7 The Nature-Nurture Question

This is an edited and adapted chapter originally written by Eric Turkheimer PhD for the NOBA series in psychology.  For full attribution please see the end of this chapter.

People have a deep intuition about what has been called the “nature–nurture question.” Some aspects of our behavior feel as though they originate in our genetic makeup, while others feel like the result of our upbringing or our own hard work. The scientific field of behavior genetics attempts to study these differences empirically, either by examining similarities among family members with different degrees of genetic relatedness, or, more recently, by studying differences in the DNA of people with different behavioral traits. The scientific methods that have been developed are ingenious, but often inconclusive. Many of the difficulties encountered in the empirical science of behavior genetics turn out to be conceptual, and our intuitions about nature and nurture get more complicated the harder we think about them. In the end, it is an oversimplification to ask how “genetic” some particular behavior is. Genes and environments always combine to produce behavior, and the real science is in the discovery of how they combine for a given behavior.

Learning Objectives

  • Understand what the nature–nurture debate is and why the problem fascinates us.
  • Understand why nature–nurture questions are difficult to study empirically.
  • Know the major research designs that can be used to study nature–nurture questions.
  • Appreciate the complexities of nature–nurture and why questions that seem simple turn out not to have simple answers.

Introduction

There are three related problems at the intersection of philosophy and science that are fundamental to our understanding of our relationship to the natural world: the mind–body problem, the free will problem, and the nature–nurture problem. These great questions have a lot in common. Everyone, even those without much knowledge of science or philosophy, has opinions about the answers to these questions that come simply from observing the world we live in. Our feelings about our relationship with the physical and biological world often seem incomplete. We are in control of our actions in some ways, but at the mercy of our bodies in others; it feels obvious that our consciousness is some kind of creation of our physical brains, at the same time we sense that our awareness must go beyond just the physical. This incomplete knowledge of our relationship with nature leaves us fascinated and a little obsessed, like a cat that climbs into a paper bag and then out again, over and over, mystified every time by a relationship between inner and outer that it can see but can’t quite understand.

It may seem obvious that we are born with certain characteristics while others are acquired, and yet of the three great questions about humans’ relationship with the natural world, only nature–nurture gets referred to as a “debate.” In the history of psychology, no other question has caused so much controversy and offense: We are so concerned with nature–nurture because our very sense of moral character seems to depend on it. While we may admire the athletic skills of a great basketball player, we think of his height as simply a gift, a payoff in the “genetic lottery.” For the same reason, no one blames a short person for his height or someone’s congenital disability on poor decisions: To state the obvious, it’s “not their fault.” But we do praise the concert violinist (and perhaps their parents and teachers as well) for their dedication, just as we condemn cheaters, slackers, and bullies for their bad behavior.

The problem is, most human characteristics aren’t usually as clear-cut as height or instrument-mastery, affirming our nature–nurture expectations strongly one way or the other. In fact, even the great violinist might have some inborn qualities—perfect pitch, or long, nimble fingers—that support and reward their hard work. And the basketball player might have eaten a diet while growing up that promoted his genetic tendency for being tall. When we think about our own qualities, they seem under our control in some respects, yet beyond our control in others. And often the traits that don’t seem to have an obvious cause are the ones that concern us the most and are far more personally significant. What about how much we drink or worry? What about our honesty, or religiosity, or sexual orientation? They all come from that uncertain zone, neither fixed by nature nor totally under our own control.

