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Why Zebras Don’t Get Ulcers Chapter 14. Stress and Depression

Author Robert Sapolsky Publisher: New York, NY: Henry Holt and Company. Publish Date: 2004 Review Date: 2023-5-29 Status:⌛️

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The defining feature of a major depression is loss of pleasure.

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This trait is called anhedonia: hedonism is “the pursuit of pleasure,” anhedonia is “the inability to feel pleasure”

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This is the classic picture of depression, and some recent research, much of it built around work of the psychologist Alex Zautra of the University of Arizona, shows that the story is more complex. Specifically, positive and negative emotions are not mere opposites. If you take subjects and, at random times throughout the day, have them record how they are feeling at that moment, the frequencies of feeling good and feeling bad are not inversely correlated. There’s normally not much of a connection between how much your life is filled with strongly positive emotions and how much with strongly negative ones. Depression represents a state where those two independent axes tend toward collapsing into one inverse relationship—too few positive emotions and too many negative ones. Naturally, the inverse correlation isn’t perfect, and a lot of current research focuses on questions like: Are different subtypes of depression characterized more by the absence of positive emotions or the overabundance of negatives?

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Accompanying major depression are great grief and great guilt. We often feel grief and guilt in the everyday sadnesses that we refer to as “depression.” But in a major depression, they can be incapacitating, as the person is overwhelmed with the despair. There can be complex layers of these feelings: not just obsessive guilt, for example, about something that has contributed to the depression, but obsessive guilt about the depression itself—what it has done to the sufferer’s family, the guilt of not being able to overcome depression, a life lived but once and wasted amid this disease. Small wonder that, worldwide, depression accounts for 800,000 suicides per year.*

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In a subset of such patients, the sense of grief and guilt can take on the quality of a delusion. By this, I do not mean the thought-disordered delusions of schizophrenics; instead, delusional thinking in depressives is of the sort where facts are distorted, over- or underinterpreted to the point where one must conclude that things are terrible and getting worse, hopeless.

An example: a middle-aged man, out of the blue, has a major heart attack. Overwhelmed by his implied mortality, the transformation of his life, he slips into a major depression. Despite this, he is recovering from the attack reasonably well, and there is every chance that he will resume a normal life. But each day he’s sure he’s getting worse.

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Cognitive therapists, like Aaron Beck of the University of Pennsylvania, even consider depression to be primarily a disorder of thought, rather than emotion, in that sufferers tend to see the world in a distorted, negative way. Beck and colleagues have conducted striking studies that provide evidence for this. For example, they might show a subject two pictures. In the first, a group of people are gathered happily around a dinner table, feasting. In the second, the same people are gathered around a coffin. Show the two pictures rapidly or simultaneously; which one is remembered? Depressives see the funeral scene at rates higher than chance. They are not only depressed about something, but see the goings-on around them in a distorted way that always reinforces that feeling. Their glasses are always half empty.

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Another frequent feature of a major depression is called psychomotor retardation. The person moves and speaks slowly. Everything requires tremendous effort and concentration. She finds the act of merely arranging a doctor’s appointment exhausting. Soon it is too much even to get out of bed and get dressed. (It should be noted that not all depressives show psychomotor retardation; some may show the opposite pattern, termed psychomotor agitation.)

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major depressives often experience elevated levels of glucocorticoids. This is critical for a number of reasons that will be returned to, and helps to clarify what the disease is actually about. When looking at a depressive sitting on the edge of the bed, barely able to move, it is easy to think of the person as energy-less, enervated. A more accurate picture is of the depressive as a tightly coiled spool of wire, tense, straining, active—but all inside. As we will see, a psychodynamic view of depression shows the person fighting an enormous, aggressive mental battle—no wonder they have elevated levels of stress hormones.

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glucocorticoids can impair aspects of memory that depend on the hippocampus, and the frequently elevated glucocorticoid levels in depression may help explain another feature of the disease, which is problems with hippocampal-dependent memory.

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the pure process of storing and retrieving memories via the hippocampus is often impaired. As we’ll see shortly, this fits extraordinarily well with recent findings showing that the hippocampus is smaller than average in many depressives.

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it is a real disease, rather than merely the situation of someone who simply cannot handle everyday ups and downs.

