Why We Get Sick

by Randolph M. Nesse

  Love joins hate; aggression, fear; expansiveness, withdrawal; and so on; in blends designed not to promote the happiness and survival of the individual, but to favor the maximum transmission of the controlling genes.

  But much emotional pain is not useful. Some useless anxiety and depression arise from normal brain mechanisms, others from brain abnormalities. Major genetic factors contribute to the causation of anxiety disorders, depression, and schizophrenia. In the next decade, specific genes will no doubt be found responsible for certain kinds of mental disorders. Physiological correlates have been found for all of these disorders, and neuroscientists are hard at work unraveling the responsible proximate mechanisms. The resulting knowledge has already improved the utility of drug treatments and offers the possibility of prevention. This is a bright time for psychiatry and for people with mental disorders. The advances in pharmacologie treatment have come so fast that many people remain unaware of their safety and effectiveness. Treatment is now more effective than the wildest hopes of psychiatrists who went into practice just thirty years ago.

  Much confusion attends these advances. The human mind tends to oversimplify this issue by attributing most bad feelings either to genes and hormones or to psychological and social events. The messy truth is that most mental problems result from complex interactions of genetic predispositions, early life events, drugs and other physical effects on the brain, current relationships, life situations, cognitive habits, and psychodynamics. Paradoxically, it now is much easier to treat many mental disorders than it is to understand them.

  Just as there are several components of the immune system, each of which protects us against particular kinds of invasions, there are subtypes of emotion that protect us against a variety of particular kinds of threats. Just as arousal of the immune system usually occurs for a good reason, not because of an abnormality in its regulation mechanism, we can expect that most incidents of anxiety and sadness are precipitated by some cause, even if we cannot identify it. On the other hand, the regulation of the immune system can be abnormal. The immune system can be too active and attack tissues it shouldn’t, causing autoimmune disorders such as rheumatoid arthritis. Comparable abnormalities in the anxiety system cause anxiety disorders. The immune system can also fail to act when it should, causing deficiencies in immune function. Might there be anxiety disorders that result from too little anxiety?

  ANXIETY

  Everyone must realize that anxiety can be useful. We know what happens to the berry picker who does not flee a grizzly bear, the fisherman who sails off alone into a winter storm, or the student who does not shift into high gear as a term-paper deadline approaches. In the face of threat, anxiety alters our thinking, behavior, and physiology in advantageous ways. If the threat is immediate, say from the imminent charge of a bull elephant, a person who flees will be more likely to escape injury than one who goes on chatting nonchalantly. During flight, our survivor experiences a rapid heartbeat, deep breathing, sweating, and an increase in blood glucose and epinephrine levels. Physiologist Walter Cannon accurately described the functions of these components of the “fight or flight” reaction back in 1929. It is curious that his adaptationist perspective has never been extended to other kinds of anxiety.

  While anxiety can be useful, it usually seems excessive and unnecessary. We worry that it will rain at the wedding next June, we lose our concentration during exams, we refuse to fly on airplanes, and we tremble and stumble over our words when speaking in front of a group. Fifteen percent of the U.S. population has had a clinical anxiety disorder; many of the rest of us are just nervous. How can we explain the apparent excess of anxiety? In order to determine when it is useful and when it is not, we need to ask how the mechanisms that regulate anxiety were shaped by the forces of natural selection.

  Because anxiety can be useful, it might seem optimal to adjust the mechanism so that we are always anxious. This would be distressing, but natural selection cares only about our fitness, not our comfort. The reason we are sometimes calm is not because discomfort is maladaptive but because anxiety uses extra calories, makes us less fit for many everyday activities, and damages tissues. Why does stress damage tissues? Imagine a host of bodily responses that offer protection against danger. Those that are “inexpensive” and safe can be expressed continually, but those that are “expensive” or dangerous cannot. Instead, they are bundled into an emergency kit that is opened only when the benefits of using the tools are likely to exceed the costs. Some components are kept sealed in the emergency kit precisely because they cause bodily damage. Thus, the damage associated with chronic stress should be no cause for surprise and certainly no basis for criticizing the design of the organism. In fact, recent work has suggested that the “stress hormone” cortisol may not defend against outside dangers at all but instead may mainly protect the body from the effects of other parts of the stress response.

  If anxiety can be costly and dangerous, why isn’t the regulatory mechanism adjusted so that it is expressed only when danger is actually present? Unfortunately, in many situations it is not clear whether or not anxiety is needed. The smoke-detector principle, described previously, applies here as well. The cost of getting killed even once is enormously higher than the cost of responding to a hundred false alarms. This was demonstrated by an experiment in which guppies were separated into timid, ordinary, and bold groups on the basis of their reactions when confronted by a smallmouth bass: hiding, swimming away, or eyeing the intruder. Each group of guppies was then left in a tank with a bass. After sixty hours, 40 percent of the timid guppies and 15 percent of the ordinary guppies were still there, but none of the bold guppies had survived.

