THE DUTCH VIOLENCE STUDY gave a much needed boost to the morale of the Lohengrins of behavioral genetics, who had, on several occasions, thought they had found their Holy Grail, only to have it prove an alluring fake. Even the Dutch study’s results, persuasive as they were, lacked replication by others, leaving the well-publicized failures looming over the field. Most behavioral geneticists, however, saw the failures as temporary misfires in a contest in which bull’s-eyes were only a few volleys away.
In addition to the damage to morale, the premature cries of “eureka” had the inevitable effect of making everyone in the field exceptionally slow to claim success. This was particularly apparent in 1994, when a group researching manic depression under Wade Berrettini, a psychiatrist at Jefferson Hospital in Philadelphia, was certain they had found a gene that in their guarded words, “increases the susceptibility to bipolar illness.” This time the depression-gene “sighting” was no place near the locations pegged by the Amish and Israeli studies, but on a different chromosome altogether, number 18.
While admirably muted in their announcement, the group’s finding seemed to herald a game of follow the bouncing genes—not to be confused with Barbara McClintock’s hopping genes—and maintained to a degree the shooting-from-the-hip impression gene hunters were making on outsiders. Of course, because the genome is such a vast molecular configuration, for a broadly defined disorder like depression, there is no reason why all three locations couldn’t be correct—each for a different type of depression or each an ingredient in a depression that stemmed from a combination of genetic anomalies.
Unlike the earlier behavioral-gene studies that had been trumpeted from newspaper front pages, the Berrettini study was announced in a discreet throat-clearing in the July 1994 issue of Proceedings of the Academy of Natural Sciences. The project had been begun ten years earlier, so had been in progress at the same time as the Amish and Israeli studies; its team of researchers was all too aware of the embarrassment that can come from premature announcements. Its first six years were spent locating a number of afflicted families, enough for a meaningful study. Eventually the team found twenty-two families, each averaging about seventeen members and, each with approximately seven or eight cases of depression, for a total of 365 individuals. (One family had been “borrowed” from the Amish study, which was a nice instance of scientific cooperation.)
Starting with no prior assumptions and no clues such as a probable X chromosome linkage, the Berrettini group adopted a strategy of searching the entire genome, a task so colossal as to have been inconceivable a few years earlier. As if in punishment for their ambition, the group was as unlucky as the Huntington’s people had been lucky in their choice of the area of DNA to start their search. Three years passed before the Berrettini group found the anomaly they were seeking on chromosome 18, one of the last places they looked.
When I spoke with Dr. Berrettini, he downplayed his find. “I wouldn’t call if a breakthrough,” he said. When I asked him, however, if his research had succeeded where the Amish study had failed, he was a bit more upbeat. “I hope so,” he said, then added, “The gold standard for this sort of research is whether or not independent confirmation can be observed. That is, can you collect a second series of families and see the same results? I understand this has now been done.”
WITH TWO FIRM VICTORIES in establishing a genes-behavior link on the DNA itself, few human geneticists doubted that others would be coming rapidly. By the summer of 1994, the process appeared so solidly on track that attention was jumping ahead to the next step in enlightenment: the mechanism by which gene expression translated into behavior. Much of the process appeared to involve gene products like hormones, enzymes, and neurotransmiters, as Jerome Kagan, Brunner, and others were discovering. One hormone in particular, testosterone, was receiving considerable attention, in part because of its relevance to the hot topic of gender but also because it was proving so interesting in itself. In his 1994 book Social Structure and Testosterone, Theodore Kemper of Rutgers University summarized the extensive research on testosterone and its influence on behavior. His central thesis went beyond the increasingly established effect the body’s internal chemistry has on human behavior but rather examined the surprising effect the environment has on body chemistry.
A noteworthy example Kemper offered involves leadership. A number of studies had shown that testosterone levels are higher in men in leadership positions than in subordinates. On hearing just this part of the findings, few would sense anything remarkable about it, assuming the higher testosterone level was a reason, perhaps the reason, that the men were leaders. As logical and pro-intuitive as such an assumption might seem, it would be wrong. It was later discovered that the testosterone level rose after the men became leaders (which, for the ambitious, may well be an important secret of the universe). The added testosterone was an effect, not a cause. Similar environmentally induced fluctuations have been noted as well with serotonin. At a time when psychologists were discovering that the environment has less effect on personality development than previously thought, biochemists were coming along and saying the environment can have profound effects on internal biochemistry, which in turn affects personality.
The responsiveness of testosterone to life situations was demonstrated in studies involving different environmental situations. One of the more interesting found that U.S. Naval Academy midshipmen had far lower testosterone levels in their first year, when they were miserable plebes, than when they reached the exalted upper grades. An added curiosity that turned up in an unrelated study was that after having sex with a partner, a male’s testosterone level rose, but after the same men masturbated alone, it remained the same. This would suggest that testosterone is not only highly responsive to surrounding situations but also that it is not easily fooled as to whether it has just experienced real turtle soup or merely the mock.
