Chapter 4
Genetics and the Environment

[N]ature prevails enormously over nurture when the differences in nurture do not exceed what is commonly found among persons of the same rank in society and in the same country.

—Francis Galton, Memories of My Life (1908)

Although genetics clearly controls many of an organism's traits, it is simplistic and incorrect to assume that organisms, including humans, are completely defined by their genes. Even though there are some phenotypes (observable traits) that are exclusively controlled by either genetics or environment, most are influenced by a complex interaction of the two. Modern genetics study defines environment as every influence other than genetic—such as air, water, diet, radiation, and exposure to infection—and it subscribes to the overarching assumption that every trait of every organism is the product of some set of interactions between genes and the environment.

NATURE VERSUS NURTURE

The debate over the relative contributions of genetics and environment—nature versus nurture—remains unresolved in many fields of study, from education to animal behavior to human disease. Historically, scientists assumed opposing viewpoints, choosing to favor either nature or nurture, rather than exploring the ways in which both play critical and complementary roles. Proponents of nature, or a person's inborn traits, argued that human characteristics are uniquely and primarily conditioned by genetics, disputing the view of those who asserted that environmental influences and experiences (nurture) determined differences between individuals and populations.

Genes versus Environment

When researchers analyze the origins of disease, the terms used to describe causation are genetic versus environmental, but the issues are the same as those in the nature-versus-nurture debate. Conditions considered to be primarily genetic are ones in which the presence or absence of genetic mutations determines whether an individual or population will develop a disease, independent of environmental exposures or circumstances. A disease considered to be primarily environmental is one in which people of virtually any genetic background can develop the disease when they are exposed to the specific environmental factors that cause it.

Even the conditions and diseases once believed to be at either end of the continuum—caused by either purely genetic or purely environmental factors—may not be exclusively attributable to one or the other. For example, an automobile accident that results in an injury might be deemed entirely environmentally caused, but many geneticists would contend that risk-taking behaviors such as the propensity to exceed the speed limit are probably genetically mediated. Furthermore, the course and duration of rehabilitation and recovery from an injury or illness is also likely genetically influenced.

At the other end of the continuum are diseases believed to be predominantly genetic in origin, such as sickle-cell anemia. Even though this disease does not have an environmental cause, there are environmental triggers that may determine when and how seriously the disease will strike. For example, sickle-cell attacks are more likely when the body has an insufficient supply of oxygen, so people with the sickle-cell trait who live at high altitudes or those who engage in intense aerobic exercise may be at increased risk of attacks. There are many more conditions for which the risk of developing the disease is strongly influenced by both genetic and environmental factors. Multiple genes and environmental factors may be involved in causing a given condition and its expression.

Asthma: A Disease with Genetic and Environmental Causes

Asthma, a disorder of the lungs and airways that causes wheezing and other breathing problems, is a good example of how genes and the environment can interact to cause diseases. The scientific evidence that asthma had a genetic basis came from studies conducted between the 1970s and 1990s, which found patterns of inheritance in families and genetic factors involved in the severity and triggers for asthma attacks. In "Family Concordance of IgE, Atopy, and Disease" (Journal of Allergy and Clinical Immunology, February 1984), Michael D. Lebowitz, Robert Barbee, and Belton Burrows looked at 350 families and found that in those where neither parent had asthma, 6% of the children had asthma; when one parent had asthma, 20% were affected; and when both parents had the condition, 60% of their offspring were affected.

In "Genetic Factors in the Presence, Severity, and Triggers of Asthma" (Archives of Disease in Childhood, August 1995), a study of pairs of twins in which at least one twin had asthma, Edward P. Sarafino and Jarrett Goldfedder discovered that genetics and environment both made strong contributions to the development of the illness. If asthma was directed solely by genes, then 100% of the identical twins, who are exactly the same genetically, would be expected to have asthma (the concordance rate is the rate of agreement, when both members of the pair of twins have the same trait). Instead, Sarafino and Goldfedder found that just over half (59%) of twins both had asthma. If asthma was entirely environmentally caused, then genes should make no difference at all—the concordance rate would be the same for identical and fraternal (nonidentical) twins. Sarafino and Goldfedder found that the concordance rate of 59% was more than twice as high in identical twins as in fraternal twins (24%). This research offers clear confirmation that asthma has a significant genetic component.

