Why We Get Sick (34 page)

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Authors: Randolph M. Nesse

BOOK: Why We Get Sick
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E
MOTIONS

U
npleasant emotions can be thought of as defenses akin to pain or vomiting. Just as the capacity for physical pain has evolved to protect us from immediate and future tissue damage, the capacity for anxiety has evolved to protect us against future dangers and other kinds of threats. Just as the capacity for experiencing fatigue has evolved to protect us from overexertion, the capacity for sadness may have evolved to prevent additional losses. Maladaptive extremes of anxiety, sadness, and other emotions make more sense when we understand their evolutionary origins and normal, adaptive functions. We also need proximate explanations of both the psychological and brain mechanisms that regulate and express these emotions. If we find what look like abnormalities in the brains of people who are anxious or sad, we cannot conclude that these brain changes cause the disorder in any but the most simplistic sense. Brain changes associated with anxiety or sadness may merely reflect the normal operation of normal mechanisms.

Knowledge about the normal functions of the emotions would provide, for psychiatry, something like what physiology provides for the rest of medicine. Most mental disorders are emotional disorders, so you might think that psychiatrists are well versed in the relevant scientific research, but no psychiatric training program systematically teaches the psychology of the emotions. This is not as unfortunate as it seems, since research on the emotions has been as fragmented and confused as psychiatry itself. In the midst of ongoing technical debates, however, many emotions researchers are reaching consensus on a crucial point:
our emotions are adaptations shaped by natural selection
. This principle holds substantial promise for psychiatry. If our emotions are subunits of the mind, they can be understood, just like any other biological trait, in terms of their functions. Doctors of internal medicine base their work on understanding the functions of cough and vomiting and the liver and the kidneys. An understanding of the evolutionary origins and functions of the emotions would begin to provide something similar for psychiatrists.

Many scientists have studied the functions of the emotions. Some have emphasized communication, especially University of California psychologist Paul Ekman, whose studies of the human face demonstrate the cross-cultural universality of emotions. Others emphasize the utility of emotions for motivation or other internal regulation, but emotions have not been shaped to perform one or even several functions. Instead, each emotion is a specialized state that simultaneously adjusts cognition, physiology, subjective experience, and behavior, so that the organism can respond effectively in a particular kind of situation. In this sense, an emotion is like a computer program that adjusts many aspects of the machine to cope efficiently with the challenges that arise in a particular kind of situation. Emotions are, in the felicitous phrase coined by University of California psychologists Leda Cosmides and John Tooby, “Darwinian algorithms of the mind.”

Emotional capacities are shaped by situations that occurred repeatedly in the course of evolution and that were important to fitness. Attacks by predators, threats of exclusion from the group, and opportunities for mating were frequent and important enough to have shaped special patterns of preparedness, such as panic, social fear, and sexual arousal. Situations that are best avoided shape aversive emotions, while situations that involve opportunity shape positive emotions. Our ancestors seem to have faced many more kinds of
threats than opportunities, as reflected by the fact that twice as many words describe negative as positive emotions. This perspective gives the boot to the modern idea that “normal” life is free of pain. Emotional pain is not only unavoidable, it is normal and can be useful. As E. O. Wilson put it,

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?

A
NXIETY

E
veryone 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.

N
OVEL
D
ANGERS

I
n 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.

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