ONE

It Runs in the Family

IN 1952, DIMITRI BELYAEV, A RUSSIAN GENETICIST, had an idea for a creative and audacious experiment. He was interested in the domestication of animals that had been important to human civilization, such as dogs, pigs, horses, sheep, and cattle. Dogs are thought to be the first domesticated species, derived from Eurasian gray wolves by hunter-gatherers over fifteen thousand years ago.¹ Belyaev wanted to know how some wild wolves, which are famously averse to human contact and occasionally aggressive, evolved into the affectionate and loyal companions we know and love. Why, as first described by Charles Darwin, did domesticated mammals often share certain physical characteristics—like rounder, more juvenile-appearing faces, floppier ears, curvier tails, and patches of lighter fur or hide—in contrast to their wild forebears? And why did most wild mammals have a single, brief breeding season every year, but their domesticated counterparts could often breed twice or more per year?

Belyaev believed that the single most important trait selected for in the initial process of domestication was not size or breeding capacity but tameness. He hypothesized that the defining characteristic of all the animal species domesticated by our ancestors was a reduction in aggression toward, and fear of, humans. To test his theory, he went to some of the industrial-scale silver fox farms that had been established for fur production in the Soviet Union and instructed the animal breeders there to select only the tamest foxes, a tiny fraction of the total, and breed them together. He believed that by repeatedly selecting for tameness over many generations, he could ultimately approximate wolf-to-dog domestication and produce a friendly, loyal, doglike fox.

In carrying out these experiments, Belyaev hoped to avoid the fate of his beloved older brother Nikolai, who, in 1937, had been executed by the Soviet government for the crime of performing and publishing genetic experiments. Those were dark days for Soviet biology. Stalin’s Communist government, eager to elevate an uneducated “common man” to a position of authority in the scientific leadership, promoted the charlatan Trofim Lysenko to director of the Institute of Genetics at the Soviet Academy of Sciences.

Lysenko faked his data to show that wheat and barley seeds that had been frozen before planting yielded larger crops when planted in winter, and that the second generation of seeds derived from those crops also acquired enhanced winter growth. He claimed that this method could double food production in the USSR and feed the masses, an assertion extolled in the state-controlled newspaper Pravda as a triumph of Soviet science. His seed-freezing techniques were widely adopted in the country but failed utterly, contributing to periods of widespread starvation. Lysenko rejected genetics, a discipline that had thrived in Russia before his rise to power, because simple genetic experiments could disprove his claims. He called Soviet geneticists “Western saboteurs” and, with Stalin’s backing, sought to dismantle the discipline. Those who resisted were fired and even imprisoned. The strongest supporters of genetics, like Nikolai Belyaev and the great Russian plant geneticist Nikolai Vavilov, were executed—Belyaev with a rifle, and Vavilov by slow starvation in a prison cell.

Dimitri Belyaev was fortunate to have some political support for his work. A decorated hero of the Russian Army during World War II, he had presided over improvements in the farming of wild foxes, sable, and mink for fur production. This effort was key to the Soviet economy because it brought in large amounts of foreign currency. Mindful of his brother’s fate, Belyaev conducted his domestication experiments on remote fox farms, far from the prying eyes of Moscow—first in the forests of Estonia and later in a distant part of Siberia near the Mongolian border. The cover story was that he was studying fox physiology, not genetics. To oversee the endeavor, Belyaev recruited the young scientist Lyudmila Trut, an expert in animal behavior who had been trained at the elite Moscow State University. He gave her explicit instructions: when selecting foxes for breeding, the only trait to be considered was tameness—not appearance, nor size, nor behavior toward other foxes.

There was no guarantee that this fox domestication plan would work. Nonetheless, it was a reasonable supposition. After all, dogs were domesticated from wolves, which are closely related to foxes. Yet previous attempts to domesticate wild zebras—which are so closely related to horses that the two species can sometimes be interbred (a Shetland pony-zebra cross is called a zony)—had repeatedly failed.² The reason appears to be that there is not enough genetic variation underlying the trait of tameness in zebras. You can’t effectively pick the tamest zebras for breeding if there aren’t any slightly tame zebras to start with. Fortunately, that wasn’t the case with Trut and Belyaev’s foxes.

FIGURE 1. Dr. Lyudmila Trut with one of her domesticated foxes. Used with permission of the BBC. Photo by Dan Child.