Asthma is an example of a condition that is polygenic—controlled by more than one gene. Familial studies demonstrate that asthma does not conform to simple Mendelian patterns of inheritance and that multiple independent segregating genes are required for phenotypic expression (polygenic inheritance). Nevertheless, it has long been known that the complex phenotypes of asthma have a significant genetic contribution. Researchers speculate that several genes combine to increase susceptibility to asthma and that there are also genes that lower susceptibility to developing the condition. Genes also affect asthma severity and the way people with asthma respond to various medications.

Environmental triggers for asthma include allergens such as air pollution, tobacco smoke, dust, and animal dander. Other environmental factors linked to its development are a diet high in salt, a history of lung infections, and the lack of siblings living at home. Researchers speculate that younger children in families with older siblings are less likely to develop asthma because their early exposures to foreign substances (such as dirt and germs) brought into the home by older siblings heighten their immune systems. The enhanced immune response is believed to have a protective effect against asthma and other illnesses.

Harvard Medical School researchers Michael E. Wechsler and Elliot Israel, in "The Genetics of Asthma" (Seminars in Respiratory and Critical Care Medicine, 2002), acknowledge some of the difficulties faced by researchers studying a complex disease such as asthma. They describe the following challenges faced by geneticists seeking to pinpoint the genetics of asthma:

• Population studies suggest that asthma is a polygenic disease, with many diverse locations of possible asthma genes already identified.
• The definition of asthma can vary from one health care practitioner to another. Some make the diagnosis based on changes in airway reactivity, others on levels of airway function, and still others on clinical symptoms. As a result, phenotyping methods must be examined and carefully compared because the variety of clinical symptoms a patient with asthma may present, such as cough, shortness of breath, wheezing, and chest tightness, are also common to several other conditions such as bronchitis or heart failure, and confusion may result in misdiagnosis.
• Even though a clinical history of asthma symptoms or phenotypes often suggests a diagnosis of asthma, there is no definitive, specific definition that classifies an individual as having or not having asthma. As a result, some people may be incorrectly labeled or identified, potentially yielding false data or nonreplicable results.
• Several recent epidemiological (the study of the spread of disease in a population) studies suggest that asthma may have many different phenotypic expressions at different ages as assessed by their risk factors and prognosis. For example, children under age six who at various times experience wheezing are labeled as asthmatic. However, most of these children do not continue to have asthma symptoms as they age—they seem to outgrow the condition.
• Asthma differs in terms of severity (mild, moderate, or severe and intermittent or persistent), suggesting different genetic or environmental influences and triggers. There are also several different subgroups of asthma patients, including aspirin-sensitive asthmatics and exercise-induced asthmatics. Each of these variations may have a different biological mechanism that accounts for each individual's phenotype.

Wechsler and Israel conclude that while a small percentage of cases of asthma may result from a single gene defect or a single environmental factor, asthma is a complex genetic disease that cannot be explained by single-gene models. In most instances it appears to result from the interaction of multiple genetic and environmental factors. Similar to other complex diseases such as diabetes and hypertension (high blood pressure), the complexity of asthma genetics may be characterized by the contribution of different genes and different environments in different populations. Population studies of asthma face challenges comparable to genetics studies of other common complex traits. They are complicated by genetic factors such as incomplete penetrance (transmission of disease genes without the appearance of the disease), genetic heterogeneity (mutations in any one of several genes that may result in similar phenotypes), epistasis (when the effects of multiple genes have a greater effect on phenotype than individual effects of single genes), polygenic inheritance (mutations in multiple genes simultaneously producing the affected phenotype), and gene-environment interactions.

