behavioral genetics essay

Blaming Our Genes: The Heritability of Behavior

It’s easy to accept that human disorders such as phenylketonuria or cystic fibrosis or Huntington’s disease have a wholly genetic basis. And you likely have no problem believing that your risk of being afflicted with an illness such as heart disease, diabetes, or colon cancer is influenced by your personal DNA code. The question of heredity becomes more complicated, however, when we consider complex behaviors.

Is your chance of having a sunny disposition affected by your genes? How about if you are a pessimist — is pessimism an inherited trait? What if you’re an early-morning or a late-night person, or compulsively neat, or emotionally unable to connect with others — could genetic differences contribute to those traits? How much of our temperament is due to our genes? How much of our intelligence — our ability to learn and remember, to acquire language, to read and spell — is a function of our DNA code? And what about psychiatric disorders such as schizophrenia, bipolar disorder, and depression? Are those due to our circumstances, or to our genetic constitution?

The answer is: both. Nature and nurture, our genetic endowment and our life situation and experiences, determine our behavior. But we suspect that the contribution from genetics may be more than most of us imagine.

Consider, for example, Susan Middlebrook, of Colchester, Vermont. She usually gets seven or eight hours of sleep each night, but rather than going to bed at 11:30 p.m., after the late-night news, and getting up at around 7 a.m., Middlebrook goes to bed early, very early . . . like at 6:30 p.m. And between 1:30 and 3 a.m., just when you’re deep in your dreams, Middlebrook is raring to get up and go. “The net result is you can feel very isolated,” she told National Geographic News in 2005. “Who wants to party at three in the morning? Nobody I know, and I’m not headed to the local bar to see who’s there.” Instead, Middlebrook gets started on her morning chores long before your dreams are over.

Middlebrook suffers from familial advanced sleep phase syndrome (FASPS), the consequence of which is that her sleep patterns are way out of sync with the norm. To establish the norm, and the abnormal exceptions, sleep researchers ask people a series of questions about their sleep habits: At what time of day do you feel your best? How easy is it for you to get up in the morning? At what time would you go to bed if you were completely free to plan your day? At what time in the evening do you feel drowsy and begin to doze? Do you consider yourself a “morning” or an “evening” person? (The questionnaire was developed by a British scientist, James Horne, and a Swedish scientist, Olov Östberg.) Answers to these and other questions produce a score that lies on a scale running from extreme “eveningness” to extreme “morningness”; most of us fall somewhere in the middle of a broad bell-shaped curve of scores, but FASPS patients lie at the far “morningness” end of the scale, scoring higher than more than 99 percent of other respondents.

What makes Middlebrook’s syndrome so interesting is that it’s the result of an abnormality in her biological clock, known as the circadian rhythm; (“circadian” means, literally, the cycle of one complete day, from the Latin circa- , “cycle,” and dies , “day”). This circadian clock controls not just sleeping and waking but also metabolic, physiological and behavioral processes such as heart rate, hormone levels, blood pressure, mood, and alertness. Our biological clocks are reset each day by exposure to sunlight, thus keeping us in synchrony with our surroundings. But Middlebrook’s internal clock runs on a faster cycle, advanced by about four hours relative to most everyone else’s, so that she is ready for bed when her neighbors are ready to sit down to dinner.

Middlebrook’s sleep-wake cycle may seem unusual to you — it is far outside the statistical norm — but around the Middlebrook home it’s about as unusual as oatmeal for breakfast: two of her three sisters, one of her parents, and her own child all keep the same odd hours. This syndrome is clearly due to a variation present in the personal DNA code of these family members (the word “familial” in the name of the syndrome might have tipped you off to this), and not to any environmental cause.

Middlebrook’s sleep-wake cycle may seem unusual to you, but two of her three sisters, one of her parents, and her own child all keep the same odd hours.

Although FASPS affects only about three people in one thousand, its genetic basis was well worth deciphering. Findings about this syndrome may help to explain other more common sleeping disorders such as insomnia and narcolepsy, or lead to treatments for jet lag or seasonal affective disorder (SAD, in which the moods of sufferers are strongly affected by lack of sunlight in the winter), and they may provide health support and guidance for millions of workers who work the nightshift. Understanding human circadian rhythms may even enable drug treatments to be timed for better effect, or suggest ways to reduce nighttime auto accidents.

Now consider Jean, a 24-year old nurse who became obsessed with cleaning and washing. As related by Peter McGuffin and David Mawson, two psychiatrists in London to whom Jean was eventually referred, each day she would wash her hands 60 to 80 times and spend 12 hours disinfecting her house; she went through twenty liters of disinfectant a week. She made her husband stop his sports activity because it brought dirt into the house, and she gave up sexual activity because it could cause contamination. When Jean was admitted to the hospital, her hands were “roughened, red, cracked and bleeding” from the constant washing.

Jean’s identical twin, Jill, a social worker, lived apart from her sister and rarely saw her. Yet at the age of 22, Jill began displaying behavior similar to Jean’s. As soon as a meal was over she felt compelled to immediately wash the dishes and silverware, or else she would become severely anxious. Moreover, “the washing of the dishes and utensils had to proceed in a specific order, and failure to comply with the routine, or an attempt by others to relieve her of the task, provoked great discomfort.” Jill established other washing rituals, and despite her best efforts to stop carrying them out, she spent increasing amounts of time on them, to the detriment of her social life and her work.

Both twins had normal childhoods, had been outgoing children, and were academically accomplished. None of their family members had received treatment for a psychiatric disorder, although their father was “fastidiously neat and orderly in his habits.” The twins attended different universities; Jean obtained a degree in physics, Jill in history. Neither of them displayed any signs of mental illness before their obsessive-compulsive behaviors began. In fact, each of them learned of the other’s similar problem only after Jean began treatment with the drug clomipramine, which together with behavior therapy alleviated her symptoms enough to allow her to return to nursing. Jill was not treated, but experienced a spontaneous remission of her symptoms after more than a year.

What caused these identical twins to develop a similar disorder at a similar time in their lives? Was it something about the way their parents brought them up that led to their symptoms years later? Was it some food they ate, or some toxin they were exposed to as children? Or was it because their personal DNA code is identical, and some combination of variations in the genes they both inherited caused them to develop an obsessive-compulsive disorder in their early 20s? Or did the disorder develop because of a complex interplay of these factors?

Consider, finally, Lewis, the son of a well-to-do couple in Pittsburgh. Lewis looked perfect at birth and appeared to be developing normally. As detailed by his mother, at 18 months Lewis was almost saying words, but they weren’t the typical words that most toddlers begin with, such as “Mommy” and “Daddy.” Instead he babbled nonsensically. And he didn’t respond to the usual games that toddlers enjoy, such as peek-a-boo or ring-around-the-rosie. At two years of age, he had no interest in some toys but was obsessed with others, and when he played with these he was oblivious to everything going on around him. He loved to climb and to swing and to bounce on a trampoline, which he did without fear. Yet sometimes he was afraid to step off a rug onto a hardwood floor, reacting as if the next step would be off a cliff. At night, Lewis took off all his clothes and slept on the floor wrapped in a blanket and surrounded by toy soldiers and matchbox cars. Lewis also had tantrums, during which he lay on the floor screaming, unable to indicate his problem.

At three he had yet to acquire any language and had little interest in communicating with his family. He babbled only to his toy soldiers. His doctors were no longer able to dismiss his problems as simply those of a “difficult” child or one in the throes of the “terrible twos.” Lewis underwent a series of tests and the doctors concluded he had an autism spectrum disorder.

The diagnosis led to a variety of publicly and privately funded treatments, including speech and occupational therapy. Lewis made remarkable progress: He developed some language ability, and his behavior calmed down. He could hold his mother’s hand, play peek-a-boo with her and kiss her good night, and occasionally even make eye contact. When he read his favorite book, Eric Carle’s “The Very Hungry Caterpillar,” he said every word at the right time and mimicked the slurping sound of the caterpillar eating. But he still could not carry on a conversation. Lewis entered a special-education preschool class, with the hope and expectation that in a few years he could be integrated into a typical school class.

Autism is a complex developmental disorder that appears within the first three years of life. Its symptoms, which can range from mild to severe, are characterized by a lack of emotional contact with others, difficulty with verbal and nonverbal communication, and a restricted range of activities and interests. Children are born with autism or with the potential to develop it; they do not acquire the condition because of bad parenting. A fascinating feature of the chromosomes of some autistic children is that large chunks of DNA — millions or tens of millions of base-pairs — are found duplicated in some children and lost altogether in others. These regions can contain dozens of genes. The analysis of the personal DNA codes of these children may help pinpoint the specific genetic changes responsible for this complex and debilitating disease.

When a human population is measured for any characteristic, say height or weight, or blood pressure or cholesterol level, the measurements reveal a continuous spectrum between two extremes.

It’s no different for a complex behavior, such as how we deal with stress. Even very young babies display a broad range of responses, from those who cry easily to those who seem unbothered by almost any challenge. Similar patterns are observed in the extent or degree to which children are active or sedentary, whether they persist at pursuing a task or lose their focus, or the extent of their introversion or extroversion. Among adults, the amounts of alcohol, nicotine, or drugs that are consumed show the same broad distributions. Some part of these traits is likely due to genetics, and some is surely due to environmental components. But how much is due to each?

The measure of the amount of the genetic effect is termed “heritability.” A trait or behavior that is wholly due to genetics has 100 percent heritability; one that is wholly due to the environment has zero heritability.

The environmental component could be due to factors shared among family members, such as the home environment, the food preferences of the family, or the level of pollution in the town where the family resides. Or it could be due to factors that are not shared, such as the specific set of friends or teachers of each family member, or unusual life events such as accidents, or diseases unique to each individual.

How do we measure, or quantify, heritability? It’s actually pretty easy. All that is needed is a set of individuals whose genetic relatedness is known, and a measurement of some trait or condition for each individual.

The easiest of these studies to understand exploits the genetic similarity of twins. The personal DNA codes of identical twins are identical, because they develop from a single fertilized egg. That is, the DNA sequence of each gene in one twin is identical to its sequence in the other twin. Fraternal twins also shared the same womb at the same time, but have the same version of only about half of their genes (like any siblings), so the genetic contribution to a trait is twice as great in identical twins as it is in fraternal twins. Thus, the more similar a trait is in identical twins as compared to fraternal ones, the greater the genetic contribution to it is likely to be.

A large number of studies suggest a heritability for intelligence of around 50 percent; some studies put this number at greater than 80 percent.

Another type of study compares siblings from the same parents (who have the same version of about half of their genes), to adopted siblings who are not genetically related but share the same surroundings. A genetic influence on a trait is apparent when biological siblings are more similar than adopted ones; an environmental influence is obvious when adopted and thus genetically unrelated siblings resemble each other more than they do other unrelated people who grew up in other families.

A third type of analysis uses family genetic studies that compare how often a disease occurs in a family in which one member is known to be affected to how often it occurs in the general population. Diseases with a genetic basis occur more frequently in members of a family that has one case — in other words, genetic diseases run in families.

With these ways to quantify heritability, let’s examine some human traits. We’ll start with intelligence — a particularly thorny issue. We’d like to believe that a roomful of books, Mozart playing in the background, and a nurturing set of parents will put any infant on the road to a Nobel Prize. Those conditions can’t hurt, but they can only do so much: A large number of studies suggest a heritability for intelligence of around 50 percent; some studies put this number at greater than 80 percent.

A Swedish twin registry has information on 25,000 same-sex twins born over a period of about 70 years. Nancy Pedersen and her colleagues at the Karolinska Institute in Stockholm studied about 300 of these twin pairs, including identical twins reared apart, identical twins reared together, fraternal twins reared apart, and fraternal twins reared together. They found that intelligence scores of identical twins who grew up apart (most having been separated by the time they were two years old) correlated much more closely than the intelligence scores of fraternal twins who grew up in the same home.