When Lyudmila Trut first slowly introduced her hand into the fox cage, she wore a thick padded glove and held a small stick. The most common reaction to this gentle intrusion was snarling and biting. Other foxes cowered, highly agitated, in the rear of the cage. But about 10 percent of the foxes stayed calm throughout, observing her intently but not approaching.³ These were the animals that she selected for the first round of breeding. Trut was also careful not to breed closely related foxes and thereby introduce inbreeding artifacts that could confound the experiment. To increase the probability that the observed tameness resulted purely from genetic selection, the foxes were not trained and their interactions with humans were strictly limited.

Trut’s initial finding, that there was some partial tameness to serve as a basis for subsequent breeding, was encouraging. But the experiment could still easily fail in a different way: it simply might take too many generations to see any significant changes in fox behavior. It has been suggested, from analysis of the archeological record, that wolf-to-dog domestication proceeded in fits and starts, beginning thousands of years ago. Trut and Belyaev didn’t have that much time and were limited by the slow pace of fox breeding: one mating season per year. So it was cause for joy when, only four years into the experiment, clear behavioral changes emerged. A few of the fourth-generation foxes showed no aggression or fear, and even displayed doglike tail wagging in response to humans. By the sixth generation, some of the fox pups exhibited whining, licking, and whimpering behavior as they eagerly sought human attention. Today, over 80 percent of the adult foxes derived from these crosses are as loyal and tame as any domesticated dog (figure 1).⁴

If you wish, you can go on the internet and obtain your own tame fox from Trut and Belyaev’s experiment, delivered from Siberia to you for $9,000, shipping included.⁵ But be aware that, while domesticated foxes are much friendlier than those in the wild, they are much harder to train than dogs. “[You can be] sitting there drinking your cup of coffee and turning your head for a second, and then taking a swig and realizing, ‘Yeah, Boris came up here and peed in my coffee cup,’” said domesticated fox expert Amy Bassett. “You can easily train and manage behavioral problems in dogs, but there are a lot of behaviors in foxes… that you will never be able to manage.”⁶

THE ORIGINAL FARMED SILVER foxes looked like wild foxes: they had erect ears, low-slung tails, and uniformly silver-black fur, save for a white tail tip. As breeding for tameness continued through the generations, the foxes often developed floppy ears, shorter, curved tails, and patchy, pale fur, particularly on the face. They reached sexual maturity earlier than wild foxes, and some even bred twice per year. It is important to emphasize that the only criterion used for breeding was tameness; the other physical traits just came along for the ride. The remarkable thing is that these particular bodily changes have emerged in many other domesticated animals—from cattle to pigs to rabbits—at various times in history.

When Trut and Belyaev measured the levels of resting stress hormones produced by the adrenal glands, they found significant reductions in the tame foxes. They also found that levels of the neurotransmitter serotonin and its metabolites were increased in the brains of the tame foxes, which is consistent with a reduction in aggressive behavior. One overarching hypothesis for the biochemical, behavioral, and structural changes seen in domesticated foxes and other animals is that their development is somehow arrested at an earlier state than their wild cousins. Perhaps the variation in genes responsible for developmental timing is what gives rise to variation in tameness. When animals are bred for tameness, the other youthful traits noticed by Darwin—like floppy ears, round faces, and curly tails—follow along.

TRUT AND BELYAEV SHOWED that a behavioral trait (tameness) in foxes is heritable, that it can be changed by selective breeding in just a few generations, and that physical changes will accompany selection for this trait. Can these conclusions about the heritability of behavioral and physical traits from the fox taming experiment be usefully applied to us? After all, we humans are not confined to cages in Siberia. And, for the most part, we choose our own mates, rather than having them forced upon us by alien overlords. We even have OkCupid and Bumble to expand our mating possibilities.

Insights about the heritability of human traits can be gleaned from studies of twins. This type of analysis can be used to estimate the degree of variation in a trait that is heritable within a particular group of people (or foxes), from 0 to 100 percent. The key thing to remember about heritability is that it measures variation across an entire population, not individuals. Just because a particular trait is 70 percent heritable doesn’t mean that, for any individual from that population, genes are responsible for 70 percent and other factors for 30 percent.