Genetic Susceptibility

Genetic susceptibility is the concept that the genes an individual inherits affect how likely he or she is to develop a particular condition or disease. When an individual is genetically susceptible to a particular disease, his or her risk of developing the disease is higher. Genetic susceptibility interacts with environmental factors to produce disease, but genes and environment do not necessarily make equal contributions to causation. Genes can cause a slight or a strong susceptibility. When the genetic contribution is weak, the environmental influence must be strong to produce disease, and vice versa.

In most instances a susceptibility gene strongly influences the risk of developing a disease only in response to a specific environmental exposure. If the environmental exposure occurs infrequently, the gene will be of low penetrance, and it may seem that the environmental exposure is the primary cause of the disease, even though the gene is required for developing the disease. For this reason, even when environmental agents are suspected to be a major cause of a particular disease, there is still the possibility that genetic factors also play a major part, particularly genetic mutations with low penetrance. Similarly, a critical mix of nature and nurture is likely to determine individual traits and characteristics. Genetic factors may be considered as the foundation on which environmental agents exert their influence. Based on this premise, it is now widely accepted that while certain environmental factors alone and certain genetic factors alone may explain the origins of some traits and diseases, most of the time the interaction of both genetic and environmental factors will be required for their expression.

Since the 1990s researchers have identified more and more genes that influence an individual's susceptibility to disease. Scientists have already linked specific deoxyribonucleic acid (DNA) variations with increased risk of common diseases and conditions, including cancer, diabetes, hypertension, and Alzheimer's disease (a progressive neurological disease that causes impaired thinking, memory, and behavior). The questions that persist in the genes-versus-environment debate no longer focus on whether a particular trait or disease is caused exclusively by a specific gene. Instead, researchers continue to explore the extent to which genes and environment influence the development of specific traits, especially conditions linked to health and susceptibility to disease.

Examples of the kinds of questions about susceptibility that geneticists and other medical researchers hope to answer include:

• Why do some tobacco smokers live long, healthy lives while others develop lung cancer and die early?
• Why do some people who are repeatedly exposed to the human immunodeficiency virus, the virus that causes acquired immune deficiency syndrome, resist contracting the virus?
• Why do common allergens (substances that cause allergies) cause moderate discomfort for some people and life-threatening asthma for others?

TWIN STUDIES

The English anthropologist Francis Galton, a cousin of Charles Darwin, conducted some of the first reported twin studies. Advancing his cousin's theories of evolution, he performed twin studies in 1876 to investigate the extent to which the similarity of twins changes over the course of development. He is considered the originator of the field of medical genetics because of his considerable contributions to the nature-versus-nurture debate and the research methods he developed for evaluating heritability. Genetic determination is the combination of genes that creates a trait or characteristic, and heritability is what causes differences in those characteristics.

Twin studies, meaning comparisons of identical (monozygotic) twins to fraternal or nonidentical (dizygotic) twins, are performed to estimate the relative contributions of genes and environment—that is, the extent to which environmental-versus-genetic influences operate on specific traits. Twin studies also help to determine the proportion of the variability in a trait that might be because of genetic factors. The studies aim to identify the causes of familial resemblance by comparing the concordance rates of monozygotic twins and dizygotic twins. Monozygotic twins share the same genetic material—they have 100% of their genes in common—and dizygotic twins share only half their genetic material—they have 50% of their genes in common. Most twin studies report their results in terms of pairwise concordance rates, which measure the number of pairs, or probandwise concordance rates, which count the number of individuals.

Monozygotic twins serve as excellent subjects for controlled experiments because they share prenatal environments and those reared together also share common family, social, and cultural environments. Furthermore, studies of twins can both point to hereditary effects and estimate heritability, a term that describes the magnitude of the genetic effect. The limitations of such studies include the potential to overestimate or underestimate the role of genetics if environmental influences treat twins as more alike or more different than they actually may be. In addition, in some studies it has been difficult to control for other potential causes or sources of variation.