Two nearly identical puppies stand side by side.
Researchers have learned a great deal about the nature-nurture dynamic by working with animals. But of course many of the techniques used to study animals cannot be applied to people. Separating these two influences in human subjects is a greater research challenge. [Image: Sebastián Dario, https://goo.gl/OPiIWd, CC BY-NC 2.0, https://goo.gl/FIlc2e]

One major problem with answering nature-nurture questions about people is, how do you set up an experiment? In nonhuman animals, there are relatively straightforward experiments for tackling nature–nurture questions. Say, for example, you are interested in aggressiveness in dogs. You want to test for the more important determinant of aggression: being born to aggressive dogs or being raised by them. You could mate two aggressive dogs—angry Chihuahuas—together, and mate two nonaggressive dogs—happy beagles—together, then switch half the puppies from each litter between the different sets of parents to raise. You would then have puppies born to aggressive parents (the Chihuahuas) but being raised by nonaggressive parents (the Beagles), and vice versa, in litters that mirror each other in puppy distribution. The big questions are: Would the Chihuahua parents raise aggressive beagle puppies? Would the beagle parents raise nonaggressive Chihuahua puppies? Would the puppies’ nature win out, regardless of who raised them? Or… would the result be a combination of nature and nurture? Much of the most significant nature–nurture research has been done in this way (Scott & Fuller, 1998), and animal breeders have been doing it successfully for thousands of years. In fact, it is fairly easy to breed animals for behavioral traits.

With people, however, we can’t assign babies to parents at random, or select parents with certain behavioral characteristics to mate, merely in the interest of science (though history does include horrific examples of such practices, in misguided attempts at “eugenics,” the shaping of human characteristics through intentional breeding). In typical human families, children’s biological parents raise them, so it is very difficult to know whether children act like their parents due to genetic (nature) or environmental (nurture) reasons. Nevertheless, despite our restrictions on setting up human-based experiments, we do see real-world examples of nature-nurture at work in the human sphere—though they only provide partial answers to our many questions.

The science of how genes and environments work together to influence behavior is called behavioral genetics. The easiest opportunity we have to observe this is the adoption study. When children are put up for adoption, the parents who give birth to them are no longer the parents who raise them. This setup isn’t quite the same as the experiments with dogs (children aren’t assigned to random adoptive parents in order to suit the particular interests of a scientist) but adoption still tells us some interesting things, or at least confirms some basic expectations. For instance, if the biological child of tall parents were adopted into a family of short people, do you suppose the child’s growth would be affected? What about the biological child of a Spanish-speaking family adopted at birth into an English-speaking family? What language would you expect the child to speak? And what might these outcomes tell you about the difference between height and language in terms of nature-nurture?

Twin boys sit together dressed in matching clothes and hats and holding similar stuffed animals.
Studies focused on twins have led to important insights about the biological origins of many personality characteristics.

Another option for observing nature-nurture in humans involves twin studies. There are two types of twins: monozygotic (MZ) and dizygotic (DZ). Monozygotic twins, also called “identical” twins, result from a single zygote (fertilized egg) and have the same DNA. They are essentially clones. Dizygotic twins, also known as “fraternal” twins, develop from two zygotes and share 50% of their DNA. Fraternal twins are ordinary siblings who happen to have been born at the same time. To analyze nature–nurture using twins, we compare the similarity of MZ and DZ pairs. Sticking with the features of height and spoken language, let’s take a look at how nature and nurture apply: Identical twins, unsurprisingly, are almost perfectly similar for height. The heights of fraternal twins, however, are like any other sibling pairs: more similar to each other than to people from other families, but hardly identical. This contrast between twin types gives us a clue about the role genetics plays in determining height. Now consider spoken language. If one identical twin speaks Spanish at home, the co-twin with whom she is raised almost certainly does too. But the same would be true for a pair of fraternal twins raised together. In terms of spoken language, fraternal twins are just as similar as identical twins, so it appears that the genetic match of identical twins doesn’t make much difference.

Twin and adoption studies are two instances of a much broader class of methods for observing nature-nurture called quantitative genetics, the scientific discipline in which similarities among individuals are analyzed based on how biologically related they are. We can do these studies with siblings and half-siblings, cousins, twins who have been separated at birth and raised separately (Bouchard, Lykken, McGue, & Segal, 1990; such twins are very rare and play a smaller role than is commonly believed in the science of nature–nurture), or with entire extended families (see Plomin, DeFries, Knopik, & Neiderhiser, 2012, for a complete introduction to research methods relevant to nature–nurture).