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There are multiple types of depressions, and they can look quite different. In one variant, unipolar depression, the sufferer fluctuates from feeling extremely depressed to feeling reasonably normal. In another form, the person fluctuates between deep depression and wild, disorganized hyperactivity. This is called bipolar depression or, more familiarly, manic depression.

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Here we run into another complication because, just as we use depression in an everyday sense that is different from the medical sense, mania has an everyday connotation as well. We may use the term to refer to madness, as in made-for-television homicidal maniacs. Or we could describe someone as being in a manic state when he is buoyed by some unexpected good news—talking quickly, laughing, gesticulating. But the mania found in manic depression is of a completely different magnitude. Let me give an example of the disorder: a woman comes into the emergency room; she’s bipolar, completely manic, hasn’t been taking her medication. She’s on welfare, doesn’t have a cent to her name, and in the last week she’s bought three Cadillacs with money from loan sharks. And, get this, she doesn’t even know how to drive. People in manic states will go for days on three hours of sleep a night and feel rested, will talk nonstop for hours at a time, will be vastly distractible, unable to concentrate amid their racing thoughts. In outbursts of irrational grandiosity, they will behave in ways that are foolhardy or dangerous to themselves and others—at the extreme, poisoning themselves in attempting to prove their immortality, burning down their homes, giving away their life savings to strangers. It is a profoundly destructive disease.

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Why is it likely that there is something wrong with norepinephrine, serotonin, or dopamine in depression? The best evidence is that most of the drugs that lessen depression increase the amount of signaling by these neurotransmitters.

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On an incredibly simplistic level, you can think of depression as occurring when your cortex thinks an abstract negative thought and manages to convince the rest of the brain that this is as real as a physical stressor. In this view, people with chronic depressions are those whose cortex habitually whispers sad thoughts to the rest of the brain.

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Thus, an astonishingly crude prediction: cut the connections between the cortex and the rest of a depressive’s brain, and the cortex will no longer be able to get the rest of the brain depressed.

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Remarkably, it actually works sometimes. Neurosurgeons may perform this procedure on people with vastly crippling depressions that are resistant to drugs, ECT, or other forms of therapy. Afterward, depressive symptoms seem to abate.*

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Obviously, this is a simplified picture—no one actually disconnects the entire cortex from the rest of the brain. After all, the cortex does more than mope around feeling bad about the final chapter of Of Mice and Men. The surgical procedure, called a cingulotomy, or a cingulum bundle cut, actually disconnects just one area toward the front of the cortex, called the anterior cingulate cortex (ACC). The ACC is turning out to have all the characteristics of a brain region you’d want to take offline in a major depression. It’s a part of the brain that is very concerned with emotions. Show people arrays of pictures: in one case, ask them to pay attention to the emotions being expressed by people in the pictures; in another case, ask them to pay attention to details like whether these are indoor or outdoor photographs. In only the former case do you get activation of the ACC.

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And the emotions that the ACC is involved in seem to be negative ones. Induce a positive state in someone by showing something amusing, and ACC metabolism decreases. In contrast, if you electrically stimulate the ACC in people, they feel a shapeless sense of fear and foreboding. Moreover, neurons in the ACC, including in humans, respond to pain of all sorts. But the ACC response isn’t really about the pain; it more concerns feelings about the pain. As was discussed in chapter 9, give someone a hypnotic suggestion that they will not feel the pain of dipping their hand into ice water. The primary parts of the brain that get pain projections from the spinal cord get just as active as if there were no hypnotic suggestion. But this time, the ACC doesn’t activate.

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In addition, the ACC and adjacent brain regions activate when you show widows pictures of their lost loved ones (versus pictures of strangers). As another example of this, put a volunteer in a brain-imaging machine and, from inside, ask them to play some game with two other people, via a computer console. Rig up the flow of the game so that, over time, the other two (actually, a computer program) gradually begin just playing with each other, excluding the test subject. Neuronal activity in the ACC lights up, and the more left out the person feels, the more intensely the ACC activates. How do you know this has something to do with that dread junior high school feeling of being picked last for the team? Because of a clever control in the study: set the person up to play with the supposed other two players. Once again, it winds up that the other two only play against each other. The difference, this time, though, is that early on the subject is told there’s been a technical glitch and that their computer console isn’t working. Excluded because of a snafu in the technology, there’s no ACC activation.