Some of the most conclusive twin study research has analyzed identical and fraternal twins who were raised apart. Researchers have sought to establish whether characteristics such as personality traits, aptitudes, and occupational preferences are the products of nature or nurture. Similar characteristics among identical twins reared apart might indicate that their genes played a major role in developing that trait. Different characteristics might indicate the opposite—that environmental influences assume a much stronger role. By comparing monozygotic and dizygotic twins, investigators can test their hypotheses and confirm the findings of earlier research. For example, if identical twins raised in different homes have many similarities, but fraternal twins raised apart have little in common, researchers may conclude that genes are more important than environment in determining specific characteristics, traits, susceptibilities, and diseases.

Paul Lichtenstein et al., in "Environmental and Heritable Factors in the Causation of Cancer—Analyses of Cohorts of Twins from Sweden, Denmark, and Finland" (New England Journal of Medicine, July 13, 2000), looked at nearly 45,000 pairs of twins to determine if the likelihood of developing certain kinds of cancers is more closely linked to environmental exposures than genetics. The results of this large-scale study revealed that environmental factors are linked to twice as many cancers as genetic factors. In fact, the risk of developing only three types of cancer (albeit some of the most common cancers)—breast, colorectal, and prostate cancers—show a significant genetic correlation.

Prostate cancer is found to have the strongest genetic link, with 42% of risk explained by genetic factors and 58% by environmental factors. The other cancers with a demonstrable genetic link, breast and colorectal cancers, are found to have less than a 35% link to genetics. Lichtenstein and his colleagues conclude that inherited genetic factors make a minor contribution to susceptibility to most types of cancer.

Do Genes Govern Sexual Orientation?

The role of genetics in establishing sexual orientation (the degree of sexual attraction to men or women) and its link to homosexuality have been hotly debated in the relevant scientific literature and the media. Studies of identical twins reveal that sexual orientation, like the overwhelming majority of human traits and characteristics, is not exclusively governed by genetics, but is more likely the result of a gene-environment interaction. For example, if homosexuality was exclusively controlled by genes, then either both members of a set of identical twins would be homosexual or neither would be. Multiple studies show that if one twin is homosexual his or her sibling is also homosexual less than 40% of the time.

J. Michael Bailey, Michael P. Dunne, and Nicholas G. Martin systematically evaluated gender identity and sexual orientation of twins and reported their findings in "Genetic and Environmental Influences on Sexual Orientation and Its Correlates in an Australian Twin Sample" (Journal of Personality and Social Psychology, March 2000). Bailey, Dunne, and Martin observed that both male and female homosexuality appears to run in families and that studies of unseparated twins suggest that this is primarily because of genetic rather than familial environmental influences. They also observe that previous research suffers from limitations such as recruiting subjects via publications aimed at homosexuals or by word of mouth—strategies likely to bias the samples and results.

To overcome these limitations, Bailey, Dunne, and Martin assessed twins from the Australian Twin Registry rather than recruiting twins especially for the purpose of their research. Using probandwise concordance (an estimate of the probability that a twin is nonheterosexual given that his or her co-twin is nonheterosexual), they found lower rates of twin concordance for nonheterosexual orientation than in previous studies. The most striking difference was between the researchers' probandwise concordance rates and those of past twin studies of sexual orientation. Previously, the lowest concordances for single-sex identical twins were 47% for women and 48% for men. This study documents concordances of just 20% for women and 24% for men, significantly lower than the rates reported for the two largest previous twin studies of sexual orientation. Bailey, Dunne, and Martin conclude that sexual orientation is familial; however, their study does not provide statistically significant support for the importance of genetic factors for this trait. They caution that this does not mean that their results entirely exclude heritability. In fact, they consider their findings consistent with moderate heritability for male and female sexual orientation, even though their male monozygotic concordance suggests that any major gene for homosexuality has either low penetrance or low frequency.

