Why We Get Sick (36 page)

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Authors: Randolph M. Nesse

BOOK: Why We Get Sick
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Our new technology also dissolves supportive social groups. For members of our socially oriented species, the worst punishment is solitary confinement, but many modern, anonymous groups are not much better. They often consist mostly of competitors with only an occasional comrade and no blood relatives. Extended families disintegrate as individuals scatter to pursue their economic goals. Even the nuclear family, that last remnant of social stability, seems doomed, with more than half of all marriages now ending in divorce and more and more children being born to single women.

We have a primal need for a secure place in a supportive group. Lacking family, we turn elsewhere to meet this need. More and more people have their social base in groups of friends, twelve-step programs such as Alcoholics Anonymous, support groups of all kinds, or psychotherapy. Many people turn to religion in part because of the group it provides. Some people advocate “family values” in hopes of preserving a threatened but cherished way of life. Most of us want most of all to be loved by someone who cares about us for ourselves, not for what we can do for them. For many, the search is bitter and fruitless.

L
ACK OF
A
TTACHMENT

P
re-evolutionary theories, both psychoanalytic and behavioral, explained the bond between mother and child as the result of feeding and caretaking. Primatologist Harry Harlow began to challenge these theories with studies of monkeys at the University of Wisconsin in the early 1950s. Infant monkeys were
separated from their mothers and provided with two surrogate mothers, one a wire form with a baby bottle full of milk, the other a soft cloth-covered form without a bottle. Although infants got milk from the wire mother, it was the cloth surrogate they clung to, screaming if it was removed. Harlow concluded that there must be a special mechanism that evolved
to
facilitate the bonding of mother and infant. Inspired by Rene Spitz’s studies of the social inadequacy of children raised in orphanages, Harlow next raised monkey infants in isolation. Such monkeys never became normal. They could not get along with other monkeys, had great difficulty in mating, and neglected or attacked any babies they had.

John Bowlby, an English psychiatrist, attended seminars with biologist Julian Huxley in 1951 and was inspired to read the imprinting experiments done by Nobel Prize-winning ethologist Konrad Lorenz. During a very specific critical period early in life, baby goslings imprint on their mothers or any other appropriate-sized moving object they encounter. Konrad Lorenz’s boots were sufficiently similar, and many photos show him being trailed by a line of goslings. Bowlby wondered if many of his patients’ difficulties were sequelae of problems with early attachment. As he looked at their first relationships, he found problems everywhere. Some had mothers who had never wanted them, others had mothers who were too depressed to respond to smiles and coos. Many had heard their mothers threaten to kill themselves and had grown up under this specter. People’s early difficulties matched the problems they experienced as adults. They could not trust people, they expected to be rejected, and they felt they had to please people or they would be abandoned. Bowlby perceptively recognized that some of the clinging and withdrawal behavior of neglected babies might be adaptive attempts to engage the mother. Instead of criticizing patients for being “dependent,” he recognized that they were trying to protect themselves from a feared separation.

Psychologist Mary Ainsworth and her colleagues did the controlled studies that brought Bowlby’s theories to mainstream psychology. She put young children into a room and observed their behavior when the mother left and later returned. On the basis of this “strange situation” test, she classified babies into those who were securely attached and those who were anxiously attached or who avoided their mothers on reunion. Which group the child fit into strongly predicted many other characteristics from group-play patterns to personality characteristics many years later. Much remains
to be done to determine what the relationship is between attachment problems and adult psychopathology and how it relates to genetic factors. Psychiatrists should not forget that mothers provide not only early experiences for their children; they also provide genes. At present we have reason to believe that many problems adults have in getting along with other people may have their origins in problems with the first attachment.

C
HILD
A
BUSE

C
hild abuse seems to have become epidemic among us. How can this be? Why would we attack our own children, the vehicles of our reproductive success? Are some parents more likely to abuse than others? Canadian psychologists Martin Daly and Margo Wilson’s evolutionary perspective led them to wonder if the presence or absence of a blood relationship between parents and children might predict the likelihood of child abuse. Because of the vagaries in the reporting of child abuse, they looked at an outcome that was easy to count and hard to hide—murders of children by their parents. The correlation was stronger than even they had dared to imagine. The risk of fatal child abuse for children living with one nongenetic parent is seventy times higher than it is for children living with both biological parents. This finding was not explainable by any tendency of families with stepparents to have more alcoholism, poverty, or mental illness. In several decades of research, no other risk factor has proved anywhere near as powerful in predicting child abuse. Many who have studied child abuse for decades never thought to look at the significance of kinship, but to evolutionists this was an obvious suspect.

Daly and Wilson were inspired, in part, by studies on infanticide in animals carried out by California anthropologist Sarah Hrdy and others. When Hrdy reported in 1977 that male languar monkeys routinely tried to kill the infants of females in a group they had just taken over from another male, no one wanted to believe her. She reported that the monkey mothers tried to protect their infants but often did not succeed. When they failed, nursing stopped, estrus came quickly, and the monkey mothers promptly mated with the males who had killed their infants. Hrdy noted that males who killed existing infants
would increase their reproductive success because the cessation of nursing brought the females into estrus so they could become pregnant with the offspring of the new male sooner.

Subsequent field research has confirmed Hrdy’s findings and extended them to many other species. Male lions kill existing cubs when they begin mating with new females. Among mice, the mere smell of a strange male often induces miscarriage—apparently an adaptation to prevent wasting investment on babies that are likely to be killed. Animals are inevitably designed to do whatever will increase the success of their genes, grotesque though the resulting behavior may seem.