Another study, the Texas Adoption Project , followed about 300 children who were adopted within a few days of birth and grew up entirely with their adopted families. John Loehlin and his coworkers at the University of Texas at Austin looked at results of intelligence tests given to the children at age seven and at age 17, to their adoptive parents, and to their biological mothers. The test scores of the biological mothers correlated significantly with those of their children who had been given away for adoption 17 years earlier, whereas there was no correlation between intelligence scores of the children and their adoptive parents. The researchers estimated that 78 percent of intelligence is inherited.

Addictive behavior, or the predilection to become addicted, is another trait whose heritability is controversial. Addiction includes physical dependence and symptoms of craving after chronic substance use, as well as behavioral dependence — the inability to stop an activity even though the consequences are severe. Alcohol, tobacco, and illicit drug use is estimated to contribute to one in eight deaths worldwide.

Yet most people who try habit-forming substances do not become addicted. One study estimates that the probability that someone who tries a substance once will become dependent on it ranges from about one in three or four for tobacco and heroin to about one in six or seven for cocaine and alcohol to about one in 11 for marijuana. The effect of genetics on the vulnerability of individuals to becoming addicted to these substances varies widely. Studies of twins suggest that persistent smoking and nicotine dependence is about 70 percent heritable, alcohol dependence is 50 to 60 percent heritable, and addiction to most other substances is 20 to 35 percent heritable. These studies also indicate that other disorders such as antisocial personality disorder and conduct disorder are often associated with addictive behavior.

Studies of twins suggest that persistent smoking and nicotine dependence is about 70 percent heritable, alcohol dependence is 50 to 60 percent heritable, and addiction to most other substances is 20 to 35 percent heritable.

Psychiatric disorders often have a large — sometimes, surprisingly large — genetic component. Schizophrenia, for which the lifetime risk is approximately 1 percent, has a heritability estimated at around 85 percent. Bipolar disorder (also known as manic-depressive illness because it is characterized by episodes of extreme elation (mania) alternating with episodes of depression) also has an individual lifetime risk of about one percent. Twin, sibling, and family studies all point to a strong genetic basis of bipolar disorder: a heritability of 80 to 90 percent. Depression (also known as unipolar disorder), for which we have an individual lifetime risk of around 10 to 20 percent in the United States, undoubtedly has a genetic basis: Its heritability may be as high as 70 percent.

Susan Middlebrook’s unusual sleep-wake cycle is obviously heritable. This syndrome has revealed something striking about circadian rhythms. Much of what’s known about these rhythms was originally worked out in Drosophila melanogaster, the tiny fruit fly that buzzes about the bananas left on a kitchen counter. Remarkably, the fly’s clockwork mechanism, the proteins it uses to reset its timing each day, works much like ours does. The first mutations to be identified that affect these rhythms, which caused flies to have either a shorter or a longer cycle, or no rhythmic cycle at all, were in a gene given the name period .

In 2001, Louis Ptácek, Ying-Hui Fu, and their colleagues at the University of Utah identified a human mutation that causes FASPS. It turned out to be in a gene that encodes a protein with an amino acid sequence very similar to the fly period protein, so the human gene was dubbed Period2 . This was extraordinary evidence of gene conservation over hundreds of millions of years of evolution. Even stronger evidence came from the finding that the single amino acid change in the Period2 protein that advanced Susan Middlebrook’s clock corresponds to a mutation in fruit flies that advances the clock of that simple organism.

What about the heritability of obsessive-compulsive disorder, the illness that struck Jean and Jill? This disease, affecting about 2 percent of the population, has remarkably diverse symptoms but generally includes four major ones: obsessions and checking behavior; a need for symmetry and order; excessive washing; and hoarding tendencies. Individuals differ in their age of onset, the duration of the illness, and the types of symptoms they display. Many sufferers have tics, and some also have depression, phobias, separation anxiety, or disruptive behavior. Some are troubled by harmful sexual or religious obsessions, or by trichotillomania, compulsive hair pulling. Others may exhibit grooming behaviors.

This diversity of symptoms suggests that obsessive-compulsive disorder may exist in different forms that have different genetic causes — in other words, there may be multiple genetic routes to a group of disorders that have all been given a single name. So it is not surprising that twin studies almost always point to a substantial heritable component for this illness, ranging from 25 percent to 80 percent. Thus, the most probable explanation for Jean and Jill’s similar illnesses at similar ages is the young women’s genetic similarity, although other factors may have contributed to their condition.

Autism is a heart-breaking diagnosis for a parent to receive, and so it was for Lewis’s parents. The prevalence of autism went up more than five-fold in the 1990s, and now may be as high as 1 percent of children. Much of the increase may be due to broader diagnostic criteria and increased physician and parent awareness.

Numerous studies indicate that genetic factors are the main cause of autism. For example, siblings of an autistic child have about 10 times the risk of having the syndrome as the general population. A twin study in the United Kingdom yielded a heritability estimate of more than 90 percent for a broad set of autistic symptoms. Many genes are suspected of being involved in the syndrome. They haven’t been identified yet, but when they are, the diagnosis of autism, which can be difficult and often confusing, will be easier and more precise. Accurate and early diagnosis will also enable earlier intervention, which will greatly improve the prognosis for these children.

Estimating the genetic component of human behaviors and psychiatric disorders may help to remove a lingering stigma attached to people with mental illness — a misplaced sense that these are character flaws — and it may inspire more people to seek treatment. In addition, these studies all point to environmental components — generally still to be teased out — that interact with the genetic ones. That’s good news, since we have some control over the environmental inputs to disease. It is notable that even for the most heritable illnesses, such as schizophrenia or bipolar disorder, the heritability is never 100 percent, and even identical twins are never 100 percent concordant. Thus, even when genetics has a strong effect, it is not absolutely deterministic, so hope should never be abandoned. Finally, identification of the gene variants contributing to a disorder can assist and sharpen diagnosis, which will lead to earlier and possibly more effective treatments.

A high heritability does not imply that just a single gene is involved. In fact, for most of these disorders it is clear that many genes are involved, and no single gene is likely to explain most of the variability. By establishing a genetic basis for these disorders and identifying families that carry the causative changes in their DNA, geneticists can pinpoint the genes that are responsible.

Identification of such genes often leads to insight into the disease that can be tested in organisms suitable for experimentation, such as the fruit fly or the mouse. Analysis of those genes is sure to illuminate disease mechanisms. Just knowing what the relevant genes are will allow individuals to be tested for the gene variants that put them at risk of the disease, and, should they carry some of those variants in their personal DNA code, make them or their parents vigilant about early signs of the disease. And the genes and proteins that are implicated provide potential targets for new drugs that promise to improve the lives of people like Susan, Jean and Jill, Lewis, and many of the rest of us.

Stanley Fields is Professor of Genome Sciences and Medicine at the University of Washington and a Howard Hughes Medical Institute Investigator. Mark Johnston is Professor and Chair of the Department of Biochemistry and Molecular Genetics at the University of Colorado School of Medicine and Editor-in-Chief of the journal Genetics. Fields and Johnston are the authors of “ Genetic Twists of Fate ,” from which this article is excerpted.

Why it is useful to understand the role of genetics in behaviour

PhD candidate in Epidemiology/Public Health, Health Behaviour Research Center, UCL

University Academic Fellow, University of Leeds

Lecturer in Behavioural Obesity Research, UCL

Disclosure statement

Clare Llewellyn is an elected trustee for the UK Association for the Study of Obesity.

Alison Fildes, Andrea Smith, and Moritz Herle do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.

University College London and University of Leeds provide funding as founding partners of The Conversation UK.

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Scientists have studied twins for many years to understand how genes and environments influence differences among individuals, spanning conditions such as cancer and mental health to characteristics such as intelligence and political beliefs .

Although the twin method is well-established, findings from twin studies are often controversial. Critics of twin research question the value of establishing that characteristics, such as health behaviours, have a strong genetic basis. A primary concern is that these types of findings will result in complacency or fatalism, effectively undermining motivation to change lifestyle. But there is very little evidence to support these fears.

Genetic influence on human characteristics is often misinterpreted. It is wrongly assumed that a behaviour that has strong genetic influence (highly heritable) must be biologically hardwired. However, genes are not destiny. Genes are often dependent on environmental exposure, such that genes can have a stronger effect, or no effect, depending on the environment.

For example, people with a genetic predisposition to lung cancer are unlikely to develop the disease unless they smoke. The same is true of behaviour. Behaviour is only elicited in response to environmental cues. Establishing that a behaviour has an important genetic basis does not imply that this behaviour cannot be changed through environmental means.

What’s the benefit?

Twin studies provide important insights into when and how genes and environments shape human nature. Studies following twins over many years have shown that the importance of genes can change dramatically with development . Genetic influence tends to increase with age for many characteristics – for example, body weight and intelligence . It is thought that with increasing maturity comes the ability to make independent choices in line with our genetic predispositions. For example, a child who is genetically predisposed to be good at reading might join a library to gain access to more books and meet like-minded people once he or she is a teenager. Twins can therefore identify the windows of opportunity when environmental influences might be strongest, and when behaviours may be easier to change.

Twin studies also inform researchers where best to target environmental interventions. Interventions targeting characteristics influenced by shared environments might best be directed at the family environment. But policymakers may have greater success if interventions are oriented towards the wider environment for characteristics shaped by factors unique to each person.

On a broader level, twin studies are also the first step towards molecular genetic research identifying specific genes involved. One classic example is body weight. We have known from twin studies that weight has a strong genetic basis , which led researchers to identify approximately 100 genetic variants involved.

The most important of these is FTO (the fat mass and obesity gene); and adults carrying two copies of the risk variant are heavier and at increased risk for obesity. The discovery of FTO and other variants paved the way for researchers to study the mechanisms through which genes influence weight in order to develop new drugs, and to help people with obesity to understand their vulnerability better.

What are the risks?

Undeniably there are concerns that promoting the knowledge that healthy behaviour is partially down to genes may somehow stop people from taking responsibility for managing their own, or their child’s behaviour. However, studies exploring individual feedback on DNA-based disease risk suggest that knowing your genetic predisposition does not necessarily undermine attempts to improve health, but may increase engagement and motivation to change behaviour .

Evidence that children’s behaviours are partially influenced by their genes also serves to alleviate the blame that often rests on parents. For example, our recent study establishing considerable genetic influence on toddlers’ fussy eating could help to ease the guilt and frustration parents experience when dealing with an extremely fussy child.

Twin research has undoubtedly advanced our understanding of human nature and has revolutionised the way we discuss the complicated relationship between nature (genes) and nurture (environment). Twin research has also led to breakthroughs in molecular genetic research that has the potential to change the course of disease treatment. Twins remain a valuable tool for researchers to establish the lay of the land in relation to the complexity of human nature.

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In This Article Expand or collapse the "in this article" section Behavioral Genetics

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Behavioral Genetics by Lisabeth DiLalla , Matthew Jamnik , Riley Marshall , Emily Pali LAST REVIEWED: 29 September 2017 LAST MODIFIED: 20 February 2024 DOI: 10.1093/obo/9780199828340-0010

Behavioral genetics is the study of genetic and environmental influences on behaviors. By examining genetic influence, more information can be gleaned about how both genes and the environment operate to affect behavior. Almost all behaviors studied by psychologists are affected by our genetic makeup, and so the question is not whether genes are important, but how do they affect these behaviors? The old nature–nurture debate has been laid to rest. We know, from thousands of studies using many different methodologies, that both genes and environment are important to understand if we hope to untangle the mysteries of virtually any behavior. Among the interesting questions to be asked now: How do genes and environments work together to influence behaviors? What specific genes might be responsible for various types of behaviors and what is their mechanism of action? The field of behavioral genetics is moving forward and changing so rapidly that many of the articles included here are from relatively recent work. Some essential mainstays are included that all students of behavioral genetics should read and that both help to explain the history of this field and also represent seminal papers that still hold true. However, a large number of the articles are representative of many comparable articles. This selection is intended to get the reader started on a foray into the area. It should be noted that most research articles in this field are quantitatively quite complicated. A reading knowledge of path analysis and structural equation modeling would be beneficial. However, even readers without this knowledge can glean sufficient information from these articles by skimming the results sections and concentrating instead on the literature reviews and discussion summaries.