For better or for worse, contentions about nature–nurture have intensified because quantitative genetics produces a number called a heritability coefficient, varying from 0 to 1, that is meant to provide a single measure of genetics’ influence of a trait. In a general way, a heritability coefficient measures how strongly differences among individuals are related to differences among their genes. But beware: Heritability coefficients, although simple to compute, are deceptively difficult to interpret. Nevertheless, numbers that provide simple answers to complicated questions tend to have a strong influence on the human imagination, and a great deal of time has been spent discussing whether the heritability of intelligence or personality or depression is equal to one number or another.

A DNA single strand.
Quantitative genetics uses statistical methods to study the effects that both heredity and environment have on test subjects. These methods have provided us with the heritability coefficient which measures how strongly differences among individuals for a trait are related to differences among their genes. [Image: EMSL, https://goo.gl/IRfn9g, CC BY-NC-SA 2.0, https://goo.gl/fbv27n]

One reason nature–nurture continues to fascinate us so much is that we live in an era of great scientific discovery in genetics, comparable to the times of Copernicus, Galileo, and Newton, with regard to astronomy and physics. Every day, it seems, new discoveries are made, new possibilities proposed. When Francis Galton first started thinking about nature–nurture in the late-19th century he was very influenced by his cousin, Charles Darwin, but genetics per se was unknown. Mendel’s famous work with peas, conducted at about the same time, went undiscovered for 20 years; quantitative genetics was developed in the 1920s; DNA was discovered by Watson and Crick in the 1950s; the human genome was completely sequenced at the turn of the 21st century; and we are now on the verge of being able to obtain the specific DNA sequence of anyone at a relatively low cost. No one knows what this new genetic knowledge will mean for the study of nature–nurture, but as we will see in the next section, answers to nature–nurture questions have turned out to be far more difficult and mysterious than anyone imagined.

What Have We Learned About Nature–Nurture?

It would be satisfying to be able to say that nature–nurture studies have given us conclusive and complete evidence about where traits come from, with some traits clearly resulting from genetics and others almost entirely from environmental factors, such as childrearing practices and personal will; but that is not the case. Instead, everything has turned out to have some footing in genetics. The more genetically-related people are, the more similar they are—for everything: height, weight, intelligence, personality, mental illness, etc. Sure, it seems like common sense that some traits have a genetic bias. For example, adopted children resemble their biological parents even if they have never met them, and identical twins are more similar to each other than are fraternal twins. And while certain psychological traits, such as personality or mental illness (e.g., schizophrenia), seem reasonably influenced by genetics, it turns out that the same is true for political attitudes, how much television people watch (Plomin, Corley, DeFries, & Fulker, 1990), and whether or not they get divorced (McGue & Lykken, 1992).

A father and his young son sit together on a blanket on the lawn on a sunny day. Each have their shirts removed and are dressed almost identically including straw hats, sunglasses, and pipes.
Research over the last half century has revealed how central genetics are to behavior. The more genetically related people are the more similar they are not just physically but also in terms of personality and behavior. [Image: Paul Altobelli, https://goo.gl/SWLwm2, CC BY 2.0, https://goo.gl/9uSnqN]

It may seem surprising, but genetic influence on behavior is a relatively recent discovery. In the middle of the 20th century, psychology was dominated by the doctrine of behaviorism, which held that behavior could only be explained in terms of environmental factors. Psychiatry concentrated on psychoanalysis, which probed for roots of behavior in individuals’ early life-histories. The truth is, neither behaviorism nor psychoanalysis is incompatible with genetic influences on behavior, and neither Freud nor Skinner was naive about the importance of organic processes in behavior. Nevertheless, in their day it was widely thought that children’s personalities were shaped entirely by imitating their parents’ behavior, and that schizophrenia was caused by certain kinds of “pathological mothering.” Whatever the outcome of our broader discussion of nature–nurture, the basic fact that the best predictors of an adopted child’s personality or mental health are found in the biological parents they have never met, rather than in the adoptive parents who raised them, presents a significant challenge to purely environmental explanations of personality or psychopathology. The message is clear: You can’t leave genes out of the equation. But keep in mind, no behavioral traits are completely inherited, so you can’t leave the environment out altogether, either.