Heritability estimates from twin studies may be used for both easily measured physical traits, like height or resting heart rate, and behavioral traits like shyness, generosity, or general intelligence, which are somewhat more subjective and harder to measure. One of the challenges with behavioral traits, which are typically measured by direct observation or with a survey, is that they are culturally constructed. The definition of and necessary criteria for the trait of shyness is probably different in Japan than it is in Italy. Concepts of generosity will not be identical for the city dwellers of Pakistan and the Hadza people of Tanzania. What this means is that the assessment of behavioral traits in individuals will be convolved with cultural factors if the individuals come from different cultural backgrounds, even if they live in the same location.

Here’s how heritability estimates work: Fraternal twins are conceived when two eggs are released during the same ovulatory cycle and each is fertilized by a separate sperm cell. The two fertilized eggs then develop separately into two embryos. Fraternal twins are as genetically similar to each other as any other pair of siblings. On average, they share 50 percent of their genes.⁷ Since fraternal twin embryos inherit their sex-determining X and Y chromosomes independently, fraternal twins are as likely to be the same sex (boy/boy or girl/girl) as the opposite sex (boy/girl or girl/boy).

By contrast, identical twins arise from a single fertilized egg that then divides to form two embryos early in development. Each twin inherits the same version of each gene from their parents, and so they are genetically identical. Because identical twin embryos also inherit the same arrangement of sex-determining X and Y chromosomes, they are always the same sex. This means that if you see mixed-sex twins, they must be fraternal, not identical.

In one simple twin study design, a particular trait, like height, is measured in members of a large number of fraternal and identical twin pairs. The difference in height is calculated for each twin pair, and then the results are compared between the fraternal and identical groups.⁸ One study of this type has shown, for example, that the average height difference between fraternal twins is 4.5 centimeters, whereas it is 1.7 centimeters for identical twins. A crucial assumption in these types of twin studies is that both twins (identical and fraternal) have been raised together, in the same household, at the same time, and will thereby have a highly shared social and physical environment, at least during childhood. Therefore, the smaller average difference between identical twins is attributed to their greater degree of genetic similarity. When these values are plugged into a standard equation, we can estimate the degree of heritability of a trait, which is about 85 percent for adult height, at least in affluent countries where basic nutrition needs are met. One can also estimate the degree of variation in height that is attributable to the twins’ shared environment, which is about 5 percent, and to the twins’ unshared environment, which is about 10 percent. Those interested in the calculation of these values are invited to check this endnote.⁹

For most twins, the shared environment is dominated by experiences in the family (both social, like being read to, and physical, like the particular foods on the dinner table) but can also include certain shared experiences at school and in the community, as well as the shared exposure to foods and infectious diseases. Unshared environment is a sort of grab bag for all of the other types of random experience, both social and biological, that individuals do not share. Importantly, this estimate of non-shared environment will also include the random nature of both fetal and postnatal development of the brain and body, which we shall explore in chapter 2.¹⁰

This type of twin analysis can be applied to any trait, not just those that are continuously variable and easily measured, such as height or weight. For example, it can be used to analyze responses to a survey question like “In the last year, have you ever felt sexual attraction to a member of your own sex?” If sexual attraction had no heritable component, we’d expect that the percentage of twin pairs where both answered yes would be roughly the same for identical and fraternal twins. Conversely, if sexual attraction were entirely heritable, then we’d expect that every homosexual/bisexual identical twin would have a homosexual/bisexual twin sibling (and every straight identical twin would have a straight twin sibling). It turns out that the best estimates to date (from a population of 3,826 randomly selected twin pairs in Sweden) are that, in men, about 40 percent of the variation in sexual orientation is heritable with no detectable effect of shared environment and 60 percent is attributable to unshared environment.¹¹ Forty percent is a significant fraction, but it still leaves room for plenty of other nonheritable factors. We’ll discuss the emerging science of sexual orientation and identity in chapter 4.

There have been critiques of these types of twin studies. Some researchers have claimed that studies comparing identical and fraternal twins raised together overestimate the heritable contribution to a trait because family members, friends, and teachers often treat identical twins more similarly than fraternal twins. This could come about in many ways, from the foods they are served to the ways in which people interact with them. Other researchers have claimed the opposite problem: they argue that since identical twins raised together seek to differentiate themselves socially from each other to a greater degree than fraternal twins, such a comparison underestimates the genetic contribution to a trait (particularly a behavioral one). In either case, the key assumption of equal shared environments between identical and fraternal twins would be violated. There have been passionate arguments for and against the validity of studies of twins raised together, and we won’t engage in a blow-by-blow recap of those brawls here. My own reading of the literature leads me to believe that, in most cases, the unequal shared environment problem in studies of twins raised together is small and rarely invalidates the general estimates of heritability that result.¹² Nonetheless, it would be best to have a twin study design that would cleanly estimate heritability without the muddled assumption of equal shared environments.