There are several texts that provide an interesting overview of the field of behavioral genetics at large and some recent books that focus on topics relevant for specific subgroups. Kim 2009 is intended to be fairly general and cover a broad array of behaviors. Plomin 2018 , written for a lay audience, is accessible and presents important food for thought about the future of DNA in our everyday lives. DiLalla 2004 and McCartney and Weinberg 2009 are edited texts resulting from Festschrifts that present chapters broadly reviewing the behavioral genetics realm with a focus on work by Irving I. Gottesman (in DiLalla) and Sandra Wood Scarr (in McCartney and Weinberg), both of whom were seminal behaviors genetics researchers. Dick 2021 summarizes behavior genetics research as it relates specifically to parenting in a book written for a lay audience, and Harden 2021 provides a general discussion of how genetics research can benefit society in terms of justice and equality. Two books by Nancy Segal ( Segal 2005 and Segal 2017 ) provide information about twins specifically. Although not recent, these are included because they provide an excellent background into research on twins.

Dick, Danielle M. 2021. The child code . New York: Avery.

This book, written for parents, discusses parenting from the perspective of each child’s unique genetic make-up, or “code.” It clarifies the importance of each individual child’s contribution to the parent-child relationship and suggests ways to parent accordingly.

DiLalla, Lisabeth Fisher, ed. 2004. Behavior genetics principles: Perspectives in development, personality, and psychopathology . Washington, DC: American Psychological Association.

Resulted from a festschrift for Professor Irving I. Gottesman, a pioneer in behavioral genetics research. This book presents research spawned by Gottesman’s work and ideas, with a specific focus on development, personality, and psychopathology. Geared to researchers and students in the field.

Harden, Kathryn Paige. 2021. The genetic lottery: Why DNA matters for social equality . Princeton, NJ, and Oxford: Princeton Univ. Press.

DOI: 10.2307/j.ctv1htpf72

This book should be read with caution, but importantly attempts to clarify to introductory readers that genetic make-up accounts for socioeconomic inequality while simultaneously trying to discredit eugenics as a pseudoscience. Harden states that awareness of human genetic variability across individuals actually should lead to a more fair, equitable society.

Kim, Yong-Kyu. 2009. Handbook of behavior genetics . New York: Springer.

DOI: 10.1007/978-0-387-76727-7

Intended for students of genetics, psychology, and psychiatry. Chapters describe research in various areas of behavior including psychopathology, intelligence, and personality. Behavioral genetic relevance is discussed, as are cutting-edge methodologies and the directions these fields will take in the future.

McCartney, Kathleen, and Richard A. Weinberg. 2009. Experience and development: A Festschrift in honor of Sandra Wood Scarr . New York: Psychology Press.

Resulted from a Festschrift for Dr. Sandra Wood Scarr, an eminent developmental behavior geneticist. Chapters written by her students and colleagues cover topics based on Scarr’s research, such as heritability of cognitive ability in impoverished children, sibling relationships, and adoption. Intended for researchers of psychology, behavior genetics, and childcare.

Plomin, Robert. 2018. Blueprint: How DNA makes us who we are . Cambridge, MA: Massachusetts Institute of Technology Press.

Written for a lay audience, Plomin uses accessible terminology to explain complicated concepts and to tease apart the roles of genes and environment as they affect behaviors. Mostly based on evidence from his own research and large, genome-wide research projects. Bottom line: children’s development is primarily a function of their genetic make-up.

Segal, Nancy L. 2005. Indivisible by two: Lives of extraordinary twins . Cambridge, MA: Harvard Univ. Press.

An arresting book by Nancy Segal. She describes several sets of twins, triplets, and quadruplets to demonstrate how both genes and environment play critical roles in behavioral development.

Segal, Nancy L. 2017. Twin mythconceptions: False beliefs, fables, and facts about twins . London: Academic Press.

In this fun book, intended for professionals, parents, and others interested in twins, Segal identifies over seventy common misconceptions about twins and twinning. She explains each one using known scientific findings, with appendixes explaining some topics in more detail.

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Course: MCAT   >   Unit 11

• Behavior and genetics questions

Genes, environment, and behavior

• Temperament, heredity, and genes
• Twin studies and adoption studies
• Heritability
• Regulatory genes
• Gene environment interaction
• Adaptive value of behavioral traits

How do genes influence who you are and what you do?

• increase the size of their fat cells or dictate how they use fat in their body
• release chemicals (like hormones) which control hunger and appetite
• influence behavior as Jennifer and Karen interact with their environment. For example, if Karen begins to gain weight, she may seek out fewer opportunities to exercise because going to the gym makes her feel uncomfortable.

How do your life experiences influence your genes?

Is there a way to tell how much of an influence genes have on a behavior, consider the following:.

• Why do you think heritability estimates cannot be generalized, or applied to different populations? Consider exactly what a heritability estimate measures - the relative influence of genes and the environment. If there was a change in the environment, the heritability estimate would change as well; an estimate from Jennifer’s neighborhood would not be applicable in Karen’s neighborhood. Each estimate is very specific to one group of individuals and their environment, which means that it could not be generalized. However, we can look at large groups of people and develop a range of estimates to tell us more about a particular trait of interest. The range allows for interpersonal and small group differences that are influenced by specific environments, but still gives us important information about the differences in people’s traits.
• The interactions between your genes and your environment are especially important during your early development. For example, exposure to toxins during and immediately after pregnancy can produce lasting effects on a baby’s health - children exposed to pesticides at a young age have a higher risk of developing mental health problems later in life.

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Chapter 12. Personality

12.3 Is Personality More Nature or More Nurture? Behavioural and Molecular Genetics

Learning objectives.

• Explain how genes transmit personality from one generation to the next.
• Outline the methods of behavioural genetics studies and the conclusions that we can draw from them about the determinants of personality.
• Explain how molecular genetics research helps us understand the role of genetics in personality.

One question that is exceedingly important for the study of personality concerns the extent to which it is the result of nature or nurture. If nature is more important, then our personalities will form early in our lives and will be difficult to change later. If nurture is more important, however, then our experiences are likely to be particularly important, and we may be able to flexibly alter our personalities over time. In this section we will see that the personality traits of humans and animals are determined in large part by their genetic makeup, and thus it is no surprise that identical twins Paula Bernstein and Elyse Schein turned out to be very similar even though they had been raised separately. But we will also see that genetics does not determine everything.

In the nucleus of each cell in your body are 23 pairs of chromosomes . One of each pair comes from your father, and the other comes from your mother. The chromosomes are made up of strands of the molecule DNA (deoxyribonucleic acid), and the DNA is grouped into segments known as genes . A gene is the basic biological unit that transmits characteristics from one generation to the next . Human cells have about 25,000 genes.

The genes of different members of the same species are almost identical. The DNA in your genes, for instance, is about 99.9% the same as the DNA in my genes and in the DNA of every other human being. These common genetic structures lead members of the same species to be born with a variety of behaviours that come naturally to them and that define the characteristics of the species. These abilities and characteristics are known as instincts  —  complex inborn patterns of behaviours that help ensure survival and reproduction (Tinbergen, 1951). Different animals have different instincts. Birds naturally build nests, dogs are naturally loyal to their human caretakers, and humans instinctively learn to walk and to speak and understand language.

But the strength of different traits and behaviours also varies within species. Rabbits are naturally fearful, but some are more fearful than others; some dogs are more loyal than others to their caretakers; and some humans learn to speak and write better than others do. These differences are determined in part by the small amount (in humans, the 0.1%) of the differences in genes among the members of the species.

Personality is not determined by any single gene, but rather by the actions of many genes working together. There is no “IQ gene” that determines intelligence and there is no “good marriage-partner gene” that makes a person a particularly good marriage bet. Furthermore, even working together, genes are not so powerful that they can control or create our personality. Some genes tend to increase a given characteristic and others work to decrease that same characteristic — the complex relationship among the various genes, as well as a variety of random factors, produces the final outcome. Furthermore, genetic factors always work with environmental factors to create personality. Having a given pattern of genes doesn’t necessarily mean that a particular trait will develop, because some traits might occur only in some environments. For example, a person may have a genetic variant that is known to increase his or her risk for developing emphysema from smoking. But if that person never smokes, then emphysema most likely will not develop.

Studying Personality Using Behavioural Genetics

Perhaps the most direct way to study the role of genetics in personality is to selectively breed animals for the trait of interest. In this approach the scientist chooses the animals that most strongly express the personality characteristics of interest and breeds these animals with each other. If the selective breeding creates offspring with even stronger traits, then we can assume that the trait has genetic origins. In this manner, scientists have studied the role of genetics in how worms respond to stimuli, how fish develop courtship rituals, how rats differ in play, and how pigs differ in their responses to stress.

Although selective breeding studies can be informative, they are clearly not useful for studying humans. For this psychologists rely on behavioural genetics  —  a variety of research techniques that scientists use to learn about the genetic and environmental influences on human behaviour by comparing the traits of biologically and nonbiologically related family members (Baker, 2004). Behavioural genetics is based on the results of family studies , twin studies , and adoptive studies .

A family study   starts with one person who has a trait of interest — for instance, a developmental disorder such as autism — and examines the individual’s family tree to determine the extent to which other members of the family also have the trait . The presence of the trait in first-degree relatives (parents, siblings, and children) is compared with the prevalence of the trait in second-degree relatives (aunts, uncles, grandchildren, grandparents, and nephews or nieces) and in more distant family members. The scientists then analyze the patterns of the trait in the family members to see the extent to which it is shared by closer and more distant relatives.

Although family studies can reveal whether a trait runs in a family, it cannot explain why. In a twin study , researchers study the personality characteristics of twins . Twin studies rely on the fact that identical (or monozygotic) twins have essentially the same set of genes, while fraternal (or dizygotic) twins have, on average, a half-identical set. The idea is that if the twins are raised in the same household, then the twins will be influenced by their environments to an equal degree, and this influence will be pretty much equal for identical and fraternal twins. In other words, if environmental factors are the same, then the only factor that can make identical twins more similar than fraternal twins is their greater genetic similarity.

In a twin study, the data from many pairs of twins are collected and the rates of similarity for identical and fraternal pairs are compared. A correlation coefficient is calculated that assesses the extent to which the trait for one twin is associated with the trait in the other twin. Twin studies divide the influence of nature and nurture into three parts:

• Heritability (i.e., genetic influence) is indicated when the correlation coefficient for identical twins exceeds that for fraternal twins, indicating that shared DNA is an important determinant of personality.
• Shared environment determinants are indicated when the correlation coefficients for identical and fraternal twins are greater than zero and also very similar. These correlations indicate that both twins are having experiences in the family that make them alike.
• Nonshared environment is indicated when identical twins do not have similar traits. These influences refer to experiences that are not accounted for either by heritability or by shared environmental factors. Nonshared environmental factors are the experiences that make individuals within the same family less alike. If a parent treats one child more affectionately than another, and as a consequence this child ends up with higher self-esteem, the parenting in this case is a nonshared environmental factor.

In the typical twin study, all three sources of influence are operating simultaneously, and it is possible to determine the relative importance of each type.

An adoption study   compares biologically related people, including twins, who have been reared either separately or apart . Evidence for genetic influence on a trait is found when children who have been adopted show traits that are more similar to those of their biological parents than to those of their adoptive parents. Evidence for environmental influence is found when the adoptee is more like his or her adoptive parents than the biological parents.

The results of family, twin, and adoption studies are combined to get a better idea of the influence of genetics and environment on traits of interest. Table 12.6, “Data from Twin and Adoption Studies on the Heritability of Various Characteristics,” presents data on the correlations and heritability estimates for a variety of traits based on the results of behavioural genetics studies (Bouchard, Lykken, McGue, Segal, & Tellegen, 1990).