  The psychiatrist’s attempt to understand how natural selection has shaped the mechanism that regulates anxiety is conceptually the same as the electronics engineer’s problem of determining if a signal on a noisy telephone line is actually information or just static. Signal detection theory provides a way to analyze such situations. With an electronic signal, the decision about whether to call a given click a signal or noise depends on four things: (1) the loudness of the signal, (2) the ratio of signals to noise, (3) the cost of mistakenly thinking that a noise is actually a signal (false alarm), and (4) the cost of mistakenly thinking that a signal is actually a noise (false negative response).

  Imagine that you are alone in the jungle and you hear a branch break behind a bush. It could be a tiger, or it could be a monkey. You could flee, or you could stay where you are. To determine the best course of action, you need to know: (1) the relative likelihood that a sound of this magnitude would come from a tiger (as opposed to a monkey), (2) the relative frequency of tigers and monkeys in this location, (3) the cost of fleeing (the cost of a false alarm), and (4) the cost of not fleeing if it really is a tiger (the cost of a false negative response). What if you hear the sound of a medium-sized stick breaking behind that bush? The individual whose anxiety level is adjusted by an intuitive, quick, and accurate signal detection analysis will have a survival advantage.

  The analogy with the immune disorders suggests that there might be a whole category of people with unrecognized anxiety disorders, namely those who have too little anxiety. Isaac Marks, the anxiety expert at the University of London, has coined the term “hypophobies” for such people. They don’t complain and don’t seek psychiatric treatment but instead end up in emergency rooms or fired from their jobs. As psychiatrists prescribe new antianxiety drugs with few side effects, we may create such conditions. For instance, one patient, shortly after starting on an antianxiety medication, impulsively told her husband that she wanted him to leave. He was very surprised but did. A week later she realized that she had three small children, a mortgage, no income, and no helpful relatives. A bit more anxiety would have inhibited such hasty action. Of course, no case is simple. This particular woman had long-standing marital dissatisfactions, and her emotional outburst might, in the long run, have left her better off. Her story illustrates one possible
function of passions, as distinct from rational decisions. As suggested by Cornell economist Robert Frank, passions motivate actions that seem impulsive but may actually benefit the person in the long run.

  NOVEL DANGERS

  In the chapter on injuries, we described experiments that showed how monkeys’ fear of snakes is “prepared.” Most of our excessive fears are related to prepared fears of ancient dangers. Darkness, being away from home, and being the focus of a group’s attention were once associated with dangers but now mainly cause unwanted fears. Agoraphobia, the fear of leaving home, develops in half of people who experience repeated panic attacks. Staying home seems senseless until you realize that most episodes of panic in the ancestral environment were probably caused by close encounters with predators or dangerous people. After a few such close calls, a wise person would try to stay home when possible, would venture out only with companions, and be ready to flee in panic at the least provocation: the exact symptoms of agoraphobia.

  Do anxiety disorders, like many other diseases, result from novel stimuli not found in our ancestral environment? Not often. New dangers such as guns, drugs, radioactivity, and high-fat meals cause too little fear, not too much. In this sense we all have maladaptive hypophobias, but few of us seek psychiatric treatment to increase our fear. Some novel situations, especially flying and driving, do often cause phobias. In both cases, the fear has been prepared by eons of exposure to other dangers. Fear of flying has been prepared by the dangers associated with heights, dropping suddenly, loud noises, and being trapped in a small, enclosed place. The stimuli encountered in an automobile zooming along at sixty miles an hour are novel, but they too hark back to ancestral dangers associated with rapid movement, such as the rushing attack of a predator. Automobile accidents are so common and so dangerous that it is hard to say if fear of driving is beneficial or harmful.

  The genetic contributions to anxiety disorders are substantial. Most people with panic disorders have a blood relative who has the same problem, and the search is on for the responsible genes. Will these genes turn out to result from mutant genes that have not been entirely selected out? Will they turn out to have other benefits? Or will we discover that genetic susceptibility to panic is simply one end of a normal distribution, like a tendency to develop a high fever with a cold or a tendency to vomit readily? When we find specific genes that predispose to panic and other anxiety disorders, we will still need to find out why those genes exist and persist.

  SADNESS AND DEPRESSION

  Depression sometimes seems like a modern plague. After motor vehicle accidents, suicide is the second leading cause of death of young adults in North America. Nearly 10 percent of young adults in the United States have experienced an episode of serious depression. Furthermore, the rates seem to have increased steadily in the past few decades, doubling every ten years in many industrial countries.

  Depression may seem completely useless. Even apart from the risk of suicide, sitting all day morosely staring at the wall can’t get you very far. A person with severe depression typically loses interest in everything—work, friends, food, even sex. It is as if the capacities for pleasure and initiative have been turned off. Some people cry spontaneously, but others are beyond tears. Some wake every morning at 4 A.M. and can’t get back to sleep; others sleep for twelve or fourteen hours per day. Some have delusions that they are impoverished, stupid, ugly, or dying of cancer. Almost all have low self-esteem. It seems preposterous even to consider that there should be anything adaptive associated with such symptoms. And yet depression is so frequent, and so closely related to ordinary sadness, that we must begin by asking if depression arises from a basic abnormality or if it is a dysregulation of a normal capacity.

