heart disease—two to five times as likely, as it turns out. And once they have the heart disease, they are more likely to die at a younger age. In a study of patients with severe coronary heart disease, Redford Williams of Duke University and colleagues found that half of those lacking social support were dead within five years—a rate three times higher than was seen in patients who had a spouse or close friend, after controlling for the severity of the heart disease.

As another variant on the helpfulness of predictability, organisms will eventually habituate to a stressor if it is applied over and over; it may knock physiological allostasis equally out of balance the umpteenth time that it happens, but it is a familiar, predictable stressor by then, and a smaller stress-response is triggered. One classic demonstration involved men in the Norwegian military going through parachute training—as the process went from being hair-raisingly novel to something they could do in their sleep, their anticipatory stress-response went from being gargantuan to nonexistent. The power of loss of predictability as a psychological stressor is shown in an elegant,

The issue of control runs through the literature on the psychology of stress. As will be discussed in the final chapter on coping, exercise can be a great stress reducer, but only so long as it is something that seems even remotely desirable. Amazingly, the same is seen in a rat—let a rat run voluntarily in a running wheel, and it makes it feel great. Force a rat to do the same amount of exercise and it gets a massive stress-response.

For most, though, occupational stress is built more around lack of control, work life spent as a piece of the machine. Endless studies have shown that the link between occupational stress and increased risk of cardiovascular and metabolic diseases is anchored in the killer combination of high demand and low control—you have to work hard, a lot is expected of you, and you have minimal control over the process. This is the epitome of the assembly line, the combination of stressors that makes for Marx’s alienation of the workers. The control element is more powerful than the demand one—low demand and low control is more damaging to one’s health than high demand and high control.

So the variable of control is extremely important; controlling the rewards that you get can be more desirable than getting them for nothing. As an extraordinary example, both pigeons and rats prefer to press a lever in order to obtain food (so long as the task is not too difficult) over having the food delivered freely—a theme found in the activities and statements of many scions of great fortunes, who regret the contingency-free nature of their lives, without purpose or striving. Loss of control and lack of predictive information are closely related. Some researchers have emphasized this, pointing out that the common theme is that the organism is subjected to novelty. You thought you knew how to manage things, you thought you knew what would happen next, and it turns out you are wrong in this novel situation. The potency of this is demonstrated in primate studies in which merely placing the animal into a novel cage suppresses its immune system. Others have emphasized that these types of stressors cause arousal and vigilance, as you search for the new rules of control and prediction. Both views are different aspects of the same issue.

A version of this can be observed among the baboons I study in Kenya. In general, when dominance hierarchies are unstable, resting glucocorticoid levels rise. This makes sense, because such instabilities make for stressful times. Looking at individual baboons, however, shows a more subtle pattern: given the same degree of instability, males whose ranks are dropping have elevated glucocorticoid levels, while males whose ranks are rising amid the tumult don’t show this endocrine trait.

As we saw, control and predictability are closely aligned; combine them with a perception of things worsening, and you have the situation of bad things happening, out of your control, and utterly unpredictable. The primatologist Joan Silk of UCLA has emphasized how, among primates, a great way to maintain dominance is for the alpha individual to mete out aggression in a randomly brutal way. This is our primate essence of terrorism.