If you look in the second column of Table 12.6 , “Data from Twin and Adoption Studies on the Heritability of Various Characteristics,” you will see the observed correlations for the traits between identical twins who have been raised together in the same house by the same parents. This column represents the pure effects of genetics, in the sense that environmental differences have been controlled to be a small as possible. You can see that these correlations are higher for some traits than for others. Fingerprint patterns are very highly determined by our genetics ( r = .96), whereas the Big Five trait dimensions have a heritability of 40% to 50%.

You can also see from the table that, overall, there is more influence of nature than of parents. Identical twins, even when they are raised in separate households by different parents (column 4), turn out to be quite similar in personality, and are more similar than fraternal twins who are raised in separate households (column 5). These results show that genetics has a strong influence on personality, and helps explain why Elyse and Paula were so similar when they finally met.

Despite the overall role of genetics, you can see in Table 12.6, “Data from Twin and Adoption Studies on the Heritability of Various Characteristics,” that the correlations between identical twins (column 2) and heritability estimates for most traits (column 6) are substantially less than 1.00, showing that the environment also plays an important role in personality (Turkheimer & Waldron, 2000). For instance, for sexual orientation the estimates of heritability vary from 18% to 39% of the total across studies, suggesting that 61% to 82% of the total influence is due to environment.

You might at first think that parents would have a strong influence on the personalities of their children, but this would be incorrect. As you can see by looking in column 7 of Table 12.6,” research finds that the influence of shared environment (i.e., the effects of parents or other caretakers) plays little or no role in adult personality (Harris, 2006). Shared environment does influence the personality and behaviour of young children, but this influence decreases rapidly as the child grows older. By the time we reach adulthood, the impact of shared environment on our personalities is weak at best (Roberts & DelVecchio, 2000). What this means is that although parents must provide a nourishing and stimulating environment for children, no matter how hard they try they are not likely to be able to turn their children into geniuses or into professional athletes, nor will they be able to turn them into criminals.

If parents are not providing the environmental influences on the child, then what is? The last column in Table 12.6,” the influence of nonshared environment, represents whatever is “left over” after removing the effects of genetics and parents. You can see that these factors — the largely unknown things that happen to us that make us different from other people — often have the largest influence on personality.

Studying Personality Using Molecular Genetics

In addition to the use of behavioural genetics, our understanding of the role of biology in personality recently has been dramatically increased through the use of molecular genetics , which is the study of which genes are associated with which personality traits (Goldsmith et al., 2003; Strachan & Read, 1999). These advances have occurred as a result of new knowledge about the structure of human DNA made possible through the Human Genome Project and related work that has identified the genes in the human body (Human Genome Project, 2010). Molecular genetics researchers have also developed new techniques that allow them to find the locations of genes within chromosomes and to identify the effects those genes have when activated or deactivated.

One approach that can be used in animals, usually in laboratory mice, is the knockout study (as shown in Figure 12.12, “Laboratory Mice”). In this approach the researchers use specialized techniques to remove or modify the influence of a gene in a line of knockout mice (Crusio, Goldowitz, Holmes, & Wolfer, 2009). The researchers harvest embryonic stem cells from mouse embryos and then modify the DNA of the cells. The DNA is created so that the action of certain genes will be eliminated or knocked out . The cells are then injected into the embryos of other mice that are implanted into the uteruses of living female mice. When these animals are born, they are studied to see whether their behaviour differs from a control group of normal animals. Research has found that removing or changing genes in mice can affect their anxiety, aggression, learning, and socialization patterns.

In humans, a molecular genetics study normally begins with the collection of a DNA sample from the participants in the study, usually by taking some cells from the inner surface of the cheek. In the lab, the DNA is extracted from the sampled cells and is combined with a solution containing a marker for the particular genes of interest as well as a fluorescent dye. If the gene is present in the DNA of the individual, then the solution will bind to that gene and activate the dye. The more the gene is expressed, the stronger the reaction.

In one common approach, DNA is collected from people who have a particular personality characteristic and also from people who do not. The DNA of the two groups is compared to see which genes differ between them. These studies are now able to compare thousands of genes at the same time. Research using molecular genetics has found genes associated with a variety of personality traits including novelty-seeking (Ekelund, Lichtermann, Järvelin, & Peltonen, 1999), attention-deficit/hyperactivity disorder (Waldman & Gizer, 2006), and smoking behaviour (Thorgeirsson et al., 2008).

Reviewing the Literature: Is Our Genetics Our Destiny?

Over the past two decades scientists have made substantial progress in understanding the important role of genetics in behaviour. Behavioural genetics studies have found that, for most traits, genetics is more important than parental influence. And molecular genetics studies have begun to pinpoint the particular genes that are causing these differences. The results of these studies might lead you to believe that your destiny is determined by your genes, but this would be a mistaken assumption.

For one, the results of all research must be interpreted carefully. Over time we will learn even more about the role of genetics, and our conclusions about its influence will likely change. Current research in the area of behavioural genetics is often criticized for making assumptions about how researchers categorize identical and fraternal twins, about whether twins are in fact treated in the same way by their parents, about whether twins are representative of children more generally, and about many other issues. Although these critiques may not change the overall conclusions, it must be kept in mind that these findings are relatively new and will certainly be updated with time (Plomin, 2000).

Furthermore, it is important to reiterate that although genetics is important, and although we are learning more every day about its role in many personality variables, genetics does not determine everything. In fact, the major influence on personality is nonshared environmental influences, which include all the things that occur to us that make us unique individuals. These differences include variability in brain structure, nutrition, education, upbringing, and even interactions among the genes themselves.

The genetic differences that exist at birth may be either amplified or diminished over time through environmental factors. The brains and bodies of identical twins are not exactly the same, and they become even more different as they grow up. As a result, even genetically identical twins have distinct personalities, resulting in large part from environmental effects.

Because these nonshared environmental differences are nonsystematic and largely accidental or random, it will be difficult to ever determine exactly what will happen to a child as he or she grows up. Although we do inherit our genes, we do not inherit personality in any fixed sense. The effect of our genes on our behaviour is entirely dependent on the context of our life as it unfolds day to day. Based on your genes, no one can say what kind of human being you will turn out to be or what you will do in life.

Key Takeaways

• Genes are the basic biological units that transmit characteristics from one generation to the next.
• Personality is not determined by any single gene, but rather by the actions of many genes working together.
• Behavioural genetics refers to a variety of research techniques that scientists use to learn about the genetic and environmental influences on human behaviour.
• Behavioural genetics is based on the results of family studies, twin studies, and adoptive studies.
• Overall, genetics has more influence than parents do on shaping our personality.
• Molecular genetics is the study of which genes are associated with which personality traits.
• The largely unknown environmental influences, known as the nonshared environmental effects, have the largest impact on personality. Because these differences are nonsystematic and largely accidental or random, we do not inherit our personality in any fixed sense.

Exercises and Critical Thinking

• Think about the twins you know. Do they seem to be very similar to each other, or does it seem that their differences outweigh their similarities?
• Describe the implications of the effects of genetics on personality, overall. What does it mean to say that genetics “determines” or “does not determine” our personality?

Baker, C. (2004). Behavioral genetics: An introduction to how genes and environments interact through development to shape differences in mood, personality, and intelligence. [PDF] Retrieved from http://www.aaas.org/spp/bgenes/Intro.pdf

Bouchard, T. J., Lykken, D. T., McGue, M., Segal, N. L., & Tellegen, A. (1990). Sources of human psychological differences: The Minnesota study of twins reared apart .  Science, 250 (4978), 223–228. Retrieved from http://www.sciencemag.org/cgi/content/abstract/250/4978/223

Crusio, W. E., Goldowitz, D., Holmes, A., & Wolfer, D. (2009). Standards for the publication of mouse mutant studies.  Genes, Brain & Behavior, 8 (1), 1–4.

Ekelund, J., Lichtermann, D., Järvelin, M. R., & Peltonen, L. (1999). Association between novelty seeking and the type 4 dopamine receptor gene in a large Finnish cohort sample.  American Journal of Psychiatry, 156 , 1453–1455.

Goldsmith, H., Gernsbacher, M. A., Crabbe, J., Dawson, G., Gottesman, I. I., Hewitt, J.,…Swanson, J. (2003). Research psychologists’ roles in the genetic revolution.  American Psychologist, 58 (4), 318–319.

Harris, J. R. (2006).  No two alike: Human nature and human individuality . New York, NY: Norton.

Human Genome Project . (2010). Information . Retrieved from http://www.ornl.gov/sci/techresources/Human_Genome/home.shtml

Långström, N., Rahman, Q., Carlström, E., & Lichtenstein, P. (2010). Genetic and environmental effects on same-sex sexual behaviour: A population study of twins in Sweden.  Archives of Sexual Behaviour , 39 (1), 75-80.

Loehlin, J. C. (1992).  Genes and environment in personality development . Thousand Oaks, CA: Sage Publications, Inc.

McGue, M., & Lykken, D. T. (1992). Genetic influence on risk of divorce.  Psychological Science, 3 (6), 368–373.

Plomin, R. (2000). Behavioural genetics in the 21st century.  International Journal of Behavioral Development, 24 (1), 30–34.

Plomin, R., Fulker, D. W., Corley, R., & DeFries, J. C. (1997). Nature, nurture, and cognitive development from 1 to 16 years: A parent-offspring adoption study.  Psychological Science, 8 (6), 442–447.

Roberts, B. W., & DelVecchio, W. F. (2000). The rank-order consistency of personality traits from childhood to old age: A quantitative review of longitudinal studies.  Psychological Bulletin, 126 (1), 3–25.

Strachan, T., & Read, A. P. (1999).  Human molecular genetics  (2nd ed.). Retrieved from http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=hmg&part=A2858

Tellegen, A., Lykken, D. T., Bouchard, T. J., Wilcox, K. J., Segal, N. L., & Rich, S. (1988). Personality similarity in twins reared apart and together.  Journal of Personality and Social Psychology, 54 (6), 1031–1039.

Thorgeirsson, T. E., Geller, F., Sulem, P., Rafnar, T., Wiste, A., Magnusson, K. P.,…Stefansson, K. (2008). A variant associated with nicotine dependence, lung cancer and peripheral arterial disease.  Nature, 452 (7187), 638–641.

Tinbergen, N. (1951).  The study of instinct  (1st ed.). Oxford, England: Clarendon Press.

Turkheimer, E., & Waldron, M. (2000). Nonshared environment: A theoretical, methodological, and quantitative review.  Psychological Bulletin, 126 (1), 78–108.

Waldman, I. D., & Gizer, I. R. (2006). The genetics of attention deficit hyperactivity disorder.  Clinical Psychology Review, 26 (4), 396–432.

Image Attributions

Figure 12.12: “ Laboratory mice ” by Aaron Logan is licensed under CC BY 1.0 license (http://creativecommons.org/licenses/by/1.0/deed.en).

• Sources: Långström, et al, 2010; Loehlin, 1992; McGue & Lykken, 1992; Plomin et al, 1997; Tellegen et al, 1988. ↵

Introduction to Psychology - 1st Canadian Edition Copyright © 2014 by Jennifer Walinga and Charles Stangor is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License , except where otherwise noted.

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Institute of Medicine (US) Committee on Assessing Interactions Among Social, Behavioral, and Genetic Factors in Health; Hernandez LM, Blazer DG, editors. Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate. Washington (DC): National Academies Press (US); 2006.

Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate.