  There are many reasons to think that the capacity for sadness is an adaptive trait. A universal capacity, it is reliably elicited by certain cues, notably those that indicate a loss. The characteristics of sadness are relatively consistent across diverse cultures. The hard part is figuring out how these characteristics can be useful. The utility of happiness is not difficult to understand. Happiness makes us outgoing and gives us initiative and perseverance. But sadness? Wouldn’t we be better off without it? One test would be to find people who do not experience sadness and see if they experience any disadvantages. Or an investigator could use a drug that blocks normal sadness, a study that we fear may soon be conducted inadvertently on a massive scale as more and more people take the new psychoactive drugs. While we wait for such studies to be done, the characteristics of sadness and the situations that arouse it provide clues that may help us to discover its functions.

  The losses that cause sadness are losses of reproductive resources. Whether of money, a mate, reputation, health, relatives, or friends, the loss is always of some resource that would have increased reproductive success through most of human evolution. How can a loss be an adaptive challenge, a situation that would benefit from a special state of preparation? A loss signals that you may have been doing something maladaptive. If sadness somehow changes our behavior so as to stop current losses or prevent future ones, this would be helpful indeed.

  How can people behave differently after a loss in a way that increases fitness? First, you should stop what you are doing. Just as pain can make us let go of a hot potato, sadness motivates us to stop current activities that may be causing losses. Second, it would be wise to set aside the usual human tendency to optimism. Recent studies have found that most of us consistently overestimate our abilities and our effectiveness. This tendency to optimism helps us to succeed in social competition, where bluffing is routine, and also keeps us pursuing important strategies and relationships even at times when they are not paying off. After a loss, however, we must take off the rose-colored glasses in order to reassess our goals and strategies more objectively.

  In addition to sudden losses, there are situations in which an essential resource is simply not available despite major expenditures and our best plans and efforts. Jobs end, friendships fade, marriages sour, and goals must be abandoned. At some point one must give up on a major life project in order to use the resources to start something else. Such giving up should not be done lightly. Quitting one’s job shouldn’t be done impulsively, because there are costs involved in retraining and starting at the bottom of another hierarchy. Likewise, it is foolish to casually give up any important relationship or life goal in which a major investment has already been made. So we don’t usually make major life changes quickly. “Low mood” keeps us from jumping precipitously to escape temporary difficulties, but as difficulties continue and grow and our life’s energies are progressively wasted, this emotion helps to disengage us from a hopeless enterprise so that we can consider alternatives. Therapists have long known that many depressions go away only after a person finally gives up some long-sought goal and turns his or her energies in another direction.

  The capacity for high and low mood seems to be a mechanism for adjusting the allocation of resources as a function of the propitiousness of current opportunities. If there is little hope of payoff, it is best to sit tight rather than to waste energy. Real estate agents who enter the business during an economic downturn may be making a mistake. Students who are failing a course would sometimes do best to drop it and try another subject. Farmers who plant their fields during a drought may go broke. If, by contrast, we come upon a short-lived opportunity, then it may be best to make a major, intense effort, despite the possible risks, in order to have a chance at a big payoff. When a million dollars in cash fell out of the back of an armored car on the streets of Detroit, a few people who made an intense, brief effort profited nicely.

  A better understanding of the functions of sadness will soon be essential. We are fast gaining the capacity to adjust mood as we choose. Each new generation of psychotropic drugs has increasing power and specificity with fewer side effects. Decades ago there was a hue and cry about “soma,” the fictional drug that made people tolerate tedious lives in Aldous Huxley�
��s Brave New World. Now that similar substances loom as a reality, strangely little is being said. Do people not realize how fast this train is moving? We certainly should try to relieve human suffering, but is it wise to eliminate normal low mood? Many people intuitively feel it is wrong to use drugs to change mood artificially, but they will have a hard time arguing against the use of nonaddicting drugs with few side effects. The only medical reason not to use such drugs is if they interfere with some useful capacity. Soon—very soon—people will be clamoring to know when sadness is useful and when it is not. An evolutionary approach provides a foundation for addressing these questions.

  We are aware that this analysis is vastly oversimplified. People are not controlled by some internal calculator that crudely motivates them to maximize their reproductive success. Instead, people form deep, lifelong emotional attachments and experience loves and hates that shape their lives. They have religious beliefs that guide their behavior, and they have idiosyncratic goals and ambitions. They have networks of friends and relatives. Human reproductive resources are not like the squirrel’s cache of nuts. They are, instead, constantly changing states of intricate social systems. All these complexities do not undercut our simple arguments; they just highlight the urgency of blazing the trail of functional understanding that the adaptationist program may provide for human emotions.