All of this had big implications for the genetics of behavior. The responsiveness of gene-produced testosterone to environmental conditions and the known effects higher levels of testosterone have on behavior raises large questions about the gene-environment interactions. Just as it is no longer possible to think of the environment as a monolithic and all-powerful molder of personality and behavior, so does the testosterone research suggest ways in which the environment, even within a normal range (pace, Sandra Scarr), can perhaps affect genetic expression.
Other research is turning up entirely new complications to the gene-enviroment equation. Stephen Suomi of the National Institute for Child Health and Human Development, in experiments with rhesus monkeys, found that when infant monkeys who had been bred to be inhibited and fearful were given to foster-mother monkeys who had opposite personalities—that is, uninhibited and fearless—not only did the infants become bold like their new mothers but they also developed the relevant brain chemistry, which for boldness meant low levels of norepinephrine. Most surprising of all, the changes appeared to be permanent.
This field of research into environmental alterations of hormone action, and in some cases gene action, is one of the last frontiers of the entire biology-environment conundrum. Other experiments indicated that repeated stressful experiences can turn laboratory animals into nervous wrecks, which is not so surprising. What was surprising, however, was that the prolonged stress-exposure brought about permanent changes in their nervous systems, including the expression of some genes. According to Suomi, “experience can push genetic constitution around. Its effect is so profound, I’d call it temperament.” This doesn’t overturn existing behavioral genetics thinking in that repeated stress falls outside Scarr and Plomin’s “normal range,” but it still bothers those who like their genes-environment dichotomies clear-cut.
THE DYNAMIC COMPLEXITY of norepinephrine may create an unnecessarily complicated example of the mysteries that lie between a gene and a behavioral trait. A clearer, more manageable example turned up late in 1993 in experiments done on an unprepossessing creature, small and furry,
the prairie vole. In the latter half of the century, animal-behavior studies have contributed mightily to the revolution in the understanding of human behavior. Numerous research projects have pried open the gene-rooted behaviors and social organization of many species and, with similarities to human behavior that were too obvious to deny, played a major role in the seismic shift in thinking about human nature over the past forty years. While this science of ethology has increased understanding of such human activities as mating, political organization, and altruistic acts, recent research on this one small mammal, the vole, is highly suggestive of the way gene-produced body chemicals lead to specific forms of behavior.
Experiments on voles done at the National Institutes of Health by Thomas Insel found that two hormones present in voles as well as in humans, oxytocin and vasopressin, had important effects on the animals’ approach to mating and to family life, aspects of behavior that are very distinctive in voles (and endlessly interesting to humans). The two hormones were long known to affect, in both voles and humans, physiological functions such as blood pressure and, in females, milk production. But by injecting the voles with a drug that blocked the hormones’ effects, Insel found not only the expected physiological changes but also marked behavioral changes as well.
Voles, like many mammals and especially rodents, have rigid mating and parenting habits. Both sexes are monogamous, for example, and as parents are obsessively doting. When the two hormones were blocked, however, dramatic changes occurred in both of these characteristics. Generally, when male voles mate for the first time, they immediately become superattentive to the female of choice and fiercely protective of her—model husbands, in short. On the other hand, when vasopressin was blocked in the males, they remained as keen on sex but after enjoying it showed a caddish lack of interest in their partner. Even worse, if other males approached the females with carnal intentions, the husbands shrugged and wandered off.
A variation on this experiment was tried with results reminiscent of Tristan and Isolde’s love potion. When a blocked male vole was given vasopressin treatments, he fell in love with the first female at hand, even before the usual coital trigger to affections. A big dose of vasopressin was enough to make him as ardent and protective as he would have been had he mounted her. With the hormone you saw the usual vole behavior, devotion with respect. Without it, you saw callous indifference.
The other hormone, oxytocin, appears to have as strong an influence on female voles’ parental instinct as vasopressin does on males’ mating behavior. For several years it has been known that the hormone makes females of a number of species eager to mate, keen on cuddling, and tireless in caring for their young. This raises the possibility that the reason human mothers submit to endless drudgery of rearing their young may not be because of parenting theories, religious upbringing, family values, or memories of their own childhoods. All such environmental elements may reinforce the self-sacrificing maternal behavior, but the real motivator may be a protein manufactured in the brain over which mothers have no control.
Curiously, other vole genuses lack these reactions to alterations in the levels of the two hormones, but evidence is accumulating that they may produce similar effects in humans. If this should turn out to be true, the commercial possibilities are limitless. Mothers who are considering abandoning their young could pop an oxytocin pick-me-up and return happily to the child-rearing grind. Or child-welfare agencies could require administering an occasional oxytocin injection before handing over cash benefits. When welfare mothers suspect their indifferent husbands are about to skip out on them, they could drop some vasopressin into their coffee and find themselves with storybook lover-dads. Yet another application would be the vasopressin nightcap, which would guarantee women that casual male pickups would send flowers or at least phone the next day.