• Hardcopy Version at National Academies Press

11 Conclusion

As discussed throughout this report, human health is determined by the interaction of several factors, including the social environment, genetic inheritance, and personal behaviors. Socioeconomic status, race/ethnicity, social networks/social support, and the psychosocial work environment all have been shown to affect health outcomes ( Chapter 2 ). These social determinants influence health at multiple levels throughout the life course. In addition to the vast array of social determinants that influence health, a person inherits a complete set of genes from each parent that contributes both directly and indirectly to the pathogenesis of disease. Genes have been identified for relatively uncommon, simple Mendelian patterns of disease inheritance, such as Tay-Sachs disease and cystic fibrosis, and recently research has begun to explore genetic susceptibility to disease as the consequence of the joint effects of many genes, each with small-to-moderate effects, often interacting among themselves and with the environment ( Chapter 3 ). Behaviors also have been shown to affect health ( Chapter 4 ). For example, tobacco use, obesity, and physical inactivity are the greatest preventable causes of morbidity and mortality in the United States ( Mokdad et al., 2004 ). Furthermore, complex traits, such as sex/gender and race/ ethnicity, pose both a challenge and an opportunity in our search for a better understanding of environmental, genetic, and behavioral interactions as determinants of health ( Chapter 5 ).

As this report demonstrates, research has documented associations between social factors and health, behaviors and health, and genetics and health. Yet, researchers are only now beginning to study in earnest the potential interactions between genetic and social environmental factors that are likely to be contributing to a large fraction of disease in most populations. Key to the success of research on these interactions is the conduct of such research in a collaborative and transdisciplinary manner, which “implies the conception of research questions that transcend the individual departments or specialized knowledge bases because they are intended to solve … research questions that are, by definition, beyond the purview of the individual disciplines” ( IOM, 2003 ). Furthermore, more comprehensive, predictive models of etiologically heterogeneous disease are needed, and this requires the development and implementation of new modeling strategies and the use of profiling approaches. In order to ensure that findings are applicable beyond a small population, research must be conducted in diverse groups and settings ( Chapter 6 ). Animal models, which are explored in Chapter 7 , have a great deal to offer in understanding the effects of interactions of social, behavioral, and genetic factors on health.

A clear formulation of the concept of interaction, and an understanding of research designs that can be used to test for it, are central to progress in assessing the impact on health of interactions among multiple factors. This report discusses several steps that are needed to advance the science of testing interactions ( Chapter 8 ). These include new, accessible statistical software for implementing tests for interaction on an additive scale and research on developing study designs that are efficient at testing interactions, including variations in interactions over time and development.

Transdisciplinary research on the impact on health of interactions among social, behavioral, and genetic factors places several demands on the research infrastructure, including the need for education and training of researchers, the enhancement and development of appropriate datasets, and the creation of incentives and rewards that will encourage investigators to move beyond the single discipline approach to research. Approaches that the National Institutes of Health can use to address these barriers include providing individual and senior fellowships, transdisciplinary institutional grants, short courses, and datasets that can be enhanced to provide the necessary information. The development of new datasets for topics that have high potential for showing interactions also would be valuable. Other incentives that foster the transdisciplinary research discussed in this report address hiring, promotion and tenure policies, peer review, and the allocation of credit for collaborative research ( Chapter 9 ).

Finally, research that elucidates how social, behavioral, and genetic factors interact to influence health raises important ethical and legal issues, including those involving how individuals and groups understand and use complex scientific findings, as well as the potential impact such findings might have on policy development ( Chapter 10 ).

Furthermore, studying interactions among variations in social, behavioral, and genetic factors requires the collection of information that could entail significant risk to research participants if it is inappropriately accessed. This report offers recommendations for communicating with policymakers and the public, for expanding the research focus to include research on how best to encourage people to engage in health-promoting behaviors, for the establishment of data-sharing policies that ensure privacy, and for improving the informed consent process.

The intent of this report is to encourage and facilitate the growth of research on the impact of interactions among social, behavioral, and genetic factors on health that will further our understanding of disease risk and aid in the development of effective interventions to improve the health of individuals and populations. This report has resulted from collaboration that has occurred between scientists from the social and the biological worlds, and it provides a template for how their theories and methods can be integrated to advance knowledge. It is timely and important because it sets out an agenda for research that is needed to advance the science of gene-environment interactions in explaining individual and population health and health disparities.

• IOM (Institute of Medicine). Who Will Keep the Public Healthy? Educating Health Professionals for the 21st Century. Washington, DC: The National Academies Press; 2003. [ PubMed : 25057636 ]
• Mokdad AH, Marks JS, Stroup DF, Gerberding JL. Actual causes of death in the United States, 2000. Journal of the American Medical Association. 2004; 291 (10):1238–1245. [ PubMed : 15010446 ]
• Cite this Page Institute of Medicine (US) Committee on Assessing Interactions Among Social, Behavioral, and Genetic Factors in Health; Hernandez LM, Blazer DG, editors. Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate. Washington (DC): National Academies Press (US); 2006. 11, Conclusion.
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The Nature of Genetic Influences on Behavior: Lessons From “Simpler” Organisms

• Kenneth S. Kendler M.D.
• Ralph J. Greenspan Ph.D.

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Substantial advances have been made in recent years in the understanding of the genetic basis of behavior in “simpler” organisms, especially the mouse and the fruit fly Drosophila . The authors examine the degree of similarity between the genetic underpinnings of psychiatric illness and genetic influences on behavior in such simpler organisms. Six topics are reviewed: 1) the extent of natural genetic variation, 2) the multigenic nature of natural variation, 3) the impact of individual genes on multiple traits, 4) gene-environment interactions, 5) genetic effects on the environment, and 6) gene-by-sex interactions. The results suggest that the pattern of results emerging in psychiatric genetics is generally consistent with the findings of behavioral genetics in simpler organisms. Across the animal kingdom, individual differences in behavior are nearly always influenced by genetic factors which, in turn, result from a substantial number of individual genes, each with a small effect. Nearly all genes that affect behavior influence multiple phenotypes. The impact of individual genes can be substantially modified by other genes and/or by environmental experiences. Many animals alter their environment, and the nature of that alteration is influenced by genes. For some behaviors, the pathway from genes to behavior differs meaningfully in males and females. With respect to the broad patterns of genetic influences on behavior, Homo sapiens appears to be typical of other animal species.

In his work on “The Descent of Man,” Darwin (1) strove to demonstrate the degree of continuity that existed between humans and other animals from which he sought to argue that “man is the modified descendent of some preexisting form.” Of the seven chapters of his book, three were devoted to the similarities of the psychological and behavioral traits of humans and “simpler” organisms.

This essay also seeks to examine the degree of continuity between humans and nonhuman animals with respect to psychological or behavioral traits. Our focus, however, differs from that of Darwin. Building on recent advances in both psychiatric and animal behavior genetics, our aim is to examine the degree of similarity in the genetic underpinnings of psychiatric illness and genetic influences on behavior in other, simpler organisms.

In short, we attempt to answer the following question: How similar, in broad outline, are the findings emerging in psychiatric genetics and the genetics of behavior in simpler organisms?

Discontinuities certainly exist between the human mental and behavioral dysfunctions that constitute psychiatric illness and the well-studied behaviors of simpler organisms. Nonetheless, as suggested by Darwin, there is potentially sufficient cross-species commonality of mechanisms that a comparison of findings will be useful. Our review will focus on, but is not limited to, behavior genetic studies of the mouse and the fruit fly Drosophila , since these two species have been the most intensively studied.

Traditionally, two distinct approaches have been taken with regard to behavior genetics in simpler organisms: the measurement and manipulation of naturally occurring variation in laboratory or wild strains, and the isolation and study of newly induced mutations. The former assesses the extent of the typically mild mutational variation that survives in nature and exerts effects on behavior. Such studies are analogous to our investigations of psychiatric disorders in human populations. The latter—which has no parallel in human research—identifies genes and mechanisms subserving particular behaviors by producing more drastic genetic lesions than would typically survive the rigors of selection in natural populations. Both methods can clarify how genetic variation contributes to behavior. However, a synthesis between the two, made possible by recent advances in molecular biology, holds the most promise for a deeper understanding of the relationship between genes and behavior.

For this essay, we identified six areas of research in psychiatric genetics where the broad pattern of results is beginning to be clear. After outlining briefly these findings, we then review what has been learned about this question in genetic studies of behavior in simpler organisms. Each of these “mini-reviews” is meant to be illustrative and not exhaustive (we do not, for example, attempt to review the genetics of mental retardation or dementia). We then examine two important areas where the findings in psychiatric genetics are too scant to permit any broad conclusions. In each of these, clear findings are emerging in behavioral genetic studies of simpler organisms that might foreshadow results that will be found in psychiatric disorders.

Extent of Natural Genetic Variation

Psychiatric disorders in humans.

Genetic risk factors have been found for every psychiatric condition that has been seriously studied (2 , 3) . For most disorders, evidence for genetic risk factors has been replicated using the same research design (most commonly twin studies) and for some disorders replicated across twin and adoption designs. Significant genetic influences have also been found for more “normative” human traits such as personality (4) that are also important risk factors for psychiatric illness (5) . Heritability—the proportion of individual differences in liability to illness that results from genetic differences between individuals in a particular population—appears to vary meaningfully between psychiatric disorders, with relatively consistent results across studies: from 20% to 30% for most anxiety disorders (6) , 30%–40% for major depression (7) , 50%–60% for alcoholism (8 , 9) , and 80% or higher for schizophrenia, bipolar illness, and autism (10 – 12) .

Behavior in Simpler Organisms

Considerable genetic variation influencing behavior appears to exist for nearly all traits, in all populations, in all species. Heritability can be estimated in several different ways in animal populations. Like twin or adoption studies in humans, these studies do not provide information about the action of specific genes at a biological level but rather estimate statistically the aggregate effects of all genes distributed across the genome within the specific population under study.

Mousseau and Roff reviewed heritability estimates for a variety of traits derived largely from parent-offspring correlations, first from Drosophila (13) and then from 75 other invertebrate and vertebrate species (14) . Of these traits, 38 from Drosophila and 105 from the other organisms were behavioral. Considerable variation in the heritability of individual traits was found with the 25th, 50th, and 75th percentiles estimated to be 12%, 25%, and 43%, respectively. In a more recent review of 57 studies of animal behavior, Meffert et al. report the mean heritability to be equal to 38% (14a) .

Another approach to assessing genetic variation in simpler organisms draws on the ancient strategy of selective breeding. Artificial selection experiments have been conducted by farmers and animal breeders for millennia, and virtually any trait seems to respond. Selection studies depend on the preexistence of genetic variation in the population undergoing selection, thereby providing an assay for the level of existing natural variation.

How extensive is natural genetic variation so assessed? The question has been concisely answered by the population geneticist Lewontin (15) : “There appears to be no character—morphogenetic, behavioral, physiological, or cytological—that cannot be selected in Drosophila .” He cited the fruit fly simply because more selection experiments had been conducted on it than any other animal, but the conclusion applies equally well to the mouse and other species. Traits responding to selection include phototaxis (movement toward light), geotaxis (movement in response to gravity), circadian rhythms, courtship behavior (a stereotypical, innate behavior in the fruit fly), and learning ability (reviewed by Greenspan [16] ). Selection studies in rodents have revealed intrinsic genetic variation for an equally wide range of behaviors, including maze learning (17) , aggression (18) , ethanol preference (19) and withdrawal (20) , anxiety (21) , and response to stress (22) .

In summary, as with psychiatric disorders, individual differences in virtually all behavioral traits examined in simpler organisms are influenced by genetic factors. Heritability estimates both for psychiatric disorders in humans and behaviors in lower organisms vary widely, although most traits appear to fall in the range of 10%–50% for the population tested.

The Multigenic Nature of Natural Variation

Although twin and adoption studies provide strong evidence for the existence of aggregate genetic effects for psychiatric disorders, several lines of evidence suggest that these effects are the result of multiple genes, each of small to modest effect. First, individual genes that strongly influence a phenotype produce a characteristic pattern of illness in pedigrees (e.g., autosomal dominant, sex-linked recessive, etc.). Despite efforts by many researchers to find pedigrees in which psychiatric disorders segregate like classic or “Mendelian” traits, these efforts have to date been largely unsuccessful. Second, linkage studies can “sweep” the human genome looking for genomic regions that impact strongly on disease risk. In such studies, genes of large effect size have a typical “signature,” which has not been found to date in any of the psychiatric disorders studied by linkage including schizophrenia, bipolar illness, panic disorder, or eating disorders. Third, a recent careful meta-analysis of 20 genome scans for schizophrenia suggests that at least 10 genomic regions are likely to contain susceptibility genes (23) . In addition, current evidence of bipolar disorder, the next most studied psychiatric disorder by linkage scans, also suggests multiple loci (24 , 24a) .

