Making the Connection: Strategies to Build Effective Personal Relationships (Collection) (60 page)

Thomas Bouchard and his colleagues at the University of Minnesota did just that.
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They tracked down more than 100 pairs of identical twins who had been raised apart and
persuaded them to volunteer for a week of psychological testing. Many twins had been raised in very different environments, some in different countries and cultures, and their reunions attracted a great deal of media attention.

A certain pair of British identical twin girls would have been especially interesting to Galton because they addressed the issue of social privilege he had wondered about. One twin had been raised by an upper-class family, had attended exclusive schools, and spoke with a refined accent to prove it; the other had been raised by a lower-class family, had quit school at 16, and spoke like Liza Doolittle did before she met Henry Higgins. Yet their test scores were very similar. The same was true of the other sets of twins. As Bouchard summed it up, “[O]n multiple measures of personality and temperament, occupational and leisure-time interests, and social attitudes, monozygotic twins reared apart are about as similar as monozygotic twins reared together.”
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These and other family and adoption studies support the conclusion that personality traits are highly heritable.
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The studies with identical twins also tell us something else that should not be ignored: They challenge the assumption that the shared family environment of those raised together is responsible for some of their similarities. Were this the case, the scores of identical twins raised together should be more similar than those raised apart. But as Bouchard pointed out, they’re not.
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Scores of genetically unrelated children who were adopted and raised in the same family also show no effect of this shared environment.
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The lack of effect of a shared family environment on these measures of personality doesn’t mean that parents are just part of the furniture. Studies indicate that parents do have some influence, but it is transmitted by their unique relationship with each child,
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including each identical twin. The studies also indicate that most environmental influences on personality cannot be specifically attributed to interactions within the family.
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How Many Gene Variants Shape a Personality Trait?

So now that we know that genes do, indeed, have a big effect on personality differences, how do they do it? To answer this question, it’s necessary to review a few facts about human genetics.

The total number of human genes is surprisingly small, about 20,000. Each is made from the four chemical building blocks of DNA—adenine (A), cytosine (C), guanine (G), and thymine (T)—strung together in a long chain whose precise sequence (such as AGACTCAAG ...)contains the instructions for manufacturing a particular protein. Each protein interacts with many others to build and maintain us. The major reason so few genes are sufficient for this complex task is that various combinations work together to control our biological and psychological functions. Furthermore, the actions of each gene and each protein can influence the actions of many others.

The main way genes interact is by turning the activities of each other on or off. To make this possible, each gene has
a specialized piece of DNA, called a promoter, that serves as a dial to control the amount of the protein that gene makes. The dial can be turned up and down by internal or environmental signals that may work through controls in other regions of DNA. This process, called regulation of gene expression,
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adjusts the amounts of the proteins that shape our bodies and minds.

Regulating the expression of a variety of genes in different cells helps explain how just 20,000 elements can give rise to such complexity. But it doesn’t explain our heritable differences. These differences are explained by
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of the genes—modifications of the sequence of bases in their DNA or the DNA of their regulatory regions—that have accumulated in the collective human genetic repertoire, called the human genome. These structural modifications of DNA, which arose through random mutations, may cause big changes in the manufacture of a specific protein or the way it functions in the body. Some of the variants, such as those that influence skin color, are carried by billions of people. Others are rare. The combined effects of the assortment of gene variants that were handed down to each of us—our own personal selection from the human genome—defines our genetic uniqueness.

But not all gene variants have such major and obvious effects as the small number that control human skin color. For example, hundreds of different genes
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influence human height, which is about 80% heritable in well-nourished human populations, and each of these genes has a tiny effect. The same is true for highly heritable personality traits.

Persuasive evidence that personality traits reflect the joint action of multiple gene variants comes from selective breeding of mice. A notable example is John DeFries’s classic study
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of a seemingly simple mouse trait: the inclination to explore an unfamiliar and potentially dangerous territory. This personality trait is related to both the excitement-seeking and anxiety facets of the Big Five, in that high excitement-seeking would increase exploration while high anxiety would inhibit it. Together these facets would also influence the risk taking that is such a cherished part of Jason Dallas’s personality.

To prepare for the experiment, DeFries randomly chose ten litters of mice and observed their behavior in a brightly lit large box called an open field. Mice prefer dim light and narrow spaces, but there are individual differences. Some mice froze in the open field, like a deer in the headlights, while others sniffed around and explored. Electronic sensors measured each mouse’s behavior, recording the total distance it traveled in a six-minute period. After DeFries had scored each animal from the initial ten litters, he selectively bred the mice to raise two extreme lines. He began by mating the most active male and female from each litter. They became the founders of what I call the fearless (F) line. He also mated the least active pairs, who became the founders of what I call the anxious (A) line. DeFries then took another ten litters and mated a randomly selected male and female from each to be the founders of the control line. He repeated this process in each generation. Because mouse pregnancies take only three weeks, and pups become sexually mature in about three
months, he was able to breed and evaluate 30 generations in the course of ten years.