TWELVE
THE UPS AND DOWNS OF HUMAN NATURE
THE NATURE-NURTURE DEBATE has been raging, in one form or another, as long as humans have reflected about themselves. Adam and Eve started things off by calling attention to their innate nature (good but weak), while their nemeses, the serpent and the apple tree, could be considered environmental influences—leaving only the question of whether the Garden of Eden, as a rearing environment, fell within Sandra Scarr’s “normal range.” There have been so many fluctuations in the fortunes of the biological versus the environmental positions that it was inevitable that in recent times apathy has set in among bystanders. First one side’s up, then the other; exhausted by these pendulum swings, much of the public has developed a cry-wolf indifference to the issue. That this reaction should happen now is both ironic and unfortunate in that science finally appears to have resolved the problem once and for all.
The conclusion that both sides now seem to agree on is that nature-or-nurture is a nonquestion. There was nothing wrong with the two concepts—nature, for genes and biology; nurture for the environment. There was plenty wrong, it turns out, with the “or.” The most cogent dismissal of this thinking must be that of Martin Daly and Margo Wilson, who wrote in their landmark 1988 book Homicide: “One might just as well ask whether hemoglobin or air is more essential to human survival.” This is a particular apt analogy, not only because both genes and environment are fundamental to development but also because their interaction is too.
The question, then, turns out to have been bogus, at least in the either-or form in which it was cast. Still, the longevity and virulence of the debate is surely a result of its relationship to fundamental questions on man’s nature that scientists and thinkers have grappled with throughout history. And because the conclusions about humans were so momentous, the matter has been the staked-out turf of powerful political and religious institutions whose systems were erected upon their conceptions of this essence, of human nature itself.
So the debate has not been an abstract conundrum, a pastime for medieval monks, dormitory bull sessions, or competing schools of psychology. It is a question that can determine the way in which humans are reared, governed, educated, punished—and how they see themselves in relationship to their gods, to their governments, and to one another. It is no wonder that throughout history entrenched powers, spiritual and temporal, have ferociously defended their dogmatic pronouncements on mankind’s essential nature—and many still do.
In looking over this history of fluctuating views about human personality and behavior, one of the most revealing areas is the changing beliefs about mental illness over the centuries. This specialized area might sound extraneous to discussions of normal behavior, but it is closely related, in that theories about mental illness invariably rest on theories about normal brain function. Because for much of this century, non-ill behavior was not seen as having any direct connection to our physical selves (mind and body were distinct entities), the approaches to mental illness provide a rare glimpse, basically the only glimpse, of the evolving view over the centuries of the mind-body connection and earlier attempts to explain individual differences.
The ancient Greeks had a simple, straightforward view: If a person was mentally ill, it was a result of a physical malfunction of the brain. According to Hippocrates, insanity was brought on by an imbalance in the four basic body fluids, or humors—blood, phlegm, yellow bile, and black bile. This analysis, which has long appeared more metaphorical than scientific, now seems to be closer to the truth—Jerome Kagan’s neurological broth, for instance—than the insanity theories that held sway for the two millennia following Hippocrates.
For many of these centuries, lunacy was explained as possession by witches or evil spirits. The condition was considered a punishment for some terrible transgression, an explanation that conveniently justified killing the afflicted or in other ways disposing of them. In the Middle Ages, this folk wisdom was given theological respectability by the Church, which held the devil himself responsible for crazed behavior. Throughout this period, more thoughtful and skeptical people toyed with other, less fanciful and more evidence-based e
xplanations; but scientific theories that conflicted with Church teaching invariably ran into trouble. With the perplexing phenomenon of insanity, few scientists were willing to go up against the Church armed with little more than hunches. In fact, for centuries there weren’t many hunches. Baffled by insanity, most people were content to shake their heads and accept the Church’s dictum that such behavioral anomalies were God’s will or the devil’s mischief.
In the eighteenth century this resignation began to weaken as more and more doctors sought medical explanations for mental problems. Prominent among these was the eminent Philadelphia physician Benjamin Rush, a signer of the Declaration of Independence, who diverted his political rebelliousness to the prevailing beliefs about many diseases, in particular, insanity. Rush was convinced it was caused not by demons and devils, nor by bad behavior, but by a physical malfunctioning of the brain.
Throughout the nineteenth century a handful of physicians pursued this concept. In 1844 another American doctor, A. L. Wigan, wrote a book entitled A New View of Insanity: The Duality of the Mind—Proved by the Structure, Functions and Diseases of the Brain. While Dr. Wigan did not make a significant advance in the treatment of mental illness, he was one of the growing number of scientists pursuing the concept that mental function resulted from the brain’s physical makeup, not from witches, spirits, or God’s will. This area of investigation was also being pursued in Europe and culminated in the science of psychiatry, a term that included all therapies aimed at curing mental disorders.
Toward the end of the century in both America and Europe, the physiological approach dominated the field. One of its leading proponents was the German psychiatrist Emil Kraepelin, who made a major contribution to the newborn discipline by classifying psychosis into two main categories: dementia praecox (later renamed schizophrenia) and manic-depressive psychosis. Kraepelin was also the first to use objective tests and measurements to study drug effects and mental disorders. As his influence in Europe grew, Kraepelin’s physiological approach to brain function appeared to be the path of the future. Instead, it was swept aside by the advent of Sigmund Freud and his revolutionary psychodynamic vision of mental illness and of personality itself.
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