Much has been learned about the number and effect size of the genes that influence behavior in simpler organisms. Most of these advances come from the application of linkage methods to the study of naturally occurring genetic variation. In linkage analysis of psychiatric disorders, the focus is typically on diseases. However, in animal linkage studies a quantitative behavior (such as motor activity or emotionality) is more commonly used. Genes that influence such traits are called “quantitative trait loci” or QTLs. In QTL analysis, a phenotypic difference between two strains is mapped against an extensive set of genetic markers that also differ between them, and chromosomal regions mediating significant effects are mapped. The power of QTL analysis in simpler organisms often substantially exceeds that available in humans because of the possibility of designing specific crosses to provide maximal linkage information.

Flint has thoroughly reviewed the literature on QTL studies of behavior in rodents, with the most commonly studied traits being circadian rhythm, drug preference or response, emotionality, motor activity, and learning (21) . He concludes that such behaviors are typically influenced by many genes of small effect. While an accurate estimation of the number of QTLs involved is problematic (and available estimates are likely to be too low), current evidence suggests that most behavioral traits in rodents are influenced by six to 24 QTLs.

In QTL studies, effect size is typically measured as the proportion of variance in the trait that results from variance at the particular QTL. (The available effect sizes are probably overestimates, since large effect genes are the ones to be first detected.) Flint concludes that—while there are exceptions—most behavioral traits are influenced by genes that account for 10% or less of the total phenotypic variance. More typically, detected genes have effect sizes of less than 5%.

In a recent, thorough QTL analysis of five anxiety-related measures in the mouse, Henderson et al. (25) found a total of 17 QTLs across all the traits and typically four to six per individual measure. While over half of the 17 loci discovered accounted for less than 1% of phenotypic variance, at least one QTL accounting for 5% of total variation was found for each of the five measures. Using a different technical approach (chromosomal substitution strains), Singer et al. (26) confirmed the presence of multiple loci influencing models of anxiety in mice. In a recent genome-wide association study in genetically heterogeneous mice, Valdar et al. (26a) examined seven behavioral phenotypes divisible into 21 more specific measures. Using a plausible statistical model, they detected a mean of nine QTLs per measure. On average, these QTLs individually accounted for 2.1% of the variation in these behaviors.

Fewer QTL studies of behavioral traits have been conducted in other organisms (27) . Two recent examples explored variation in a key feature of the courtship song of Drosophila— the mean interpulse interval—and reported results similar to those found for behaviors in the rodent, i.e., multiple QTLs each accounting for 3%–10% of the phenotypic variance (28 , 29) .

A different approach toward identifying genes involved in behavioral traits in simpler organisms has come with the advent of DNA microarray technology. With these methods, it is possible to directly examine differences in expressed levels of mRNA between strains selected for behavioral differences. This approach does not directly measure the number of allelic differences giving rise to the behavioral difference. Instead, it reveals the set of genes whose expression is changed as a result of those allelic differences. These two sets of allelic differences are surely overlapping, but not likely to be identical. This method was, for example, applied to Drosophila strains selected for differences in geotaxis and found approximately 250 genes whose expression differed in the two selected lines (30) .

The number of individual genes influencing a behavioral trait can also be estimated from surveying experimental studies of individual genes. Such studies are carried out with induced mutations (e.g., “knockouts”) or genetically engineered strains (transgenics) in which expression of the gene is altered. While not designed as a direct measure of the number of loci involved, these studies can provide a different sort of sampling than that obtained from more directed gene searches. Furthermore, such a list, if complete, will be considerably larger than that obtained from QTL studies, since many of the genes so identified would not have trait-relevant variations in natural populations. Although far from complete, recent surveys have enumerated 33 genes identified since 1995 that influence aggressive behavior in the male mouse (31) and 14 loci from mutations that altered odor-guided behavior in Drosophila (32) .

Combining these two approaches may provide the most complete picture of the multigenic foundations for behavior. In a comprehensive study of genes affecting long-term memory in Drosophila , Dubnau et al. (33) combined a large-scale mutation screen with an analysis of gene expression patterns. The mutant screen identified 60 new mutants that are selectively defective in long-term memory, and in parallel, the DNA microarray analysis identified 42 genes expressed in the brains of flies under conditions that produce long-term memory. Both sets of genes run the gamut of biological functions—transcription, translation, signal transduction, cytoskeleton, and metabolism.

How far down the phylogenetic scale of complexity does the multigenic influence over behavior extend? In the nematode C. elegans— which contains only 302 neurons—mutations in over 100 different genes impair locomotion while mutations in at least 18 genes are involved in the response to light touch (34) . Many genes appear to be able to influence behaviors in even the simplest organisms.

In summary, three distinct methods—QTL linkage analysis, examination of knockout and transgenic animals, and comparison of expression arrays in selected lines—all suggest that in simpler organisms most behavioral traits are influenced by a relatively large number of genes. Variants in these genes that exist in natural populations tend to have modest effects on the phenotype.

The Impact of Individual Genes on Multiple Traits

Psychiatric genetics in humans.

In twin and adoption studies, genetic risk factors are often not specific for individual psychiatric or drug abuse conditions but rather influence liability for a range of disorders. One recent large-scale twin study of seven psychiatric and substance use disorders found one common genetic risk factor that increased risk for drug abuse, alcohol dependence, antisocial personality disorder, and conduct disorder and a second common genetic factor influencing liability to major depression, generalized anxiety disorder, and phobia (35) . Other twin studies have also found evidence for genetic factors that have an impact on risk for multiple disorders (e.g., references 36 γ8) . This relationship is often quantified by a statistic called the “genetic correlation,” which reflects the degree of overlap of the genetic risk factors for two traits or disorders.

Using the methods of linkage and association, evidence has also accumulated for genomic regions or individual genes that convey risk to more than one disorder. A number of overlapping positive regions in linkage genome scans for bipolar illness and schizophrenia have led some to argue that this reflects shared genes between these two disorders (39) . A pair of overlapping genes on chromosome 13q (termed G30 and G72) may be associated with risk for both schizophrenia and bipolar illness (40) . Claims have been made that several functional candidate genes (e.g., serotonin transporter, dopamine transporter, D 2 receptor) are associated with a wide range of psychiatric disorders and/or psychiatrically relevant traits (41 , 42) .

Thirty years of analyzing genes affecting behavior in mice, fruit flies, and nematodes have consistently supported the contention that genes influencing behavior are pleiotropic—that is, they affect more than one trait (43 , 44) . In studies most closely analogous to human investigations, genetic correlations can be calculated between two traits when both are studied in animals that are genetically related to one another—such as parents and offspring or siblings. Reviewing such studies, Roff (45) found reports on 166 genetic correlations between behaviors from six different animal species. The mean and median absolute value of these genetic correlations were +0.59 and +0.56, respectively, indicating that most of the examined pairs of behaviors were substantially influenced by common sets of genes.

A second approach to studying pleiotropy is through selection studies. Over and over again, studies have found that, in selecting for one trait, changes are also seen in other traits. While some of these results will not always be due to pleiotropy (selection can carry along linked variants at other loci that affect the different phenotypes), when suitably analyzed, such correlated traits are often found to arise from pleiotropic effects. For example, flies selected for geotaxis preference also displayed increased behavioral stereotypy (46) , altered egg-laying behavior (47) , and altered mating preference (48) . In the many selection experiments performed on courtship and mating behavior in Drosophila , correlated responses have also been found for open field behavior (analogous to the test for emotionality in rodents) (49 , 50) , general locomotor activity (51) , and increased sensitivity to disturbance (49) . An example with more cognitive phenotypes comes from experimental selection for an increase in sensitization (“central excitatory state”) in the blowfly Phormia regina . These flies showed correlated responses in both associative conditioning (52) and in food search behavior (53) .

In summary, evidence from breeding studies, selection experiments, and single gene mutants all suggest that genes that alter behavior in simpler organisms frequently influence a variety of often quite disparate behaviors.

Gene-Environment Interactions

Commonsense etiologic models in psychiatry assume that genetic and environmental risk factors add together to produce disease liability. However, classical genetics and biomedicine provide many examples where genetic effects are modified by environmental exposure, thereby producing “gene-environment interaction.” Twin and adoption studies have produced evidence for such interactions for major depression with exposure to stressful life events (63 , 64) , and schizophrenia, conduct disorder, and aggression with exposure to a dysfunctional rearing environment (65 , 66) . Genotype-environment interactions have also been shown in twin studies for a range of psychiatrically relevant traits including aggression, disinhibition, and smoking (3) . In many of these studies, heritability of traits increases in more permissive environments. Caspi and colleagues have found evidence for interactions between environmental factors and polymorphisms in the association of monamine oxidase with risk for antisocial behavior (67) and the association of serotonin transporter with risk for depression (68) .

Clear examples of genotype-environment interaction have emerged in studies of the genetics of behavior in simpler organisms. In contrast to the foregoing examples, many of these have come from work in behavioral ecology on various species studied initially in the field and then brought into the laboratory.

For example, a range of hybrid strains of the paradise fish Macropodus opercularis were exposed to four environments that differed in their level of novelty and threat, which provided an ethologically valid test of “anxiety.” Significant gene-by-environment interactions were observed, with the ordering of the strains (from most to least “anxious”) varying widely across the different environments (69) .

In a similar test in mice, Wahlsten et al. (70) systematically examined eight different strains on five behavioral tests in three laboratories. Of these tests, three produced robust evidence for genotype-environment interaction—meaning that the genetic differences between strains varied as a function of the laboratory in which the tests were performed. In the detailed study of genetically heterogeneous mice noted above, Valdar et al. (70a) examined interactions on the behaviors examined between background genetic liability and 10 environmental covariates. Six percent of the interactions tested (10 in total) met rigorous criteria for statistical significance.

Two sets of rodent studies of genotype-environment interaction have particularly close analogies with human studies (63 , 66) . Investigations with both Y-chromosomal variants and the oxytocin gene show that their phenotypic effect on aggressive behavior in mice was substantially modified by the maternal environment (31) . The effects of the social stress of crowding and frequent cage reassignment on both aggression and hypertension varied dramatically between different rat strains (71) .

Henderson (72) studied the heritability of a complex motor food-seeking task for mice raised in standard or enriched laboratory cages. Heritability was much higher in the enriched (40%) than standard conditions (10%), perhaps because the enriched environment was more “permissive,” i.e., permitting mice with high innate skills to practice the needed complex motor behaviors.

As has been seen in a more limited range of conditions in human studies of psychiatric disorders, the examination of behavior in simpler organisms suggests that genetic effects can frequently be modified by environmental exposure.

Genetic Effects on the Environment

In the traditional view of gene action, genetic expression takes place entirely in a physiological “internal milieu,” or “inside the skin.” The environment, by contrast, exists outside the skin with the causal relationship between organism and environment flowing only from environment to organism. When considering behavior, however, a revised view of gene action is indicated. Through an influence on behavior, genes can also have an impact on the external milieu. In humans, this effect is seen in the social environment from which emerge a number of risk factors for psychiatric and substance use disorders. Studies in twin populations have now suggested that genetic factors, through “outside the skin” pathways, influence exposure to a range of environmental risk factors, including stressful life events (73 – 75) , low levels of social support and marital quality (76 , 77) , both the elicitation and provision of poor parenting (78 – 80) , and deviant peer groups in adolescence (81) . For psychiatric and substance use disorders, one pathway from gene to illness involves self-selection into high-risk environments that then feed back to increase risk of illness.