Trying to untangle the various ways nature-nurture influences human behavior can be messy, and often common-sense notions can get in the way of good science. One very significant contribution of behavioral genetics that has changed psychology for good can be very helpful to keep in mind: When your subjects are biologically-related, no matter how clearly a situation may seem to point to environmental influence, it is never safe to interpret a behavior as wholly the result of nurture without further evidence. For example, when presented with data showing that children whose mothers read to them often are likely to have better reading scores in third grade, it is tempting to conclude that reading to your kids out loud is important to success in school; this may well be true, but the study as described is inconclusive, because there are genetic as well as environmental pathways between the parenting practices of mothers and the abilities of their children. This is a case where “correlation does not imply causation,” as they say. To establish that reading aloud causes success, a scientist can either study the problem in adoptive families (in which the genetic pathway is absent) or by finding a way to randomly assign children to oral reading conditions.

The outcomes of nature–nurture studies have fallen short of our expectations (of establishing clear-cut bases for traits) in many ways. The most disappointing outcome has been the inability to organize traits from more– to less-genetic. As noted earlier, everything has turned out to be at least somewhat heritable (passed down), yet nothing has turned out to be absolutely heritable, and there hasn’t been much consistency as to which traits are more heritable and which are less heritable once other considerations (such as how accurately the trait can be measured) are taken into account (Turkheimer, 2000). The problem is conceptual: The heritability coefficient, and, in fact, the whole quantitative structure that underlies it, does not match up with our nature–nurture intuitions. We want to know how “important” the roles of genes and environment are to the development of a trait, but in focusing on “important” maybe we’re emphasizing the wrong thing. First of all, genes and environment are both crucial to every trait; without genes the environment would have nothing to work on, and too, genes cannot develop in a vacuum. Even more important, because nature–nurture questions look at the differences among people, the cause of a given trait depends not only on the trait itself, but also on the differences in that trait between members of the group being studied.

The classic example of the heritability coefficient defying intuition is the trait of having two arms. No one would argue against the development of arms being a biological, genetic process. But fraternal twins are just as similar for “two-armedness” as identical twins, resulting in a heritability coefficient of zero for the trait of having two arms. Normally, according to the heritability model, this result (coefficient of zero) would suggest all nurture, no nature, but we know that’s not the case. The reason this result is not a tip-off that arm development is less genetic than we imagine is because people do not vary in the genes related to arm development—which essentially upends the heritability formula. In fact, in this instance, the opposite is likely true: the extent that people differ in arm number is likely the result of accidents and, therefore, environmental. For reasons like these, we always have to be very careful when asking nature–nurture questions, especially when we try to express the answer in terms of a single number. The heritability of a trait is not simply a property of that trait, but a property of the trait in a particular context of relevant genes and environmental factors.

Another issue with the heritability coefficient is that it divides traits’ determinants into two portions—genes and environment—which are then calculated together for the total variability. This is a little like asking how much of the experience of a symphony comes from the horns and how much from the strings; the ways instruments or genes integrate is more complex than that. It turns out to be the case that, for many traits, genetic differences affect behavior under some environmental circumstances but not others—a phenomenon called gene-environment interaction, or G x E. In one well-known example, Caspi et al. (2002) showed that among maltreated children, those who carried a particular allele of the MAOA gene showed a predisposition to violence and antisocial behavior, while those with other alleles did not. Whereas, in children who had not been maltreated, the gene had no effect. Making matters even more complicated are very recent studies of what is known as epigenetics, a process in which the DNA itself is modified by environmental events, and those genetic changes transmitted to children.