The tendency for male animals to kill the offspring of other males in certain circumstances is an evolved adaptation. Is child abuse in humans in any way related? We had thought not, both because human males don’t routinely take over a group of breeding females with young offspring and because many foster fathers are obviously capable of providing excellent care for children who are not their own. We had guessed that children are abused not because of an evolved adaptation but because a normal adaptation failed when one of the parents had too little early contact with the child to facilitate normal attachment. However, studies by anthropologist Mark Flinn in Trinidad have found that stepparents still treat their stepchildren more harshly than their natural children, regardless of the amount of early contact with the baby. More is involved in forming human attachments than merely spending time together. Much more research is needed to explore this murky intersection of biology and culture.

S
CHIZOPHRENIA

T
he symptoms of schizophrenia, unlike those of anxiety and depression, are not a part of normal functioning. Hearing voices, thinking that others can read your mind, emotional numbness, bizarre beliefs, social withdrawal, and paranoia appear together as a syndrome not because they are parts of an evolved defense. It is more likely that one kind of brain damage can cause many malfunctions, just as heart damage can cause shortness of breath, chest pain, and swollen ankles. Schizophrenia disrupts the
perceptual-cognitive-emotional-motivational system. This is another way of saying that we still don’t know how to describe the higher levels of brain function.

Schizophrenia affects about 1 percent of the population in diverse societies worldwide. The notion that it is a disease of civilization seems to be incorrect, although there have recently been suggestions that the course of the disease is worse in modern societies. Compelling evidence suggests that susceptibility to schizophrenia depends on certain genes. Relatives of schizophrenics are several times more likely than other people to get the disease, even if they were raised by nonschizophrenic adoptive parents. If one identical twin has schizophrenia, the chance of the other getting it is about 50 percent, while the risk for a nonidentical twin is about 25 percent. There is also evidence that schizophrenia decreases reproductive success, especially in men.

These observations call up our standard question: What can account for the high incidence of genes that can decrease fitness? Selection against the genes that cause schizophrenia is strong enough that they should be far less common if their presence were due simply to mutation balanced by selection. Furthermore, the relatively uniform rates of schizophrenia suggest that the responsible genes did not arise recently but have been maintained for millennia. It appears that the genes that cause schizophrenia must somehow confer an advantage that balances the severe costs.

The most likely possibility is that these genes are advantageous in combination with certain other genes, or in certain environments, much in the way a single sickle-cell gene is advantageous even though having two such genes causes sickle-cell anemia. Or it might be that the genes that predispose to schizophrenia have other effects that offer a slight advantage in most people who have them, even though a small proportion develop the disease. A number of authors have speculated on the kinds of advantages that might accrue to people who have genes that predispose to schizophrenia: perhaps they increase creativity or sharpen a person’s intuitions about what others are thinking. Perhaps they protect against some disease. Some have suggested that the tendency to suspiciousness itself may compensate somewhat for the disadvantages of schizophrenia. Evidence for these ideas remains scattered, but they are worth pursuing. Support is provided by evidence of high levels of accomplishment in relatives of schizophrenics who are not affected by the disease. This whole area is just beginning to be explored.

S
LEEP
D
ISORDERS

S
leep, like so many other bodily capacities, commands our attention only when it goes awry, which it does for many people in many ways. For sleep, as for so many things, timing is often the crucial factor. Most sleep problems involve an inability to sleep at the proper time or a tendency to sleep at the wrong time. Insomnia affects more than 30 percent of the population and is the spur to a huge industry, from over-the-counter sleeping pills to specialized medical clinics. The people who suffer from daytime sleepiness are often the same ones who don’t sleep well at night. Sleepiness is a bother when you are trying to read in the evening, a handicap after the alarm rings in the morning, and a positive danger if it happens while you are driving.

Then there are dreams and their disorders, nightmares and night terrors. Some people experience a kind of lack of coordination of the aspects of sleep and become conscious while still dreaming and unable to move, a frightening state indeed. People with narcolepsy slip suddenly into dreaming sleep in the midst of everyday activities, sometimes so swiftly that they fall and injure themselves. And then there are the people with sleep apnea, who intermittently stop breathing during sleep with resulting nighttime restlessness, daytime tiredness, and even brain damage. In order to understand these problems, we need to know more about the origins and functions of normal sleep.

Is sleep a trait that has been shaped by natural selection? There are several reasons to think so. First, the trait is widespread among animals and perhaps universal among vertebrates. In some animals that seem not to sleep, such as dolphins, one half of the brain in fact sleeps while the other stays awake, possibly because they must repeatedly swim to the surface to breathe. Second, all vertebrates seem to share the same sleep regulation mechanisms, with the center that controls dreaming sleep consistently located in the ancient parts of the brain. Third, the patterns of mammalian sleep, with its periods of rapid eye movement and rapid brain waves, are also shared with birds, whose evolution diverged from ours before the time of the dinosaurs. Fourth, the wide variation in the actual patterns of sleep, even in closely related mammals, suggests that whatever kind of sleeping was done by our most recent common ancestor could evolve
rapidly to match the species’ particular ecological niche. Finally, if deprived of sleep, all animals function poorly.

In order to better understand sleep difficulties, we would like to understand how the capacity and necessity for sleep increase fitness. One major contribution to the problem came in 1975 from British biologist Ray Meddis, who proposed that the amount and timing of our sleep are set by our potential for productive activity in different phases of the day-night cycle. As one reviewer of Meddis’s book put it, our motivation to sleep at night arises from the desirability of staying off the streets. If there are special dangers in being abroad in the dark and little likelihood of positive accomplishment then, we are better off resting. This explains why humans and other animals benefit from a daily cycle of activity, but it does not explain why we sleep instead of just spending the night quietly awake, ready for any opportunities or dangers that may arise. It also does not explain why we have become so dependent on sleep that its lack makes us barely able to function.

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