In what is called “niche construction,” animals modify their physical environment through building burrows, webs, and dams and constructing nursery environments for their offspring (82) . While there are well demonstrated strain and species differences in such behaviors, few have been analyzed genetically. In addition to the physical environment, in social animals, an organism’s genes can, through behavior, also have an impact on key aspects of the social environment such as parent-offspring, mate and adult-peer relations.

Lynch (83) performed a selection study for nest construction in female mice and achieved nearly a 10-fold divergence in behavior after 15 generations, with a realized heritability of 28%. Maestripieri et al. (84) found that infant abuse “ran in families” in pigtail macaques but could not discriminate genetic from familial-environmental transmission. In rodents, genetic effects are seen with both the provision and elicitation of parental care. Hurnik et al. (85) performed a selection experiment for the speed of maternal retrieval behavior in two inbred mouse strains. Over only five generations, substantial divergence was seen in the groups selected for slow and fast retrieval, respectively. Eisen et al. (86) conducted a selection experiment for 12-day litter weight and concluded that 11% of the variance in this trait was due to genes in the mother which, via quality of care and feeding, influenced weight gain in her offspring. Roubertoux et al. (87) studied genetic influences on vocalizations in newborn mice, a primary method by which newborns communicate distress to their mother. Substantial differences in a range of vocalizations were found among seven inbred strains. Single gene effects have also been seen on maternal behavior. For example, female mice homozygous or heterozygous for knockout of their prolactin receptor exhibit relatively specific impairment in maternal behavior (88) .

The effect of individual genes on affiliative behavior has been studied in two species of voles. The prairie vole Microtus ochrogaster is monogamous, biparental, and highly social. By contrast, the montane vole Microtus montanus is promiscuous, maternal, and minimally social (89) . The hormones oxytocin and vasopressin exert complementary effects on these behaviors in the prairie vole, as they appear to do in rats and mice. Moreover, the anatomical distribution of oxytocin and vasopressin receptors in the brain differs markedly between the two vole species (90) .

Vasopressin administration stimulates affiliative behavior in prairie voles but neither in montane voles nor in mice. When a prairie vole vasopressin receptor gene (V 1a ) was transferred into mice, thereby creating an anatomical distribution similar to that of the prairie vole, the mice began to exhibit affiliative behavior in response to vasopressin. This result argues that changing the pattern of V 1a distribution is sufficient to alter this social behavior. This interpretation is further supported by the fact that the V 1a receptor genes are virtually identical between the two vole species that differ in affiliative behavior, except for the presence in prairie voles of a small segment in the region of the gene that is likely to regulate its expression. The presence of this DNA segment correlates well with behavioral and anatomical features of two other species, the pine vole Microtus pinetorum , which is like the prairie vole behaviorally as well as in its anatomical and molecular characteristics of V 1a , and the meadow vole Mictotus pennsylvanicus , which is like the montane vole in all of these respects. Thus, it appears that subtle changes in the expression pattern of the vasopressin receptor V 1a may account for these substantial differences in social behavior in these rodent species.

This interesting case is an exception to our earlier assertion that natural genetic variants tend to have modest effects on a phenotype and tend to act in concert with many other genes. The large preponderance of studied examples is consistent with our earlier statement but, as in all things biological, there are exceptions. Two other examples of large single gene effects on complex behavior are the neuropeptide-Y-receptor-like gene in the nematode C. elegans and the cGMP-dependent protein kinase gene in Drosophila , both of which affect foraging behavior (54 , 91) .

Aggression is another important social behavior that has been shown, in simpler organisms, to be influenced by genetic factors. Enhanced aggression has been achieved through selection experiments in Drosophila (92) and mice (18) . Finally, variation in a gene influencing eye color in Drosophila influences preference of flies for different microenvironments differing in ambient light conditions (93) . This study shows how genetic variation can have an impact on the active selection of environments.

In summary, given prior strong evidence for genetic influences on a wide range of behavior, it is not surprising that increasing evidence in both human and nonhuman animal populations suggests that genes also influence an organism’s social and physical environment. With respect to behavior, gene action does not stop at the physiologic boundary of the organism, the skin.

Gene-by-Sex Interactions

Twin studies have suggested that the aggregate genetic risk factors for major depression (94) , some forms of phobias (95) , and alcoholism (96) are not entirely the same in males and females. Of two genome scan linkage studies for major depression, one presented evidence for a male-specific locus (97) while a second revealed several loci specific in their effect on women (98) . A genome scan for the personality trait of neuroticism—closely related genetically to risk for major depression (99) —revealed three loci on chromosomes 1q, 12q, and 13q that appeared to be female specific (100) .

Since sexual differences start out developmentally as differences in gene expression in the sex determination pathway, it is not surprising that many genetic influences on behavior also have differential effects on females and males. Initially, in selection experiments on behavioral traits, sex-specific results were obtained. One sex was found to respond more to selection than the other, and in some cases that differential response was true at one phenotypic extreme and not the other. This is illustrated in two different experiments, one in Drosophila selecting for differential geotaxis response (101) , and one in the blow fly Phormia selecting for the conditioned response to a sucrose stimulus (102) . When such selected strains are bred to produce various classes of progeny, sex-by-gene interactions can often be seen at the aggregate gene level, as seen in a Drosophila study of response to an unconditioned stimulus (103) .

Sex-specific behavioral responses have been shown, in several instances, to reflect underlying differences in gene expression. This is merely a more restricted aspect of the emerging data from whole-genome expression analysis, which has shown that 50%–60% of all genes are differentially expressed between the sexes (104 , 105) . In one study, sex was shown to have the strongest single effect on the variance in gene expression (106) . Whereas many of these are genes directly involved in sex determination and sex-specific development and show an all-or-none difference, many more are not. Fruit flies also show sexually dimorphic responses to cocaine (107 , 108) , and this is reflected in a differential sensitivity to the induction of stereotypical locomotor behavior.

Such sex-specific effects are by no means confined to the fruit fly. For example, studies have shown sex-specific QTLs for several different alcohol-related traits in mice including preference (109) , duration of loss of righting reflex (110) , and severity of withdrawal (111) . Other studies in the mouse have shown sex-specific effects on basal gene expression in brain (112 , 113) as well as in response to caffeine administration (114) .

In summary, evidence on psychiatric and substance use disorders in human populations and a range of behavioral phenotypes in simpler animals suggest that modification of genetic effects by sex is probably a common phenomenon.

Gene-Gene Interactions

We now turn to two areas where clear findings in psychiatric genetics have yet to emerge. The first of these, termed gene-gene interaction or “epistasis,” occurs when two alleles at different genetic loci interact in a nonadditive fashion on a phenotype (115) . While widely suspected to be important in psychiatric genetics, gene-by-gene interactions have been little studied. In part this is because the standard “work horses” of genetic epidemiology—twin and adoption studies—are very weak at detecting such effects (116) .

While methods have been developed for linkage studies to detect gene-gene interactions (117) , they have not been widely validated, may have quite low power, and have been applied only rarely to human behavioral traits (118) . Theoretically, association studies provide substantially greater power to detect such interactions. However, all the difficulties with association studies of the main effect of genes (e.g., low a priori probabilities, multiple testing, liberal alpha values, and false positive rates [ 119 , 120 ]) are further exacerbated in studying interactions. A number of association studies have reported interactions, but we are unaware of any that have been widely replicated or supported by meta-analyses. Applying statistical models to risk of illness in various classes of relatives, Risch suggests that gene-by-gene interactions are important in the etiology of schizophrenia (121) .

In contrast to human studies, robust methods are available in simpler organisms to detect gene-gene interactions. One powerful approach is to observe the effects of induced mutations that influence behavior in different laboratory strains. These strains provide varying “genetic backgrounds” that could modify the effects of the mutated gene.

Mouse geneticists have long noted the sensitivity of mutations to genetic background (122) . In one striking example, a mutation in the serotonin transporter (5-HTT) showed dramatically different effects when placed in two different strains. In B6 mice, the 5-HTT mutation produced increased anxiety-like behavior and reduced exploratory locomotion. However, the same mutation in 129S6 mice produced no change in either measure (123) . (Of note, the 5-HTT mutation in the 129S6 strain was shown to produce expected changes in serotonin receptor binding and function, thus proving that the mutation was “active” but its behavioral effect was “suppressed” by the genetic background of 129S6 mice.) Similarly, a knockout of the nitric oxide synthase 1 (NOS1) enzyme increased attack behavior in one mouse strain (C57BL/6By) but not in a related substrain (C57BL/6J) (31) . The effect of NOS1 inactivation on agonistic behavior must depend critically on one or more of the rather small number of genes that distinguish the two mouse substrains.

Epistasis can also be examined using a defined set of mutant genes. Such an approach was illustrated for odor-guided behavior in Drosophila . Fourteen distinct smell-impaired mutant lines were isolated (124) . Interactions among the 14 genes were assessed by constructing pairwise combinations of the mutants and testing them for their olfactory responsiveness. The majority of pairwise combinations showed gene-gene interactions in which the combination of the two mutations produced a greater phenotypic effect than would have been predicted from the average effect of each mutation on its own (125) .

The molecular basis of gene-gene interactions is illustrated in the following example. Beginning with the cAMP phosphodiesterase gene dunce , introduced here as having pleitropic effects on both learning and egg-laying, mutations were screened to find one that would suppress the effects of dunce . One was found in the gene encoding the synthetic enzyme for cAMP: adenyl cyclase (61) , which was already known as the learning mutant rutabaga (126 , 127) . One mutant gene could mask the effect of the other, apparently due to a restoration of a balance between the level of cAMP synthesis and degradation when mutations impaired the function of both enzymes.

In conclusion, the impact of gene-gene interactions on behavior is much more easily studied in simpler organisms than in humans. The available evidence suggests that such interactions certainly occur and may be relatively common. Available human data, however, indirectly suggest that for psychiatric disorders, genetic effects will not be limited to only gene-gene interactions. This inference is based on the following line of thought: Every time an egg or sperm is made, specific set of genes that might be interacting on a trait will commonly be broken up by recombination. If most genetic effects were mediated by such gene-gene interactions, resemblance in relatives for psychiatric disorders would be restricted to monozygotic twins who share all their genes in common. However, all well studied psychiatric disorders robustly “run in families.” This pattern of findings suggests that at least a reasonable proportion of genetic effects are what statistical geneticists call “additive,” which means that genes have reliable average effects that are not highly dependent on the presence or absence of other genes.

What Sits Under Linkage Peaks

For complex human syndromes like psychiatric disorders, linkage “peaks” are large, often spanning tens of millions of base pairs and hundreds of possible genes (128) . The last several years have seen some initial success—most notably in schizophrenia—in what has been called “fine mapping”: using different techniques to localize a specific susceptibility gene under the linkage peak (40 , 129) . However, this task has proven more difficult than might have been initially thought. Furthermore, some of the genes found may not account for the entire linkage signal.

Further progress has been made, in simpler organisms, in the fine mapping of QTL peaks (analogous to linkage peaks in human research). In many cases, on closer examination, a single QTL fractionates into multiple tightly linked QTLs. In a recent review, Mackay (130) notes QTL studies with just this result for the Drosophila traits of “starvation resistance,” “olfactory behavior,” and longevity. In one study, two QTLs influencing longevity resolved, on fine mapping, into eight distinct peaks. Yalcin et al. (131) have fine mapped in the mouse a QTL shown to influence anxiety-related behaviors and found that it too “broke apart” into three discrete peaks. If true, these results have two implications. First, prior QTL and linkage studies may have substantially underestimated the number of loci that have an impact on behavioral phenotypes. Second, the task of fine mapping traits in humans under linkage peaks, where we have fewer and less powerful methods than in lower animals, may be even more difficult than we have previously estimated.