A mother smiles broadly as she nuzzle noses with her toddler son.
The answer to the nature –nurture question has not turned out to be as straightforward as we would like. The many questions we can ask about the relationships among genes, environments, and human traits may have many different answers, and the answer to one tells us little about the answers to the others. [Image: Sundaram Ramaswamy, https://goo.gl/Bv8lp6, CC BY 2.0, https://goo.gl/9uSnqN]Epigenetics  is the study of changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself.  Epigenetics has the potential to provide answers to these important questions and refers to the transmission of phenotype in terms of gene expression in the absence of changes in DNA sequence—hence the name epi- (Greek: επί- over, above) genetics (Waddington, 1942; Wolffe & Matzke, 1999). The genotypephenotype distinction is drawn in genetics. “Genotype” is an organism’s full hereditary information. … The genes contribute to a trait, and the phenotype is the observable expression of the genes (and therefore the genotype that affects the trait). Genotype studies have provided insights into epigenetic regulation of developmental pathways in response to a range of external environmental factors (Dolinoy, Weidman, & Jirtle, 2007). These environmental factors during early childhood and adolescence can cause changes in expression of genes conferring risk of mental health and chronic physical conditions. Thus, the examination of genetic–epigenetic–environment interactions from a developmental perspective may determine the nature of gene misregulation in psychological disorders. Identical twins develop from a single fertilized egg, they have the same genome. However recent studies have shown that many environmentally induced differences are reflected in the epigenome for identical twins. The epigenome refers to the genomic pattern and information made up of chemical compounds and proteins that can attach to DNA and direct such actions as turning genes on or off, controlling the production of proteins in particular cells and changing the expression of a gene. These changes in the epigenome may be passed down through heritance, or may be changed by environmental experiences.

The video above explains basics of epigenetics, and shares the story of two “clones” or persons that were born identical, but had very different life circumstances. One person was stressed and ate poorly, the other had an easier life and ate healthy ways. If you and your clone person were examined at age 50, you would look quite different. The one who had eaten poorly would probably look more tired. If scientists looked at your DNA however, your DNA would be still the same, or your genomes would be the same. However you would have different epigenomes – meaning that some markers on your genes would look differently. If you think of DNA and genes as a paragraph, then epigenomes could be the punctuation of the paragraph. As you know, punctuation changes the meaning and expression of a paragraph. The epigenome is the “marching orders” for what the gene is supposed to do, and can be affected by environmental experiences. What we do, what we eat, what we smoke, who we hang out with, all of these affect our epigenomes or the expression of our genes.

One of the most educational findings (and historically tragic events) on the impact of adverse environmental conditions (phenotype experiences)  and physical health (genotype experiences) comes from studies of the children of women who were pregnant during two civilian famines of World War II: the Siege of Leningrad (1941–44) (Bateson, 2001) and the Dutch Hunger Winter (1944–1945) (Stanner et al., 1997). In the Netherlands famine, women who were previously well nourished were subjected to low caloric intake and associated environmental stressors. Women who endured the famine in the late stages of pregnancy gave birth to smaller babies (Lumey & Stein, 1997) and these children had an increased risk of insulin resistance later in life (Painter, Roseboom, & Bleker, 2005). In addition, offspring who were starved prenatally later experienced impaired glucose tolerance in adulthood, even when food was more abundant (Stanner et al., 1997). Famine exposure at various stages of gestation was associated with a wide range of risks such as increased obesity, higher rates of coronary heart disease, and lower birth weight (Lumey & Stein, 1997). Interestingly, when examined 60 years later, people exposed to famine prenatally showed reduced DNA methylation compared with their unexposed same-sex siblings (Heijmans et al., 2008).