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Given these functions of the ACC, it is not surprising that its resting level of activity tends to be elevated in people with a depression—this is the fear and pain and foreboding churning away at those neurons. Interestingly, another part of the brain, called the amygdala, seems to be hyperactive in depressives as well. We will hear lots about the role of the amygdala in fear and anxiety in the next chapter. However, in depressives, the amygdala seems to have been recruited into a different role. Show a depressed person a fearful human face and his amygdala doesn’t activate all that much (in contrast to the response you’d see in the amygdala of a control subject). But show him a sad face and the amygdala gets a highly exaggerated activation.

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Sitting just in front of the ACC is the frontal cortex which, as we saw in chapter 11, is one of the most distinctly human parts of the brain. Work by Richard Davidson of the University of Wisconsin has shown that one subregion called the prefrontal cortex (PFC) seems highly responsive to mood, and in a lateralized way. Specifically, activation of the left PFC is associated with positive moods, and activation of the right PFC, with negative. For example, induce a positive state in someone (by asking him to describe the happiest day of his life), and the left PFC lights up, in proportion to the person’s subjective assessment of his pleasure. Ask him to remember a sad event, and the right PFC dominates. Similarly, separate an infant monkey from its mother and right PFC metabolism rises while left PFC decreases. Thus, not surprisingly, in depressives, there is decreased left PFC activity and elevated activity in the right PFC.

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It is hard to look at the biology of anything these days without genes coming into the picture, and depression is no exception. Depression has a genetic component. As a first observation, depression runs in families. For a long time, that would have been sufficient evidence for some folks that there is a genetic link, but this conclusion is undone by the obvious fact that not only do genes run in families, environment does as well. Growing up in a poor family, an abusive family, a persecuted family, can all increase the risk of depression running through that family without genes having anything to do with it.

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So we look for a tighter relationship. The more closely related two individuals are, the more genes they share in common and, as it turns out, the more likely they are to share a depressive trait. As one of the most telling examples of this, take any two siblings (who are not identical twins). They share something like 50 percent of their genes. If one of them has a history of depression, the other has about a 25 percent likelihood, considerably higher than would be expected by chance. Now, compare two identical twins, who share all of their genes in common. And if one of them is depressive, the other has a 50 percent chance. This is quite impressive—the more genes in common, the more likelihood of sharing the disease. But there remains a confound: the more genes people share within a family, the more environment they share as well (starting with the fact that identical twins grow up treated more similarly than are non-identical twins).

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Tighten the relationship further. Look at children who were adopted at an early age. Consider those whose biological mother had a history of depression, but whose adoptive mother did not. They have an increased risk of depression, suggesting a genetic legacy shared with their biological mother. But the confound there, as we saw in chapter 6, is that “environment” does not begin at birth, but begins much earlier, with the circulatory environment shared in utero with one’s biological mother.

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For any card-carrying molecular biologist in the twenty-first century, if you want to prove that genes have something to do with depression, you’re going to have to identify the specific genes, the specific stretches of DNA that code for specific proteins that increase the risk for depression. As we’ll see shortly, precisely that has occurred in recent years.

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people who are undergoing a lot of life stressors are more likely than average to succumb to a major depression, and people sunk in their first major depression are more likely than average to have undergone recent and significant stress.

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Laboratory studies also link stress and the symptoms of depression. Stress a lab rat, and it becomes anhedonic. Specifically, it takes a stronger electrical current than normal in the rat’s pleasure pathways to activate a sense of pleasure. The threshold for perceiving pleasure has been raised, just as in a depressive.

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Critically, glucocorticoids can do the same. A key point in chapter 10 was how glucocorticoids and stress could disrupt memory. Part of the evidence for that came from people with Cushing’s syndrome (as a reminder, that is a condition in which any of a number of different types of tumors wind up causing vast excesses of glucocorticoids in the bloodstream)

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This has been a bit tricky to demonstrate. First, when someone is initially treated with synthetic glucocorticoids, the tendency is to get, if anything, euphoric and even manic, perhaps for a week or so before the depression kicks in. You can immediately guess that we are dealing with one of our dichotomies between short- and long-term stress physiology; chapter 16 will explore in even more detail where that transient euphoria comes from.