Bailey, Dunne, and Martin attribute their markedly different results to the observation that in previous studies twins deciding whether to participate in research that was clearly designed to study homosexuality probably considered the sexual orientation of their co-twins before agreeing to participate. In contrast, the more general focus of the Bailey, Dunne, and Martin study and its anonymous response format made such considerations less likely.

Even though it remains unclear from recent studies whether concordance is closer to 50% or 30%, all researchers concur that it is not 100%. This finding suggests that the influence of genes on sexual orientation is indirect and influenced by environment. Neil Whitehead and Briar Whitehead claim in My Genes Made Me Do It (1999) that "genes make proteins, not preferences." Similarly, they contend that "genes create a tendency, rather than a tyranny" and conclude that all the identical twin studies reveal that in terms of determining sexual orientation, neither genetic nor family-related factors are overwhelming. Furthermore, Whitehead and Whitehead believe that all influences—genetic and environmental—are subject to change and that it is possible to "foster or foil genetic or family influences."

IS THERE A GAY GENE?

In "New Genetic Regions Associated with Male Sexual Orientation Found" (WebMD Medical News Archive, January 28, 2005), Jennifer Warner described research that examined the entire human genetic makeup—genetic information on all chromosomes—in an effort to identify possible genetic determinants of male sexual orientation. Investigators looked at the genetic makeup of 456 men from 146 families with two or more gay brothers and found the same genetic patterns among the gay men on three chromosomes: 7, 8, and 10. Sixty percent of the gay men in the study shared these common genetic patterns, which was slightly more than the 50% expected by chance alone. Patterns involving chromosomes 7 and 8 were associated with sexual orientation regardless of whether the man received them from his father or his mother; however, the areas on chromosome 10 were only associated with male sexual orientation if they were inherited from the mother. The identification of these regions has spurred further research to identify the individual genes in these regions that are linked to sexual orientation.

GENETIC AND ENVIRONMENTAL INFLUENCES ON INTELLIGENCE

The role of genetics in determining a person's intelligence is a controversial subject. Few would deny that genes play some role, but many are uncomfortable with the idea that genes determine intelligence. For if intelligence is a genetic trait, the implication is that some people are born to be smart, others are not, and education and upbringing cannot change it. The results of many studies and contentious debate in the scientific community have produced little consensus about the relationship between genetics and intelligence. At least part of the problem stems from the fact that the term intelligence is defined differently by different people.

Although this issue has been argued since the 1870s—when Galton proposed his controversial and arguably racist notions about the heritability of intelligence—the debate was reignited during the 1990s when Richard J. Herrnstein and Charles Murray published The Bell Curve: Intelligence and Class Structure in American Life (1994). Herrnstein and Murray expressed their beliefs that between 40% and 80% of intelligence is determined by genetics and that it is intelligence levels, not environmental circumstances, poverty, or lack of education, that are at the root of many of our social problems. Critics argued that Herrnstein and Murray not only manipulated and misinterpreted data to support their contention that intelligence levels differ among ethnic groups but also reintroduced outdated and harmful racial stereotypes. Many observers did agree with Herrnstein and Murray's premises that intellect is spread unevenly among individuals and population subgroups, that innate intelligence is distributed through the entire population on a "bell curve," with most people near to the average and fewer at the high and low ends, and even that the distribution varies by race and ethnicity. However, few have been willing to accept the idea that intelligence is entirely genetically encoded, permanently fixed, and unresponsive to environmental influences.