Parental investment and programming of stress responses in the offspring

The most comprehensive study to date of variations in parental investment and epigenetic inheritance in mammals is that of the maternally transmitted responses to stress in rats. In rat pups, maternal nurturing (licking and grooming) during the first week of life is associated with long-term programming of individual differences in stress responsiveness, emotionality, cognitive performance, and reproductive behavior (Caldji et al., 1998; Francis, Diorio, Liu, & Meaney, 1999; Liu et al., 1997; Myers, Brunelli, Shair, Squire, & Hofer, 1989; Stern, 1997). In adulthood, the offspring of mothers that exhibit increased levels of pup licking and grooming over the first week of life show increased expression of the glucocorticoid receptor in the hippocampus (a brain structure associated with stress responsivity as well as learning and memory) and a lower hormonal response to stress compared with adult animals reared by low licking and grooming mothers (Francis et al., 1999; Liu et al., 1997). Moreover, rat pups that received low levels of maternal licking and grooming during the first week of life showed decreased histone acetylation and increased DNA methylation of a neuron-specific promoter of the glucocorticoid receptor gene (Weaver et al., 2004). The expression of this gene is then reduced, the number of glucocorticoid receptors in the brain is decreased, and the animals show a higher hormonal response to stress throughout their life. The effects of maternal care on stress hormone responses and behaviour in the offspring can be eliminated in adulthood by pharmacological treatment (HDAC inhibitor trichostatin A, TSA) or dietary amino acid supplementation (methyl donor L-methionine), treatments that influence histone acetylation, DNA methylation, and expression of the glucocorticoid receptor gene (Weaver et al., 2004; Weaver et al., 2005). This series of experiments shows that histone acetylation and DNA methylation of the glucocorticoid receptor gene promoter is a necessary link in the process leading to the long-term physiological and behavioral sequelae of poor maternal care. This points to a possible molecular target for treatments that may reverse or ameliorate the traces of childhood maltreatment.

Several studies have attempted to determine to what extent the findings from model animals are transferable to humans. Examination of post-mortem brain tissue from healthy human subjects found that the human equivalent of the glucocorticoid receptor gene promoter (NR3C1 exon 1F promoter) is also unique to the individual (Turner, Pelascini, Macedo, & Muller, 2008). A similar study examining newborns showed that methylation of the glucocorticoid receptor gene promoter maybe an early epigenetic marker of maternal mood and risk of increased hormonal responses to stress in infants 3 months of age (Oberlander et al., 2008). Although further studies are required to examine the functional consequence of this DNA methylation, these findings are consistent with our studies in the neonate and adult offspring of low licking and grooming mothers that show increased DNA methylation of the promoter of the glucocorticoid receptor gene, decreased glucocorticoid receptor gene expression, and increased hormonal responses to stress (Weaver et al., 2004). Examination of brain tissue from suicide victims found that the human glucocorticoid receptor gene promoter is also more methylated in the brains of individuals who had experienced maltreatment during childhood (McGowan et al., 2009). These finding suggests that DNA methylation mediates the effects of early environment in both rodents and humans and points to the possibility of new therapeutic approaches stemming from translational epigenetic research. Indeed, similar processes at comparable epigenetic labile regions could explain why the adult offspring of high and low licking/grooming mothers exhibit widespread differences in hippocampal gene expression and cognitive function (Weaver, Meaney, & Szyf, 2006).

However, this type of research is limited by the inaccessibility of human brain samples. The translational potential of this finding would be greatly enhanced if the relevant epigenetic modification can be measured in an accessible tissue. Examination of blood samples from adult patients with bipolar disorder, who also retrospectively reported on their experiences of childhood abuse and neglect, found that the degree of DNA methylation of the human glucocorticoid receptor gene promoter was strongly positively related to the reported experience of childhood maltreatment decades earlier. For a relationship between a molecular measure and reported historical exposure, the effects size is extraordinarily large. This opens a range of new possibilities: given the large effect size and consistency of this association, measurement of the GR promoter methylation may effectively become a blood test measuring the physiological traces left on the genome by early experiences. Although this blood test cannot replace current methods of diagnosis, this unique and addition information adds to our knowledge of how disease may arise and be manifested throughout life. Near-future research will examine whether this measure adds value over and above simple reporting of early adversities when it comes to predicting important outcomes, such as response to treatment or suicide.