ON FEBRUARY 19, 1979, (at which point the tame-fox breeding experiment had been underway in the Soviet Union for over twenty-six years), the local newspaper in Lima, Ohio, reported a fun human-interest story about identical twin brothers who had been adopted by different families and raised completely apart, only to reunite at age thirty-nine. The twins were born in 1939 to a fifteen-year-old unwed mother, who immediately put them up for adoption. They were separated four weeks later, when one was adopted by Ernest and Sarah Springer, who brought him to their home in Piqua, Ohio. The second boy was adopted two weeks later by Jess and Lucille Lewis of Lima, Ohio, a town about forty-five miles away from Piqua. For reasons that have never been explained, both couples were told that their adoptive child had a twin who died at birth.¹³

But when Lucille Lewis was finalizing the legal adoption of her son, by then a toddler, a clerk at the county courthouse let the cat out of the bag. She told her, “They named the other little boy Jim, too.” In an interview with People magazine, Mrs. Lewis said, “I knew all those years that he had a brother, and I worried whether he had a home, and whether he was all right.” She waited until her son turned five before telling him about his twin. Jim Lewis couldn’t explain why, at the age of thirty-nine, he finally contacted the court to put him in touch with his brother. The Lima News reported that Jim Lewis called Jim Springer, took a deep breath, and asked, “Are you my brother?” At the other end of the line, Jim Springer answered, “Yep.” And so, the twins were reunited.¹⁴

When the Jim twins reunited, they were not mirror duplicates in either appearance (figure 2) or temperament. Nonetheless, a series of striking similarities emerged. Both brothers worked in law enforcement and enjoyed carpentry and drafting as hobbies. On vacations, they liked to drive their Chevrolets to Pass-a-Grille Beach in the Florida panhandle. In school, both had excelled in math and struggled with spelling. Both had married women named Linda, only to divorce and remarry women named Betty. Both had sons: James Alan Lewis and James Allan Springer. And, most tellingly, they preferred to wash their hands both before and after peeing.

It’s not surprising that these anecdotes were broadly appealing to readers and that the story of the Jim twins quickly made its way around the world. The day after the first story of their reunion appeared in the Lima News, it was reprinted in the Minneapolis Star Tribune, where it caught the eye of Meg Keyes, a psychology graduate student at the University of Minnesota. Keyes had recently taken a course with Professor Thomas Bouchard Jr. on individual behavioral differences. When she showed Bouchard the article, he immediately recognized how interesting it would be to study the Jim twins, and soon. He was quoted in the New York Times as saying, “[To study the Jim twins] I’m going to beg, borrow and steal and even use some of my own money if I have to. It is important to study them immediately because now that they have gotten together they are, in a sense, contaminating one another.”¹⁵

Bouchard quickly contacted the twins, who agreed to come to the University of Minnesota to spend six days undergoing a battery of psychological and medical tests and interviews. More stories of behavioral and physical similarities emerged. Both crossed their legs in the same way and suffered from chronic headaches and a heart condition. Both were described as “patient, kind, and serious.” Both had rapidly gained ten pounds at exactly the same age. These anecdotal similarities were tantalizing, but analysis of a single identical twin pair, even one as striking as the Jim twins, did not allow Bouchard to reach the holy grail: to estimate the heritability of traits without the potential confound of the equal environment assumption. That would require him to compare a sizeable population of identical twins with an equally sizeable population of fraternal twins raised apart.

FIGURE 2. Jim Springer and Jim Lewis pose for a photo shortly after being reunited in 1979. Photo courtesy of Nancy L. Segal and the Jim twins. Used with permission.

When the study of the Jim twins began, Bouchard assumed that they would be a one-off. Other researchers had tried to analyze twins raised apart but had access to so few twin pairs that their results were statistically weak. Bouchard imagined that he would have the same problem, that the cost of finding many twins raised apart would be prohibitive. What he didn’t count on was the public’s insatiable appetite for Jim twin stories. They appeared in newspapers, magazines, and on all the major television shows of the day. Some newly separated twin pairs emerged after the Jims appeared on The Tonight Show with Johnny Carson, others after seeing them on Dinah Shore.