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As a second complication, does someone with Cushing’s syndrome or someone taking high pharmacological doses of synthetic glucocorticoids get depressed because glucocorticoids cause that state, or is it because they recognize they have a depressing disease? You show it is the glucocorticoids that are the culprits by demonstrating higher depression rates in this population than among people with, for example, the same disease and the same severity but not receiving glucocorticoids. At this stage, there’s also not much of a predictive science to this phenomenon. For example, no clinician can reliably predict beforehand which patient is going to get depressed when put on high-dose glucocorticoids, let alone at what dose, and whether it is when the dose is raised or lowered to that level. Nonetheless, have lots of glucocorticoids in the bloodstream and the risk of a depression increases.

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Stress and glucocorticoids tangle up with biology in predisposing a person toward depression in an additional, critical way. Back to that business about there being a genetic component to depression. Does this mean that if you have “the gene” (or genes) “for” depression, that’s it, you’re up the creek, it’s inevitable? Obviously not, and the best evidence for this is that factoid about identical twins. One has depression and the other, sharing all the same genes, has about a 50 percent chance of having the disease as well, a much higher rate than in the general population. There, pretty solid evidence for genes being involved. But flip this the other way. Share every single gene with someone who is depressive and you still have a 50 percent chance of not having the disease.

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Genes are rarely about inevitability, especially when it comes to humans, the brain, or behavior. They’re about vulnerability, propensities, tendencies. In this case, genes increase the risk of depression only in certain environments: you guessed it, only in stressful environments. This is shown in a number of ways, but most dramatically in a recent study by Avshalom Caspi at King’s College, London. Scientists identified a certain gene in humans that increases the risk of depression. More specifically, it is a gene that comes in a few different “allelic versions”—a few different types or flavors that differ slightly in function; have one of those versions, and you’re at increased risk. What that gene is I’m not telling yet; I’m saving it for the end of this chapter, as it is a doozy But the key thing is that having version X of this gene Z doesn’t guarantee you get depression, it just increases your risk. And, in fact, knowing nothing more about someone than which version of gene Z she has doesn’t increase your odds of predicting whether she gets depressed. Version X increases depression risk only when coupled with a history of repeated major stressors. Amazingly, the same has been shown with studies of some nonhuman primate species, who carry a close equivalent of that gene Z. It’s not the gene that causes it. It’s that the gene interacts with a certain environment. More specifically, a gene that makes you vulnerable in a stressful environment.

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Not surprisingly, glucocorticoid levels are typically abnormal in people who are clinically depressed. A relatively infrequent subtype of depression, called “atypical depression,” is dominated by the psychomotor features of the disease—an incapacitating physical and psychological exhaustion. Just as is the case with chronic fatigue syndrome, atypical depression is characterized by lower than normal glucocorticoid levels. However, the far more common feature of depression is one of an overactive stress-response—somewhat of an overly activated sympathetic nervous system and, even more dramatically, elevated levels of glucocorticoids. This adds to the picture that depressed people, sitting on the edge of their beds without the energy to get up, are actually vigilant and aroused, with a hormonal profile to match—but the battle is inside them.

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Research stretching back some forty years has explored why, on a nuts-and-bolts level, glucocorticoid levels are often elevated in depression. The elevated levels appear to be due to too much of a stress signal from the brain (back to chapter 2—remember that the adrenals typically secrete glucocorticoids only when they are commanded to by the brain, via the pituitary), rather than the adrenals just getting some depressive glucocorticoid hiccup all on their own now and then. Moreover, the excessive secretion of glucocorticoids is due to what is called feedback resistance—in other words, the brain is less effective than it should be at shutting down glucocorticoid secretion. Normally, the levels of this hormone are tightly regulated—the brain senses circulating glucocorticoid levels, and if they get higher than desired (the “desired” level shifts depending on whether events are calm or stressful), the brain stops secreting CRH. Just like the regulation of water in a toilet bowl tank. In depressives, this feedback regulation fails—concentrations of circulating glucocorticoids that should shut down the system fail to do so, as the brain does not sense the feedback signal.*

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the glucocorticoid angle fits well, in that the hormones can alter features of all three neurotransmitter systems—the amount of neurotransmitter synthesized, how fast it is broken down, how many receptors there are for each neurotransmitter, how well the receptors work, and so on. Moreover, stress has been shown to cause many of the same changes as well. Sustained stress will deplete dopamine from those “pleasure” pathways, and norepinephrine from that alerting locus ceruleus part of the brain. Moreover, stress alters all sorts of aspects of the synthesis, release, efficacy, and breakdown of serotonin. It is not clear which of those stress effects are most important, simply because it is not clear which neurotransmitter or neurotransmitters are most important. However, it is probably safe to say that whatever neurochemical abnormalities wind up being shown definitively to underlie depression, there is precedent for stress and glucocorticoids causing those same abnormalities.