 

Epigenetic strategy to understanding gene-environment interactions

 

An unhappy looking little boy sits with his teddy bear on the floor of a closet.
Although there is some evidence that a dysfunctional upbringing can increase one’s likelihood for schizophrenia (an epigenetically inherited disease), some people who have both the predisposition and the stressful environment never develop the mental illness. [Image: Steve White, CC0 Public Domain, https://goo.gl/m25gce]
While the cellular and molecular mechanisms that influence on physical and mental health have long been a central focus of neuroscience, only in recent years has attention turned to the epigenetic mechanisms behind the dynamic changes in gene expression responsible for normal cognitive function and increased risk for mental illness. The links between early environment and epigenetic modifications suggest a mechanism underlying gene-environment interactions. Early environmental adversity alone is not a sufficient cause of mental illness, because many individuals with a history of severe childhood maltreatment or trauma remain healthy. It is increasingly becoming evident that inherited differences in the segments of specific genes may moderate the effects of adversity and determine who is sensitive and who is resilient through a gene-environment interplay. Genes such as the glucocorticoid receptor appear to moderate the effects of childhood adversity on mental illness. Remarkably, epigenetic DNA modifications have been identified that may underlie the long-lasting effects of environment on biological functions. This new epigenetic research is pointing to a new strategy to understanding gene-environment interactions.

 

 

Some common questions about nature–nurture are, how susceptible is a trait to change, how malleable is it, and do we “have a choice” about it? These questions are much more complex than they may seem at first glance. For example, phenylketonuria is an inborn error of metabolism caused by a single gene; it prevents the body from metabolizing phenylalanine. Untreated, it causes mental retardation and death. But it can be treated effectively by a straightforward environmental intervention: avoiding foods containing phenylalanine. Height seems like a trait firmly rooted in our nature and unchangeable, but the average height of many populations in Asia and Europe has increased significantly in the past 100 years, due to changes in diet and the alleviation of poverty. Even the most modern genetics has not provided definitive answers to nature–nurture questions. When it was first becoming possible to measure the DNA sequences of individual people, it was widely thought that we would quickly progress to finding the specific genes that account for behavioral characteristics, but that hasn’t happened. There are a few rare genes that have been found to have significant (almost always negative) effects, such as the single gene that causes Huntington’s disease, or the Apolipoprotein gene that causes early onset dementia in a small percentage of Alzheimer’s cases. Aside from these rare genes of great effect, however, the genetic impact on behavior is broken up over many genes, each with very small effects. For most behavioral traits, the effects are so small and distributed across so many genes that we have not been able to catalog them in a meaningful way. In fact, the same is true of environmental effects. We know that extreme environmental hardship causes catastrophic effects for many behavioral outcomes, but fortunately extreme environmental hardship is very rare. Within the normal range of environmental events, those responsible for differences (e.g., why some children in a suburban third-grade classroom perform better than others) are much more difficult to grasp.

The difficulties with finding clear-cut solutions to nature–nurture problems bring us back to the other great questions about our relationship with the natural world: the mind-body problem and free will. Investigations into what we mean when we say we are aware of something reveal that consciousness is not simply the product of a particular area of the brain, nor does choice turn out to be an orderly activity that we can apply to some behaviors but not others. So it is with nature and nurture: What at first may seem to be a straightforward matter, able to be indexed with a single number, becomes more and more complicated the closer we look. The many questions we can ask about the intersection among genes, environments, and human traits—how sensitive are traits to environmental change, and how common are those influential environments; are parents or culture more relevant; how sensitive are traits to differences in genes, and how much do the relevant genes vary in a particular population; does the trait involve a single gene or a great many genes; is the trait more easily described in genetic or more-complex behavioral terms?—may have different answers, and the answer to one tells us little about the answers to the others.