This unprecedented publicity allowed Bouchard to found the Minnesota Study of Twins Reared Apart (MISTRA), which ran for twenty years and analyzed eighty-one identical and fifty-six same-sex fraternal twin pairs.¹⁶ In collaboration with fellow University of Minnesota psychologist David Lykken, the study also compared twins reared apart with twins reared together. MISTRA was a major advance in twin research. The largest and most productive investigation of this type, it produced good estimates of the heritable contribution to variance in many physical traits, like body mass index (about 75 percent) and resting heart rate (about 50 percent), and behavioral traits, like extraversion (about 50 percent) and schizophrenia (about 85 percent).

One main conclusion of MISTRA and related studies was that most human traits, regardless of whether they are physical or behavioral, have a significant heritable component, usually ranging from 30 to 80 percent. Rarely are traits either entirely heritable or entirely nonheritable (we’ll talk about some notable exceptions to this later). The other main conclusion is that variation in certain traits, like IQ, is weakly heritable (about 22 percent) when tested at age five but becomes strongly heritable once school is well underway at age twelve (about 70 percent), and then remains so across the lifespan. Correspondingly, the variation in IQ explained by the shared environment is about 55 percent at age five (when most experience has been within the family) but falls to undetectable levels by age twelve, at which time children have been exposed to a broader range of experiences.¹⁷ Those of you who are doing the arithmetic will notice that the variations accounted for by heritability and shared environment are not adding up to 100 percent. That difference is the aforementioned term “unshared environment,” which, in addition to unshared social experience, also includes the random process of development. More on this in chapter 2.

For decades, the dominant thinking in the field of psychology, and in society at large, was that the most important determinant of one’s adult personality was the influence of immediate family, particularly the parents. This idea came from the twentieth-century psychological movement called behaviorism, which held that humans come into the world as blank slates, ready to be molded by social experience. As a result, it was quite a shock when the MISTRA experiments showed significantly higher correlations in personality measures in identical twin pairs than in fraternal ones. The main result was that about 50 percent of the variation in personality can be accounted for by heritability. This held for all five major standard scales of personality (openness, conscientiousness, extraversion, agreeableness, and neuroticism; abbreviated as OCEAN) and directly contradicted the blank slate hypothesis of the behaviorists.

Most psychologists were guessing that the remaining 50 percent of the variation would be largely explained by social dynamics within the family. By comparing identical twins raised together with identical twins raised apart, the MISTRA researchers estimated the contribution of “shared environment” to individual personality—a factor that includes social experience in the family as well as things like shared nutrition and shared exposure to communicable diseases. To the psychologists’ surprise, shared environment made little or no contribution to variation in personality measures (typically less than 10 percent). It’s not just identical twin results that support the idea that shared environment plays a tiny role in explaining individual personalities. Fraternal twins who grow up together are no more similar in personality than those raised in different families, and unrelated adoptive siblings raised in the same family are barely alike at all.

The failure of shared environment to affect personality goes against some popular ideas about the influence of parents. But these twin study results don’t say that parental behavior is unimportant. Rather, they show that, beyond some minimum level of parental support and encouragement, extra attention doesn’t produce large effects on personality as measured by questionnaires administered in the lab.

Importantly, personality is not the totality of one’s character. Parents can inculcate work habits and teach specific skills, like weaving or car repair. And they can transmit philosophical, religious, or political opinions that are not measured by the OCEAN personality tests. For example, altruism, sharing, and other prosocial behaviors appear to be influenced by shared environments to a greater degree than other behavioral traits.¹⁸ Religiousness is another trait where significant variation is contributed by both heritable factors and shared environment. Importantly, while one’s likelihood of having religious beliefs is influenced by both heredity and shared environment, the specific religion you choose has no hereditary component. Your genes might contribute to making you religious, but they will not specify a Hindu or Wiccan or Roman Catholic faith—that’s mostly a family and community affair.