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there may be problems with the hippocampus in people with major depression. This speculation was reinforced by the fact that the type of memory most often impaired in depression—declarative memory—is mediated by the hippocampus. As was discussed in chapter 10, there is atrophy of the hippocampus in long-term depression. The atrophy emerges as a result of the depression (rather than precedes it), and the longer the depressive history, the more atrophy and the more memory problems. While no one has explicitly shown yet that the atrophy occurs only in those depressives with the elevated glucocorticoid levels, the atrophy is most common in the subtypes of depression in which the glucocorticoid excess is most common.

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Chronic depression has also been associated in some studies with decreased volume in the frontal cortex. This was initially puzzling for those of us who view the world through glucocorticoid-tinted glasses, but has recently been resolved. In the rat, the hippocampus is overwhelmingly the target in the brain for glucocorticoid action, as measured by the density of receptors for the hormone; however, in the primate brain, the hippocampus and frontal cortex seem to be equally and markedly sensitive to glucocorticoids.

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So some pretty decent circumstantial evidence suggests that the glucocorticoid excess of depression may have something to do with the decreased volume of the hippocampus and frontal cortex. Chapter 10 noted an array of bad things that glucocorticoids could do to neurons. Some obsessively careful studies have shown loss of cells in the frontal cortex accompanying the volume loss in depression—as one point of confusion, it is those supportive glial cells rather than neurons that are lost. But in the hippocampus, no one has a clue yet; it could be the killing or atrophying of neurons, the inhibition of the birth of new neurons, or all the above.* Whatever the explanation is at the cellular level, it appears to be permanent; years to decades after these major depressions have been gotten under control (typically with medication), the volume loss is still there.

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—why is it that most of us can have occasional terrible experiences, feel depressed, and then recover, while a few of us collapse into major depression (melancholia)?

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we saw that certain features dominated as psychologically stressful: a loss of control and of predictability within certain contexts, a loss of outlets for frustration, a loss of sources of support, a perception of life worsening. In one style of experiment, pioneered by the psychologists Martin Seligman and Steven Maier, animals are exposed to pathological amounts of these psychological stressors. The result is a condition strikingly similar to a human depression.

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Although the actual stressors may differ, the general approach in these studies always emphasizes repeated stressors with a complete absence of control on the part of the animal. For example, a rat may be subjected to a long series of frequent, uncontrollable, and unpredictable shocks or noises, with no outlets.

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After awhile, something extraordinary happens to that rat. This can be shown with a test. Take a fresh, unstressed rat, and give it something easy to learn. Put it in a room, for example, with the floor divided into two halves. Occasionally, electricity that will cause a mild shock is delivered to one half, and just beforehand, there is a signal indicating which half of the floor is about to be electrified. Your run-of-the-mill rat can learn this “active avoidance task” easily, and within a short time it readily and calmly shifts the side of the room it sits in according to the signal. Simple. Except for a rat who has recently been exposed to repeated uncontrollable stressors. That rat cannot learn the task. It does not learn to cope. On the contrary, it has learned to be helpless.

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This phenomenon, called learned helplessness, is quite generalized; the animal has trouble coping with all sorts of varied tasks after its exposure to uncontrollable stressors. Such helplessness extends to tasks having to do with its ordinary life, like competing with another animal for food, or avoiding social aggression. One might wonder whether the helplessness is induced by the physical stress of receiving the shocks or, instead, the psychological stressor of having no control over or capacity to predict the shocks. It is the latter. The clearest way to demonstrate this is to “yoke” pairs of rats—one gets shocked under conditions marked by predictability and a certain degree of control, the other rat gets the identical pattern of shocks, but without the control or predictability. Only the latter rat becomes helpless.

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Seligman argues persuasively that animals suffering from learned helplessness share many psychological features with depressed humans. Such animals have a motivational problem—one of the reasons that they are helpless is that they often do not even attempt a coping response when they are in a new situation. This is quite similar to the depressed person who doesn’t even try the simplest task that would improve her life. “I’m too tired, it seems overwhelming to take on something like that, it’s not going to work anyway….”