It is tempting to predict that the more we understand the wide-ranging effects of genetic differences on all human characteristics—especially behavioral ones—our cultural, ethical, legal, and personal ways of thinking about ourselves will have to undergo profound changes in response. Perhaps criminal proceedings will consider genetic background. Parents, presented with the genetic sequence of their children, will be faced with difficult decisions about reproduction. These hopes or fears are often exaggerated. In some ways, our thinking may need to change—for example, when we consider the meaning behind the fundamental American principle that all men are created equal. Human beings differ, and like all evolved organisms they differ genetically. The Declaration of Independence predates Darwin and Mendel, but it is hard to imagine that Jefferson—whose genius encompassed botany as well as moral philosophy—would have been alarmed to learn about the genetic diversity of organisms. One of the most important things modern genetics has taught us is that almost all human behavior is too complex to be nailed down, even from the most complete genetic information, unless we’re looking at identical twins. The science of nature and nurture has demonstrated that genetic differences among people are vital to human moral equality, freedom, and self-determination, not opposed to them. As Mordecai Kaplan said about the role of the past in Jewish theology, genetics gets a vote, not a veto, in the determination of human behavior. We should indulge our fascination with nature–nurture while resisting the temptation to oversimplify it.

Vocabulary

Adoption study
A behavior genetic research method that involves comparison of adopted children to their adoptive and biological parents.
Behavioral genetics
The empirical science of how genes and environments combine to generate behavior

Epigenetics  is the study of changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself.  Epigenetics looks at all events that occur in the absence of changes in DNA sequence. Epigenetics is looking at changes of the gene expression, rather than changes in the DNA code itself.

Epigenome: epigenome refers to the genetic patterns and information made up of chemical compounds and proteins that can attach to DNA, and direct such actions as turning genes on or off, controlling the production of proteins in particular cells and changing the expression of a gene. These changes in the epigenome may be passed down through heritance, or may be changed by environmental experiences.

Heritability coefficient
An easily misinterpreted statistical construct that purports to measure the role of genetics in the explanation of differences among individuals.

Genotype: is an organism’s full hereditary information. … The genes that contribute to a trait”. Genotype is an organism’s full hereditary information.

Phenotype: is an organism’s actual observed properties, such as morphology, development, or behavior.

Twin studies
A behavior genetic research method that involves comparison of the similarity of identical (monozygotic; MZ) and fraternal (dizygotic; DZ) twins.

Quiz

References

  • Bouchard, T. J., Lykken, D. T., McGue, M., & Segal, N. L. (1990). Sources of human psychological differences: The Minnesota study of twins reared apart. Science, 250(4978), 223–228.
  • Caspi, A., McClay, J., Moffitt, T. E., Mill, J., Martin, J., Craig, I. W., Taylor, A. & Poulton, R. (2002). Role of genotype in the cycle of violence in maltreated children. Science, 297(5582), 851–854.
  • McGue, M., & Lykken, D. T. (1992). Genetic influence on risk of divorce. Psychological Science, 3(6), 368–373.
  • Plomin, R., Corley, R., DeFries, J. C., & Fulker, D. W. (1990). Individual differences in television viewing in early childhood: Nature as well as nurture. Psychological Science, 1(6), 371–377.
  • Plomin, R., DeFries, J. C., Knopik, V. S., & Neiderhiser, J. M. (2012). Behavioral genetics. New York, NY: Worth Publishers.
  • Scott, J. P., & Fuller, J. L. (1998). Genetics and the social behavior of the dog. Chicago, IL: University of Chicago Press.
  • Turkheimer, E. (2000). Three laws of behavior genetics and what they mean. Current Directions in Psychological Science, 9(5), 160–164.

 

 

 

This is an edited and adapted chapter from a chapter by Eric Turkheimer PhD, contributed to the NOBA project. The original authors bear no responsibility for this chapter. The original chapter can be found here:

Turkheimer, E. (2019). The nature-nurture question. In R. Biswas-Diener & E. Diener (Eds), Noba textbook series: Psychology. Champaign, IL: DEF publishers. Retrieved from http://noba.to/tvz92edh

 

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