Another well-entrenched idea about the influence of family on personality has to do with birth order. First children are generally thought to be socially dominant, less fearful, and more novelty seeking and risk-taking as compared to their later-born siblings. And if one observes children at home, this stereotype is borne out. Parents treat firstborns differently than their later children, and firstborns both care for and boss around their younger siblings throughout childhood. Indeed, these social patterns often persist within the family as the children become adults. But remarkably, study after study has failed to find that the domineering qualities of firstborns are present outside of the family.¹⁹ Neither at school, nor on sports teams, nor in the workplace do firstborn children show an unusual degree of social dominance or any other personality trait. In retrospect, this makes sense. The firstborn child who is the oldest and biggest at home no longer enjoys that same status on the playground, in the classroom, or in other locations outside of the family.

IF THE JIM TWINS had not been so alike and generated such appealing stories and media attention, the MISTRA study might not have happened at all. The Jim twins were certainly among the most similar in the study and hence not the most representative example of identical twins raised apart. Bouchard noted this issue: “There probably are genetic influences on almost all facets of human behavior, but the emphasis on the idiosyncratic characteristics is misleading. On average, identical twins raised separately are about 50 percent similar [in behavioral measures]—and that defeats the widespread belief that identical twins are carbon copies. Obviously, they are not. Each is a unique individual in his or her own right.”

When the MISTRA results first began to be published in the 1980s, the reception was not entirely positive. The evidence that there was a strong heritable component to complex behavioral traits like novelty seeking, traditionalism, and general intelligence, while embraced by some, was met with skepticism and hostility by others, particularly the adherents of behaviorism. Bouchard and his coworkers were called frauds, racists, and Nazis. Some opponents sought to have him fired from the University of Minnesota. However, over time, the MISTRA findings, on both behavioral and physical traits, were replicated by several well-controlled studies of twins raised apart. An important caveat is that, to date, most of these studies have been performed among more affluent populations in countries like Japan, the United States, Sweden, and Finland, where nutritious food, medical care, and decent schools are widely available. While there are still arguments to be had, most biologists today accept that most behavioral and physical traits have a substantial heritable component.²⁰

Danielle Reed, a scientist from the Monell Chemical Senses Center, credits Bouchard’s work with expanding our understanding of heredity. “He was the trailblazer,” she says. “We forget that 50 years ago things like alcoholism and heart disease were thought to be caused entirely by lifestyle. Schizophrenia was thought to be due to poor mothering. Twin studies have allowed us to be more reflective about what people are actually born with and what’s caused by experience.”²¹

FOR YEARS, PEOPLE HAVE argued about the origin of human traits. The most politically and emotionally fraught of these arguments concerns IQ tests as a measure of intelligence. Can intelligence be determined by heredity, environment, or something else? Are IQ tests even valid cross-culturally? The results from MISTRA and certain other twin studies have estimated that about 70 percent of the variation in IQ test scores is heritable. The first and most obvious point is that 70 percent is not 100 percent—this value still leaves room for significant environmental influences. The second point is more subtle. Estimates of heritability are only valid for the population that is analyzed. While the MISTRA investigators did not seek out a particular type of twin pair for their study, its population was overwhelmingly white, midwestern, and middle class, and so the 70 percent heritability estimate does not necessarily apply to other populations.

Perhaps it’s easier to think about heritability for human populations using a less politically sensitive trait, like height. In affluent populations, with good access to nutritious food, clean water, decent sleep, and basic medical care, about 85 percent of the variation in height is heritable. But if we look at a population that does not have these advantages, like poor people in rural India or Bolivia, then only about 50 percent is heritable. Without access to basic nutrition (including sufficient protein) and treatment for diseases (mostly infectious ones), poor people are not able to reach their genetic potential for height.²² Stated another way, the heritable and environmental components of a trait are not simply summed up. Heredity interacts with the environment, providing the potential for a trait, but environmental conditions influence whether that potential will be fully realized.

It’s the same situation for IQ test scores: children without access to basic human needs—not just nutrition, health care, and sanitation, but decent schools, books, sufficient sleep, and the freedom to explore and be curious—cannot fulfill their genetic potential for general intelligence. Crucially, the degree of variation in general intelligence explained by heredity is lower for poor populations than for those whose basic needs have been met.²³ To me, the political and moral lesson from the study of trait heritability is clear: if you want to improve the lives of humanity as a whole, the first job is to make sure that everyone has his or her basic needs met in order to fulfill her or his genetic potential for positive human traits. We’ll return to this issue when we explore population differences and concepts of race and racism in chapter 8.