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Animals with learned helplessness also have a cognitive problem, something awry with how they perceive the world and think about it. When they do make the rare coping response, they can’t tell whether it works or not. For example, if you tighten the association between a coping response and a reward, a normal rat’s response rate increases (in other words, if the coping response works for the rat, it persists in that response). In contrast, linking rewards more closely to the rare coping responses of a helpless rat has little effect on its response rate. Seligman believes that this is not a consequence of helpless animals somehow missing the rules of the task; instead, he thinks, they have actually learned not to bother paying attention. By all logic, that rat should have learned, “When I am getting shocked, there is absolutely nothing I can do, and that feels terrible, but it isn’t the whole world; it isn’t true for everything.” Instead, it has learned, “There is nothing I can do. Ever.” Even when control and mastery are potentially made available to it, the rat cannot perceive them. This is very similar to the depressed human who always sees glasses half empty. As Beck and other cognitive therapists have emphasized, much of what constitutes a depression is centered around responding to one awful thing and overgeneralizing from it—cognitively distorting how the world works.

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It takes surprisingly little in terms of uncontrollable unpleasantness to make humans give up and become helpless in a generalized way. In one study by Donald Hiroto, student volunteers were exposed to either escapable or inescapable loud noises (as in all such studies, the two groups were paired so that they were exposed to the same amount of noise). Afterward, they were given a learning task in which a correct response turned off a loud noise; the “inescapable” group was significantly less capable of learning the task. Helplessness can even be generalized to nonaversive learning situations. Hiroto and Seligman did a follow-up study in which, again, there was either controllable or uncontrollable noise. Afterward the latter group was less capable of solving simple word puzzles. Giving up can also be induced by stressors far more subtle than uncontrollable loud noises. In another study, Hiroto and Seligman gave volunteers a learning task in which they had to pick a card of a certain color according to rules that they had to discern along the way. In one group, these rules were learnable; in the other group, the rules were not (the card color was randomized). Afterward, the latter group was less capable of coping with a simple and easily solved task. Seligman and colleagues have also demonstrated that unsolvable tasks induced helplessness afterward in social coping situations.

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Thus humans can be provoked into at least transient cases of learned helplessness, and with surprising ease. Naturally, there is tremendous individual variation in how readily this happens—some of us are more vulnerable than others (and you can bet that this is going to be important in considering stress management in the final chapter). In the experiment involving inescapable noise, Hiroto had given the students a personality inventory beforehand. Based on that, he was able to identify the students who came into the experiment with a strongly “internalized locus of control”—a belief that they were the masters of their own destiny and had a great deal of control in their lives—and, in contrast, the markedly “externalized” volunteers, who tended to attribute outcomes to chance and luck. In the aftermath of the uncontrollable stressor, the externalized students were far more vulnerable to learned helplessness. Transferring that to the real world, with the same external stressors, the more that someone has an internal locus of control, the less the likelihood of a depression.

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But life is full of more significant examples. If a teacher at a critical point of our education, or a loved one at a critical point of our emotional development, frequently exposes us to his or her own specialized uncontrollable stressors, we may grow up with distorted beliefs about what we cannot learn or ways in which we are unlikely to be loved. In one chilling demonstration of this, some psychologists studied inner-city school kids with severe reading problems. Were they intellectually incapable of reading? Apparently not. The psychologists circumvented the students’ resistance to learning to read by, instead, teaching them Chinese characters. Within hours they were capable of reading more complex symbolic sentences than they could in English. The children had apparently been previously taught all too well that reading English was beyond their ability.

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A major depression, these findings suggest, can be the outcome of particularly severe lessons in uncontrollability for those of us who are already vulnerable. This may explain an array of findings that show that if a child is stressed in certain ways—loss of a parent to death, divorce of parents, being a victim of abusive parenting—the child is more at risk for depression years later. What could be a more severe lesson that awful things can happen that are beyond our control than a lesson at an age when we are first forming our impressions about the nature of the world? As an underpinning of this, Paul Plotsky and Charles Nemeroff of Emory University have shown that rats or monkeys exposed to stressors early in life have a lifelong increase in CRH levels in their brain.

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“According to our model,” writes Seligman, “depression is not generalized pessimism, but pessimism specific to the effects of one’s own skilled actions.” Subjected to enough uncontrollable stress, we learn to be helpless—we lack the motivation to try to live because we assume the worst; we lack the cognitive clarity to perceive when things are actually going fine, and we feel an aching lack of pleasure in everything.*

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