One traditional measure of intelligence is a standardized intelligence quotient (IQ) test, which measures an individual's ability to reason and solve problems. Nearly all studies that focus on the link between intelligence and genetics rely on results obtained from IQ tests, which generally provide an overall score along with measures of verbal ability and performance ability. Although there are several versions of IQ tests available, test takers generally perform comparably on all of them, presumably indicating that they all measure similar aspects of cognitive ability. Critics of IQ tests as measures of intelligence contend that they do not measure all abilities in the complex realm of intelligence. They observe that the tests measure one small segment of the diverse abilities that comprise intelligence, evaluate only analytic abilities, fail to assess creative or practical abilities, and measure only a small sample of the skills that define the domain of intelligent human behavior.

Despite concern about whether IQ tests fully measure intelligence, nearly all scientific study of the contributions of genetics and environment to intelligence has focused on measuring IQ and examining individuals who differ in their familial relationships. For example, if genetics plays the predominant role in IQ, then identical twins should have IQs that compare more closely than the IQs of fraternal twins, and siblings' IQs should correlate more highly than those of cousins. In "Genetics of Childhood Disorders, II: Genetics and Intelligence" (Journal of the American Academy of Child and Adolescent Psychiatry, May 1999), Alan S. Kaufman observes that scientists who argue in favor of genetic determination of IQ cite these data to support their assertion that:

• Identical (monozygotic) twins' IQs are more similar than those of fraternal (dizygotic) twins.
• IQs of siblings correlate more highly than IQs of half-siblings, which, in turn, correlate higher than IQs of cousins.
• IQ correlations between a biological parent and child living together are higher than those between an adoptive parent and child living together.

Kaufman asserts that the following results support scientists who believe that environment more strongly determines IQ:

• IQs of fraternal twins correlate more highly than IQs of siblings of different ages despite the same degree of genetic similarity.
• Unrelated siblings reared together, such as biological and adopted children, have IQs that are more similar than biological siblings reared apart.
• Correlations between IQs of an adoptive parent and a child living together are similar to correlations of a biological parent and a child living apart.
• Siblings reared together have IQs that are more similar than siblings reared apart, and the same finding holds for parents and children, when they live together or apart.

The preponderance of evidence from twin, family, and adoption studies supports increasing heritability of intelligence over time, ranging from 20% in infancy to 60% in adulthood, along with environmental factors estimated to contribute about 30%. Kaufman suggests that heredity is important in determining a person's IQ, but environment is also crucial. Based on twin studies, the heritability percentage for IQ is approximately fifty, which is comparable to the heritability value for body weight. Kaufman believes that the genetic contribution to weight and intelligence are comparable. He observes that many overweight people have a genetic predisposition for a large frame and a metabolism that promotes weight gain, whereas naturally thin people have the opposite genetic predisposition. Nonetheless, for most people environmental factors such as diet and exercise have a substantial impact on weight. Similarly, genetics and environment interact to determine IQ, and people with genetic, familial relationships such as parents and siblings frequently share common environments.

In "Virtual Twins: New Findings on Within-Family Environmental Influences on Intelligence" (Journal of Educational Psychology, September 2000), psychologist Nancy L. Segal examined virtual twins—genetically unrelated siblings (typically adopted) of the same age who were reared together from early infancy—to assess environmental influences on intelligence. The results of this study reveal that the IQ correlation of virtual twins fell considerably below correlations reported for identical twins, fraternal twins, and full siblings. Segal interprets these results as a demonstration of the modest effects of environment on intellectual development and as supporting a predominantly genetic role in determining intelligence.

Robert Plomin details similar findings from adoption studies in "Genetics of Childhood Disorders, III: Genetics and Intelligence" (Journal of the American Academy of Child and Adolescent Psychiatry, June 1999). He observes that adoption studies have a substantial estimated heritability, finding that identical twins reared apart are almost as similar for measures of intelligence as identical twins reared together. Plomin also looked at 245 children adopted in the first month of life from the Colorado Adoption Project to see if there is more of a parent-offspring or an adoptive parent-adopted children correlation of IQ scores. He finds significant correlations between biological mothers and their adopted-away children and almost no parent-offspring correlations for adoptive parents and their adopted children, suggesting that family environment shared by parents and offspring does not contribute as strongly as genetic influences to parent-offspring resemblance for selected measures of intelligence.