The results were dramatic. After 30 generations, the average member of the F line roamed freely across the open field. In contrast, the average member of the A line huddled in a corner of the box. Members of the control line maintained their original modest level of exploration, which hadn’t changed through 30 generations.

The other notable finding was that separation of the two lines was gradual, with steady increments from one generation to the next. When the open field behavior of the F line was plotted as a graph, it looked like that of a long-term growth stock that kept rising year after year over the ten-year period. In contrast, the pattern of the A line looked like the stock of a weak company in a failing industry, heading progressively downward until it hovered near zero. This pattern of gradual change has two implications: Variants of many genes together affect this personality trait; and the behavioral effects keep adding up as more of the relevant gene variants are selected in each generation. Direct analysis of the DNA of these mouse lines
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confirms these conclusions.
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Genetic Thinking vs. Genetic Testing

As behavioral scientists were accumulating evidence that many gene variants work together to influence personality differences, geneticists were busily deciphering the complete DNA sequences of the human and mouse genomes, and the structures of common gene variants. This provided the
foundation for searching the entire genome for variants that influence personality traits in people and in mice. But progress with this genome-wide approach has been slow.
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Frustrated by this limited success, some researchers have taken a more focused approach. It was based on the knowledge that drugs such as Prozac and Ritalin affect personality and that they do this by influencing the way serotonin or dopamine act in the brain. This raised the possibility that inherited variations in genes that control certain actions of serotonin or dopamine in the brain might be responsible for heritable personality differences. To look into this, researchers examined variants of several dozen of these genes to see if they were correlated with scores on personality tests.

All the genes that they examined influence the emotional circuits of the brain. Of these, the most widely studied, called SERT, was singled out because it makes the serotonin transporter protein, Prozac’s target. The SERT protein vacuums up (transports) serotonin from the fluid around nerve cells that are activated by frightening experiences so that the serotonin can be used again. By controlling the amount of serotonin that bathes these nerve cells, the SERT protein affects the intensity of the emotional response. Therefore, it is easy to imagine how variants of the SERT gene might influence the tuning of brain circuits that control traits such as fearfulness.

To see whether the SERT gene affects personality, researchers focused on two common variants, one with a long promoter and the other with a short one. Several studies have found that groups of people who have two copies of the gene
with the long promoter, which makes more SERT protein, have a slightly lower average score on Neuroticism.
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Furthermore, brain imaging studies indicate that if such people are shown frightening pictures, they have less activation of the amygdala, a brain structure involved in fear processing.
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Taken together, the studies suggest that these differences in the amount of SERT protein account for a fraction—but only a tiny fraction—of the variation in the tendency to be frightened.

A similar conclusion emerged in studies of another gene, DRD4, which makes a receptor for dopamine. Scientists studied this gene because Ritalin and amphetamine stimulate behavior by releasing dopamine, which activates dopamine receptors. Researchers found that groups of people with variants of DRD4 had different average scores on novelty-seeking and impulsivity, traits expected to be influenced by dopamine.
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Once again, the gene variants accounted for just a tiny fraction of the variation in these traits.
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So don’t rush out to your nearest DNA testing service to have your SERT or DRD4 genes examined: They are just two examples of the thousands of gene variants that work together to influence personality,
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sometimes in unexpected ways.
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And even though new techniques, such as the complete sequencing of a person’s DNA,
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will eventually be used to search for variants that influence specific traits, it will still be very difficult to identify the mixture that shapes a particular personality.

But the fact that such genetic testing hasn’t proved useful, at least for now, doesn’t mean that you can also dismiss
genetic thinking. When trying to make sense of someone, it still helps to remember that a person’s specific combination of gene variants has a substantial effect on his or her personality. And we have a good idea where these many variants came from.

The Deep Roots of Our Diversity

Our view of the accumulation of so many variants in the human genome is based on Darwin’s key insight that the environment keeps selecting those that increase fitness. For example, a consistent environmental factor, such as the relatively low amount of sunlight, exerted a relentless selective force on gene variants that eventually made Northern Europeans white. But Darwin also realized that environments keep changing over the course of evolution and that this led to the selection of variants that were suitable for different contingencies. Among them were those that influence personality.

To see what I mean, consider the environments that influenced the selection of the variants that control the open field behavior of mice. In dangerous territories with many predators, variants that favor caution would be selected because those who carried them would be more likely to live long enough to reproduce. But when the cats are away, the mice will play. In such safer environments, the variants that favor exploration would be selected because those who carried them might find more food and more sexual partners. Fluctuations of these alternative environments would lead to retention of both types of variants in the group’s genetic repertoire.
Furthermore, many of them would be kept as the species continued to evolve. This explains why some that arose in distant ancestors have been passed down to you and me.
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Predators are not the most important instruments of selection of heritable human personality traits. People are. They are the ones we depend on and compete with, and there are benefits and costs in the many tactics they and we use to interact. These fluctuating social environments have contributed to the selection of the wide range of gene variants that influence our personalities.
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