TWIN STUDIES CAN MEASURE the average contribution of heritability to variation in human traits across a population, but they cannot reveal the underlying biological mechanisms responsible for this variation. In order to do that, we’ll need to consider the biochemical machinery of life. Heredity is encoded in DNA, which resides in the nucleus of cells. It is organized into genes, each of which contains the instructions to make a different protein. Some proteins are structural: they are the girders and cables that determine the shapes of cells. Others have specific biochemical functions, such as creating or breaking down an important chemical in the body, like a digestive enzyme in the stomach. Yet other proteins are receptors, specialized micromachines that allow cells to respond to chemical signals like hormones or neurotransmitters. Still more are transducers that help us sense things about the world around us, like the proteins in the retina that allow us to see light or those in the inner ear that allow us to hear sounds, converting those forms of energy into electrical signals that ultimately travel to the brain.

DNA is composed of long chains of chemical groups called nucleotides that come in four flavors: A, C, T, or G. Humans have about three billion nucleotides organized into about nineteen thousand different genes, with vast gaps of more poorly understood DNA between them.²⁴ Together, all of this DNA is the human genome. We now know the complete nucleotide sequence of the human genome, as well as that of some plants, animals, and bacteria. In turns out that nineteen thousand genes is not an unusual number for an animal. The tiny roundworm C. elegans has about the same number. By comparison, a fruit fly has about thirteen thousand and a rice plant about thirty-two thousand. A particular type of poplar tree is the present winner with about forty-five thousand genes. Clearly, the number of genes in an organism’s genome does not determine the anatomical complexity, much less the mental capacity of that critter or plant.²⁵

On average, considering the entire DNA sequence (both the genes and the stretches of other DNA between them), each human is about 99.8 percent similar to any other human, 98 percent similar to a chimpanzee, and 50 percent similar to a fruit fly. This is because, if you go back far enough in evolutionary time, about eight hundred million years, humans, chimps, and fruit flies all share a common ancestor.

If only a 2 percent difference separates us from chimps, then it follows that small differences in the DNA sequence can sometimes have a big effect on traits. Indeed, there are certain locations in the human genome where a change in a single nucleotide (called a point mutation) will be fatal. Sometimes, if the change acts early in development, the embryo will die. There are other places where changes in a single nucleotide can cause a serious disease. For example, certain tiny changes in the gene that instructs the production of an enzyme that metabolizes the amino acid phenylalanine will break it. As a result, when an infant carrying this mutation eats phenylalanine-containing foods, the amino acid builds up to toxic levels and impairs development of the brain and other organs, producing the disease phenylketonuria (known as PKU).²⁶ There are many other examples of single-nucleotide mutations in genes, but it’s worthwhile to note that, unlike PKU, most have no functional consequences at all.²⁷

We generally carry two copies of each gene, each called an allele: one from our mother and one from our father. For most genes, both the maternal and paternal copies are active.²⁸ So, to have PKU, you need to inherit broken copies of the gene instructing production of phenylalanine from both your mother and your father. This qualifies PKU as a recessive genetic disease. There are other genetic diseases that are inherited in a dominant fashion, like Marfan syndrome (a disease of overly stretchy connective tissue), where receiving a single copy of a particular gene variant from either parent is sufficient to produce the disease.

HERE’S A FUN FACT you can use to impress your friends: everyone has either wet or dry earwax. If your ancestors are from Europe or Africa, there’s a very high chance (greater than 90 percent) that you have the wet type. If your ancestors are from Korea, Japan, or northern China, then you almost certainly have the dry type. If your people hail from South Asia, or if you are of mixed northeast Asian and European/African ancestry, then your chance of having dry earwax is somewhere in the middle. To study the genetics of earwax, a group of scientists led by Norio Niikawa of the Nagasaki University School of Medicine obtained DNA and earwax samples from people all around the world.²⁹

They determined that the dry earwax trait is due to a single-nucleotide mutation in a gene that controls various forms of secretion (ABCC11). Like PKU, having dry earwax is recessive; it requires inheriting a mutant form of the gene from both of your parents. To put this back in the context of twin studies, the dry earwax trait (and the PKU trait) is 100 percent heritable. There is no contribution of either shared or individual environment. It doesn’t matter how your parents raised you or what kind of experiences you had in school or what foods you ate. If you inherited two mutant copies of the dry earwax gene variant, you are going to have dry earwax—end of story.