Scientists Identify the Gene Involved in Human Brain Development

The genetic underpinnings of human intelligence were further supported by the discovery in 2006 of a key gene—HAR1F—that helped the human brain evolve from its primate ancestors. Kerri Smith et al. report in "Honing in on the Genes for Humanity" (Nature, August 17, 2006) that after examining forty-nine areas of genetic code that have changed the most between the human and chimpanzee genomes, they pinpointed an area of the human genome that appears to have evolved seventy times faster than the balance of human genetic code. Smith and her colleagues observed eighteen differences in the HAR1F gene that took place in humans but not in chimps and may have prompted the rapid growth of the brain's cerebral cortex (the part of the brain where thought processes occur). It may also explain why human brains are three times the size of chimp brains.

HOW DO GENES INFLUENCE BEHAVIOR AND ATTITUDES?

The question of interest is no longer whether human social behavior is genetically determined; it is to what extent.

—Edward O. Wilson, On Human Nature (1978)

Heredity is what sets the parents of a teenager wondering about each other.

—Laurence J. Peter, author of The Peter Principle (1968)

Most people accept the premise that genes at least in part influence personality and behavior. Families have long decried a characteristic "bad temper" or "wild streak" appearing in a new generation, or boasted about inherited musical or artistic talents. It seems intuitively correct to assume that some of our behaviors and attitudes, both the desirable and less desirable ones, are in part genetically mediated. In "The DNA Age: That Wild Streak? Maybe It Runs in the Family" (New York Times, June 15, 2006), Amy Harmon asserts that an increasing understanding of genetics has renewed consideration about the degree to which individuals can actually control how they behave.

Studies of families and twins strongly suggest genetic influences on the development and expression of specific behaviors, but there is no conclusive research demonstrating that genes determine behaviors. In "The Interplay of Nature, Nurture, and Developmental Influences: The Challenge ahead for Mental Health" (Archives of General Psychiatry, November 2002), psychiatrist Michael Rutter observes that a range of mental health disorders from autism and schizophrenia to attention deficit hyperactivity disorder (ADHD) involve at least indirect genetic effects, with heritability ranging from 20% to 50%. He further asserts that genetically influenced behaviors also bring about gene-environment correlations.

Rutter explains the mechanism of genetic influence on behavior: genes affect proteins, and through the effects of these proteins on the functioning of the brain there are resultant effects on behavior. Rutter views environmental influences as comparable to genetic influences in that they are strong and pervasive but do not determine behaviors, and studies of environmental effects show that there are individual differences in response. Some individuals are severely affected and others experience few repercussions from environmental factors. This has given rise to the idea of varying degrees of resiliency—that people vary in their relative resistance to the harmful effects of psychosocial adversity—as well as the premise that genetics may offer protective effects from certain environmental influences.

Jan Strelau, in "The Contribution of Genetics to Psychology Today and in the Decade to Follow" (European Psychologist, December 2001), asserts that the proportion of phenotypic variance that may be attributed to genetic variance shows that personality traits, including temperament as well as specific behaviors and intelligence, have a heritability ranging from 40% to about 60%, but that it is primarily environmental influences that explain individual differences. He states that genetics influence the environment experienced by individuals, which explains how, for example, children growing up in the same family often experience and interpret their environments differently. This also explains why individuals who share the same genes though living apart show some concordance in selecting or creating similar experiences.

Traditional psychological theory holds that attitudes are learned and most strongly influenced by environment. In "The Heritability of Attitudes: A Study of Twins" (Journal of Personality and Social Psychology, June 2001), James M. Olson et al. examine whether there is a genetic basis for attitudes by reviewing earlier studies and conducting original research on monozygotic and dizygotic twins. Olson and his collaborators argue that the premise that attitudes are learned is not incompatible with the idea that biological and genetic factors also influence attitudes. They hypothesize that genes probably influence predispositions or natural inclinations, which then shape environmental experiences in ways that increase the likelihood of the individual developing specific traits and attitudes. For example, children who are small for their age might be teased or taunted by other children more than their larger peers. As a result, these children might develop anxieties about social interaction, with consequences for their personalities, such as shyness or low self-esteem discomfort with large groups.