Conclusions

In the spirit of Darwin’s “Descent of Man,” we set ourselves the task in this essay of trying to determine the level of continuity in the broad patterns of the genetic influences on behavior from “simpler organisms” to humans. We framed for ourselves the question of the degree of similarity in general outline of results obtained in psychiatric genetics and in the behavior genetics research in simpler organisms. On the basis of this review, our response to this question would be “Quite similar.” An analogous answer would have been obtained had we examined complex nonbehavioral traits such as blood pressure or immune function. Throughout the animal kingdom, individual differences in behavior are, almost without exception, influenced by genetic factors. Most commonly, these genetic effects are of moderate rather than overwhelming importance and sometimes genetic influences are quite modest in magnitude. Across a wide variety of species, including humans, the genetic influences on behavior are typically the result of a moderate to large number of individual genes each of which, on its own, has a rather small effect on the behavior. In both humans and simpler organisms, the interrelationship between genes and the environment in their impact on behavior is, at least for a number of traits, likely to be complex. Gene-environment interaction, while still much underresearched, may be widespread in its effects. It is equally likely that genes, through “outside the skin pathways” play critical roles in influencing important aspects of the social environment to which the organism is exposed. For a number of behaviors across most organisms, the pathway from genes to behavior may differ meaningfully in males and females.

Studies in simpler organisms suggest that gene-gene interactions may play an important etiologic role for many behavioral traits. Whether this also holds for genetically influenced traits in humans remains an open question; it seems a reasonable expectation, given all of the other similarities between genetics of behavior in humans and model organisms, but the data are lacking. Studies in Drosophila and mice suggest that our prior assumption that linkage or QTL peaks are the result of a single susceptibility gene is likely to be incorrect for a substantial number of such peaks.

Given that Darwin was correct when he argued over 130 years ago that “man is the modified descendent of some preexisting form” (1) , our results are not surprising. They should, however, further encourage dialogue and collaboration between those trying to understand the genetic basis of psychiatric disorders and those studying the genetic influences on behavior in “simpler” organisms.

Received Aug. 28, 2004; revisions received Dec. 31, 2004, and April 11, 2005; accepted April 28, 2005. From the Virginia Institute for Psychiatry and Behavioral Genetics and the Departments of Psychiatry and Human Genetics, Medical College of Virginia, Virginia Commonwealth University; and The Neurosciences Institute, San Diego. Address correspondence and reprint requests to Dr. Kendler, Department of Psychiatry, Medical College of Virginia of Virginia Commonwealth University, P.O. Box 980126, Richmond, VA 23298-0126; [email protected] (e-mail).Dr. Kendler and Dr. Greenspan report no competing interests.Supported by the Fritz Redlich Fellowship at the Center for Advanced Study in the Behavioral Sciences to Dr. Kendler. Dr. Greenspan is the Dorothy and Lewis B. Cullman Fellow at The Neurosciences Institute, which is supported by the Neurosciences Research Foundation. The authors thank Jonathan Flint, M.D., and Robert Karp, Ph.D., for their comments on an earlier version of this manuscript.

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Essay On Behavioral Genetics

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Topic: Education , Psychology , Science , Behavior , Human , Biology , Brain , Study

Published: 01/13/2020

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Introduction

Biological Psychology is the biological study of human behavior through various theories. It is said that every behavior, action, emotion and thought originates from the brain. In the past, this study was known as physiological psychology due to the fact that the methods employed to study the brain functions and behavior correlates with the physiology. For instance, stimulation and lesioning are among the methods used. There are three major theories that try to link the biology of humans to their behavior. They include: evolutionary psychology, behavioral genetics and behavioral neuroscience. These three theories hold different backgrounds in regard to the biological explanation of the human behavior (Downes, 2008). Evolutionary psychology is one of the biological methods used in the study of human behavior. It holds to the fact that, most of the human acts can be explained through the call to internal psychological mechanism. In this theory, adaptation is the major factor that contributes to the behavior of human beings. It is indicated that every behavior is a product of natural selection which enabled people to suit to the environment and survive to the present time. This is what distinguishes it from other cognitive theories of human behavior (Downes, 2008). Behavioral genetics also seeks to understand the influence of genetics in the behavior of human beings. It extends its study to include the environmental influence on individual variations that is observed in human beings. This study was based on certain assumptions or observations. These assumptions were that the behavior of living things is habitually species specific. This is observed in a number of species such as birds, plants and animals. For example, during mating, birds of the same species tend to behave the same but totally different from the other species. Another observation was that behaviors are always likely to breed through. This means that a behavior can be reproduced through perpetuating a successive generation of living things. Thirdly, the alterations in biological structures results in changes in behaviors. Other factors are observed through the human understanding such persistence of a particular behavior in a specific family tree of human beings (McInerney, 2008). The studies on behavioral genetics entail the use of people who have a similar background such as twins to monitor their behaviors. The consideration in this case is the environmental influence. It has been found out that genetics has become a vital organ of biological science that helps to establish the cause of some disorders in human beings. The same case is with the human behavior. Hence, it is even easier to use the study of chromosomes or single- gene disorders to establish a behavior than the use studying complex behaviors (McInerney, 2008). The study of human behavior as it is influenced by the brain is termed as behavioral neuroscience. In this study, the transmissions of neurons and substances across the body organs are investigated. The study of the way neurons affect the behavior of human beings is studied. The objective of such studies is aim at reaching to a solution or an explanation that will help in stopping or eliminating certain abnormal behaviors. The study entails the examination of the receptor cells of the brain to find any damages that may cause neurons not elicit certain responses to stimuli. It is through this study that some of the disorders’ causes have been known. Consequently, some medicines and surgical procedures have been established to deal with these conditions (Behavioral Neuroscience, 2012). The procedure of these studies is normally conducted with animals that have almost similar conditions like those under study. Some parts of the brain of these animals are damaged intentionally and their behaviors monitored. After this, the physicians try to formulate possible explanations on the causes of such behaviors. It must be noted that it is through the neuroscience study that some pharmaceuticals are manufactured that help in restoration of neurotransmissions so that neurons are able to reach their respective receptor cells. Behavioral neuroscience holds the view that the brain controls every activity and behavior of human beings and all organisms at large (Behavioral Neuroscience, 2012).

In summary, the human behavior is explained using the biological approach, behavioral genetics and the neuroscience mechanism. These three theories have varied explanations as to why human beings as well as other organisms behave the way they do. Their characteristics are associated with particular patterns.

References:

Behavioral Neuroscience. (2012). Behavioral Neuroscience: Our Hope for the Future. Retrieved from http://www.behavioralneuroscience.net/ Downes, S. M. (2008). Evolutionary Psychology. Retrieved from http://plato.stanford.edu/entries/evolutionary-psychology/ McInerney, J. (2008). Behavioral Genetics. Retrieved from http://www.ornl.gov/sci/techresources/Human_Genome/elsi/behavior.shtml

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Mental health care is hard to find, especially for people with Medicare or Medicaid

Rhitu Chatterjee

With rates of suicide and opioid deaths rising in the past decade and children's mental health declared a national emergency , the United States faces an unprecedented mental health crisis. But access to mental health care for a significant portion of Americans — including some of the most vulnerable populations — is extremely limited, according to a new government report released Wednesday.

The report, from the Department of Health and Human Services' Office of Inspector General, finds that Medicare and Medicaid have a dire shortage of mental health care providers.

The report looked at 20 counties with people on Medicaid, traditional Medicare and Medicare Advantage plans, which together serve more than 130 million enrollees — more than 40% of the U.S. population, says Meridith Seife , the deputy regional inspector general and the lead author of the report.

Medicaid serves people on low incomes, and Medicare is mainly for people 65 years or older and those who are younger with chronic disabilities.

The report found fewer than five active mental health care providers for every 1,000 enrollees. On average, Medicare Advantage has 4.7 providers per 1,000 enrollees, whereas traditional Medicare has 2.9 providers and Medicaid has 3.1 providers for the same number of enrollees. Some counties fare even worse, with not even a single provider for every 1,000 enrollees.

"When you have so few providers available to see this many enrollees, patients start running into significant problems finding care," says Seife.

The findings are especially troubling given the level of need for mental health care in this population, she says.

"On Medicare, you have 1 in 4 Medicare enrollees who are living with a mental illness," she says. "Yet less than half of those people are receiving treatment."

Among people on Medicaid, 1 in 3 have a mental illness, and 1 in 5 have a substance use disorder. "So the need is tremendous."

The results are "scary" but "not very surprising," says Deborah Steinberg , senior health policy attorney at the nonprofit Legal Action Center. "We know that people in Medicare and Medicaid are often underserved populations, and this is especially true for mental health and substance use disorder care."

Among those individuals able to find and connect with a provider, many see their provider several times a year, according to the report. And many have to drive a long way for their appointments.

"We have roughly 1 in 4 patients that had to travel more than an hour to their appointments, and 1 in 10 had to travel more than an hour and a half each way," notes Seife. Some patients traveled two hours each way for mental health care, she says.

Mental illnesses and substance use disorders are chronic conditions that people need ongoing care for, says Steinberg. "And when they have to travel an hour, more than an hour, for an appointment throughout the year, that becomes unreasonable. It becomes untenable."

"We know that behavioral health workforce shortages are widespread," says Heather Saunders , a senior research manager on the Medicaid team at KFF, the health policy research organization. "This is across all payers, all populations, with about half of the U.S. population living in a workforce shortage."

But as the report found, that's not the whole story for Medicare and Medicaid. Only about a third of mental health care providers in the counties studied see Medicare and Medicaid patients. That means a majority of the workforce doesn't participate in these programs.

This has been well documented in Medicaid, notes Saunders. "Only a fraction" of providers in provider directories see Medicaid patients, she says. "And when they do see Medicaid patients, they often only see a few."

Lower reimbursement rates and a high administrative burden prevent more providers from participating in Medicaid and Medicare, the report notes.

"In the Medicare program, they set a physician fee rate," explains Steinberg. "Then for certain providers, which includes clinical social workers, mental health counselors and marriage and family therapists, they get reimbursed at 75% of that rate."

Medicaid reimbursements for psychiatric services are even lower when compared with Medicare , says Ellen Weber , senior vice president for health initiatives at the Legal Action Center.

"They're baking in those discriminatory standards when they are setting those rates," says Steinberg.

The new report recommends that the Centers for Medicare & Medicaid Services (CMS) take steps to increase payments to providers and lower administrative requirements. In a statement, CMS said it has responded to those recommendations within the report.

According to research by Saunders and her colleagues at KFF, many states have already started to take action on these fronts to improve participation in Medicaid.

Several have upped their payments to mental health providers. "But the scale of those increases ranged widely across states," says Saunders, "with some states limiting the increase to one provider type or one type of service, but other states having rate increases that were more across the board."

Some states have also tried to simplify and streamline paperwork, she adds. "Making it less complex, making it easier to understand," says Saunders.

But it's too soon to know whether those efforts have made a significant impact on improving access to providers.

CMS has also taken steps to address provider shortages, says Steinberg.

"CMS has tried to increase some of the reimbursement rates without actually fixing that structural problem," says Steinberg. "Trying to add a little bit here and there, but it's not enough, especially when they're only adding a percent to the total rate. It's a really small increase."

The agency has also started covering treatments and providers it didn't use to cover before.

"In 2020, Medicare started covering opioid treatment programs, which is where a lot of folks can go to get medications for their substance use disorder," says Steinberg.

And starting this year, Medicare also covers "mental health counselors, which includes addiction counselors, as well as marriage and family therapists," she adds.

While noteworthy and important, a lot more needs to be done, says Steinberg. "For example, in the substance use disorder space, a lot of addiction counselors do not have a master's degree. And that's one of their requirements to be a counselor in the Medicare program right now."

Removing those stringent requirements and adding other kinds of providers, like peer support specialists, is key to improving access. And the cost of not accessing care is high, she adds.

"Over the past two decades, [in] the older adult population, the number of overdose deaths has increased fourfold — quadrupled," says Steinberg. "So this is affecting people. It is causing deaths. It is causing people to go to the hospital. It increases [health care] costs."

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