The mutation in the ABCC11 gene that causes dry earwax also eliminates armpit odor.³⁰ That’s the main reason why the subway at rush hour in Seoul smells so much better than it does in New York City. The ABCC11 gene plays a role in secretions from the apocrine glands, the special sweat glands in the armpits (and the external genitals) that secrete oily substances that are then metabolized by bacteria to create funky odors.³¹ Because of the ABCC11 mutation, nearly all Korean people (and most Japanese and northern Han Chinese people) have odorless armpits along with dry earwax. It is rumored that, in some cases, armpit odor has been a sufficient condition to excuse Japanese men from military service. Stinky armpits are so rare in Japan that some Japanese people who have the stinky-armpit trait seek surgical removal of their armpit apocrine glands. But anxiety about armpit odor is not just a Japanese phenomenon. Revealing the power of advertising and social conformity, one study showed that, among those rare women in the United Kingdom who have the odorless-armpit trait, most (78 percent) still buy and use deodorant.³²

AFTER HEARING ABOUT PKU and dry earwax, one could begin to think that there are single genes that drive many human traits. In fact, such traits are quite rare, occupying the far end of the heritability spectrum. The other end consists of traits, like speech accent, that appear to have no heritable basis whatsoever. While there are heritable factors that contribute to the quality of your voice (high or low pitched, resonant or thin, raspy or clear), and these voice qualities will be equally evident in both your speech and singing voice, your accent is entirely determined by your experience of hearing the speech of others. There is no genetic contribution at all. Interestingly, the speech that we imitate most strongly is that of our peers, not our parents. That is why the children of immigrants tend to have the accents of the community where they were raised.

Most traits are neither entirely heritable, like earwax type, nor entirely environmental, like speech accent. Rather, 30 to 80 percent of their variation across a population can be explained by genes. In recent years, a new approach, called a genome-wide association study (GWAS), has helped to show why that is the case. Let’s say that you want to know what genes contribute to variation in height (which we know is about 85 percent heritable in affluent populations). You’d assemble thousands of people chosen at random, spanning the range of adult human height. Then you’d collect DNA samples and look at variation across all nineteen thousand or so genes in the genome, as well as the long stretches of DNA between genes. In fact, this very study was done with over seven hundred thousand people, and it showed that height was not determined by changes in a single gene or even a handful of genes, but rather by variation in at least seven hundred genes. Some of these genes were known to contribute to the growth of bone, muscle, or cartilage and so weren’t a surprise. But many others would never have been guessed beforehand, reflecting the fact that there are many genes in the genome whose functions remain poorly understood.³³

There is no single height gene. Rather, there are many genes, and variation in each contributes a small amount to overall height (and each of these genes also influences traits other than height). In addition, the variation in each of these many genes does not merely sum up, but rather combines in sometimes complex and unpredictable ways. Variation in two different genes can add up to more than the sum of their small effects; 1 + 1 = 5, if you will. Other times, two genes can cancel each other out, yielding a 1 + 1 = 0 situation.

The same is true of behavioral traits. There is no single gene for religiosity, neuroticism, or empathy. Genes contain the information to instruct the production of proteins (like the D2-type dopamine receptor or the enzyme tyrosine hydroxylase), not behavioral traits like shyness or risk-taking. A disorder like schizophrenia or a structural trait like height can be highly heritable (both about 85 percent) but also determined by the concerted interaction of many hundreds of genes. Please remember this the next time you see a news report about “the IQ gene” or “the empathy gene” or some such nonsense.³⁴

WITH THIS BACKGROUND ON trait heritability and genes, let’s return to Trut and Belyaev’s fox-taming experiment. One way to discover which genes are involved in the emerging trait of tameness would be to take a page from the human height studies: do a GWAS by taking DNA samples from many tame and wild foxes and compare variation across the genome with scores of tameness. Another way is called a candidate gene approach. Recent work from Monique Udell and her coworkers at Oregon State University has shown that variation in two adjacent genes in dogs is strongly associated with tameness and extreme friendliness. Deletion of these same genes (and other nearby genes) occurs in some humans and causes Williams-Beuren syndrome, one symptom of which is extreme friendliness. These findings have led to the interesting hypothesis that one important event in dog domestication has been changes in these two genes that mimic aspects of human Williams-Beuren syndrome.³⁵ Soon, we will know if the Siberian tame foxes have similar mutations in these two genes, which would be a big step in understanding the emergence of tameness in particular, and novel behavioral traits more generally.