In research supported by the National Institutes of Health, Amy Abrahamson, Laura Baker, and Avshalom Caspi examine genetic influences on attitudes of adolescents and report their findings in "Rebellious Teens? Genetic and Environmental Influences on the Social Attitudes of Adolescents" (Journal of Personality and Social Psychology, December 2002). The purpose of their study was to investigate sources of familial influence on adolescent social attitudes in an effort to understand whether and how families exert an influence on the attitudes of adolescents. They wanted to pinpoint the age when genetic influences actually emerge and to determine the extent to which parents and siblings shape teens' views about controversial issues. Abrahamson, Baker, and Caspi explored genetic and environmental influences in social attitudes in 654 adopted and nonadopted children and their biological and adoptive relatives in the Colorado Adoption Project. Conservatism and religious attitudes were measured in the children annually from ages twelve to fifteen and in the parents during the twelve-year-old visit.

The study finds that both conservatism and religious attitudes are strongly influenced by shared-family environmental factors throughout adolescence. Familial resemblance for conservative attitudes arises from both genetic and common environmental factors, and familial influence on religious attitudes is almost entirely in response to shared-family environmental factors. These findings are different from previous findings in twin studies, which suggest that genetic influence on social attitudes do not emerge until adulthood. In contrast, the Colorado Adoption Project study detects significant genetic influence in conservatism as early as age twelve, but finds no evidence of genetic influence on religious attitudes during adolescence. Abrahamson, Baker, and Caspi conclude that genetic factors exert an influence on social attitudes much earlier than previously indicated. For example, significant genetic influences on variations in conservatism are identified as early as age twelve. The study provides further evidence that shared environmental factors contribute significantly to individual differences in social attitudes during adolescence.

Psychologist David Cohen downplays environmental influences by specifically discounting parents' responsibility for mental illness and emotional problems in their children. In Stranger in the Nest: Do Parents Really Shape Their Child's Personality, Intelligence, or Character? (1999), Cohen asserts that "good parenting" cannot overcome "bad genes" and that it is impossible to separate genetic background from environmental influence. Making a strong case for genetic influence, Cohen writes, "The truth of the matter is that, if sufficiently strong, inborn potentials can trump parental influence, no matter how positive or negative. Some traits manifest themselves in such unexpected and uncontrollable ways that, for better or for worse, one's child may indeed seem like a perfect stranger."

ENVIRONMENTAL GENOME PROJECT

In many instances it is difficult to understand how genes manage to assert themselves over the myriad of complications imposed by the environment. The Environmental Genome Project (EGP) was launched by the National Institute of Environmental Health Sciences (which is one of the twenty-seven institutes and centers of the National Institutes of Health) in 1998. The EGP aims to improve understanding of human genetic susceptibility to environmental exposures, including gaining an understanding of how individuals differ in their susceptibility to environmental agents and how these susceptibilities change over time. Figure 4.1 shows the interrelationship of human health and disease to environmental exposures, susceptibility, time, and age.

Ongoing EGP research activities focus on biostatistics and bioinformatics; DNA sequencing; ethical, legal, and social implications; population-based epidemiology; and technology development. For example, research underway at the University of Colorado Health Sciences Center is examining controversies surrounding genetic research and health services with Native Americans. This research aims to help formulate guidelines for the conduct of genetic research and the delivery of genetic health services in Native American communities. Other research examines the potential link between environmental exposures and childhood leukemia (cancer of the blood), the health risks of pesticide exposures among farmers, and genetic susceptibility to cancers triggered by environmental exposures such as vinyl chloride induced cancers.