Genetics and Human Behavior: I. Scientific and Research Issues
I. SCIENTIFIC AND RESEARCH ISSUES
Interest in the possible effects of genetic inheritance on human behavior is a perennial one, with its modern roots dating back the writings of Sir Francis Galton in the late nineteenth century. The issue is often framed as a debate over "nature versus nurture." After the "rediscovery" of the work of Gregor Mendel (1822–1884) in the twentieth century, the issue came to be couched in terms of genes versus environments and their respective influences on the organism, while more recently the talk has been of DNA and its role in relation to other causal factors. Themes revolving around genetics and environment are especially contentious when behavioral and mental traits (and disorders) are brought into the picture. This has been the case for views about the self and responsibility, as well as in society in general, where the specter of eugenics is quickly raised. According to the Nobel Laureate Thorsten Wiesel, "Perhaps most disturbing to our sense of being free individuals, capable to a large degree of shaping our character and our minds, is the idea that our behavior, mental abilities, and mental health can be determined or destroyed by a segment of DNA." The inflammatory appearance in 1994 of The Bell Curve by social scientists Richard Herrnstein and Charles Murray, which argued IQ is substantially inherited and may differ among races for genetic reasons, represents a major example of this social contentiousness. Another highly fractious example revolved around the University of Maryland's project on genetics and criminal behavior, and especially the September 1995 conference. The conference was strongly criticized by groups opposed to any inquiries into genetics and crime, and some of these groups' representatives invaded the conference and had to be escorted away by the authorities (Wasserman and Wachbroit).
The academic discipline that studies the effect of genetics on human behavior is termed behavior genetics or behavioral genetics. In addition to studying humans, this discipline has a long history of examining the behaviors of simpler organisms, including the round worm (C. elegans), the fruit fly, (Drosophila), and the common mouse (Mus), as well as dogs, primates, and many other organisms. The organized discipline began to coalesce from a wide variety of disciplines in the 1960s with the appearance of the first textbook in the subject, Human Genetics by John Fuller and Robert Thompson. The disciplines contributing to behavioral (and psychiatric) genetics included biology (including genetics), psychology, statistics, zoology, medicine, and psychiatry. Especially significant was the psychology of individual differences, which perhaps provided the main themes of the new subject (see psychiatric geneticist Irving Gottesman's 2003 article for a brief but excellent historical introduction and references).
In the realm of behavioral disorders and genetics, the years since 1970 have seen a shift from the view of psychiatric disorders being primarily environmental (due to poor parenting, for example) to the contemporary view that amalgamates both genetic and what are called nonshared environmental influences as major causal determinants of mental disorders. This has not been a shift without controversy, and it reflects broader shifts in psychosocial studies of the contributions of nature and nurture (Reiss and Neiderhiser). Further, though psychology has paid increasing attention to behavioral genetics, cultural anthropology and sociology have been strongly resistant to any genetic approaches (Rowe and Jacobson).
Major Methods of Studying Genetic Influences
Traditional genetics, of the type investigated by Mendel and his followers, was able to identify genes that had large effects and often displayed typical patterns, such as those involving dominant, recessive, or sex-linked traits. Genes that affect human behaviors and exhibit such patterns are well-known, including Huntington's disease (caused by an autosomal dominant mutation) and phenylketonuria, or PKU (a recessive mutation). Symptoms of Huntington's disease's include degeneration of the nervous system, usually beginning in middle age and resulting in death. In this devastating disease, there is usually a gradual loss of intellectual ability and emotional control. The genetic pattern is that of a condition caused by a rare, single, dominant gene. Since affected people have one copy of the dominant disease gene and one copy of a recessive gene (for a "normal" nervous system), half of their offspring develop the disease. Huntington's never skips a generation. Since the gene is dominant, the person who inherits it will manifest the disease (if he or she lives long enough). If one full sibling has the condition, there is a fifty-fifty chance that any other sibling will also get the disease.
In contrast to dominant conditions, recessive conditions show a very different pattern of occurrence. Recessive means that both copies of the gene must be of the same form (the same allele) in order to show the condition. Two parents, neither of whom shows a trait, can have a child affected by a recessive trait (this happens if both parents are carriers of one copy of the recessive allele—the child thus has two copies, one from each parent, and manifests the condition). Recessive traits can skip generations because parents and their offspring can carry one copy of the recessive gene and not display the associated trait. In the population there are many recessive genes that cause various abnormal conditions. Each particular recessive allele may be rare, but since there are many of them, their combined impact on a population can be substantial.
Among humans, a classic example of recessive inheritance is the condition of phenylketonuria (PKU). Individuals with PKU usually are severely mentally impaired. Most never learn to talk; many have seizures and display temper tantrums. PKU is a form of severe mental retardation that is both genetic and treatable. It is genetic in that it is caused by a recessive genetic allele. Without two copies of that particular allele, a person will not develop the set of symptoms, including mental impairment, that is characteristic of PKU. However, scientific knowledge has led to a treatment. It was discovered that the recessive PKU gene prevents the normal metabolism of a substance that is common in food, making many normal foods toxic to the individual with two PKU alleles. A special diet that is low in the offending substance can prevent or minimize the nervous system damage that leads to the profound intellectual disabilities of untreated PKU individuals.
The example of PKU demonstrates that inherited (genetic) conditions can be treated—that knowledge of specific causation can result in effective treatment. This is an extremely important point both ethically and philosophically, because it is often misunderstood and misinterpreted.
Well over one hundred different genes are known for which relatively rare recessive alleles cause conditions that include severe mental impairment among their symptoms. The rapidly developing knowledge of basic genetic chemistry, from molecular genetics to biotechnology and the Human Genome Project, which produced a mapping of some 30,000 human genes early in the twenty-first century on April 15, 2003, holds out the hope that many more of these devastating genetic conditions may soon be treatable. As part of the Human Genome Project, genes for Huntington's disease and PKU have been identified and sequenced, though as yet no new therapies have been developed for these disorders.
In spite of these clear scientific successes related to Mendelian genetic-pattern disorders, many human traits—including normal traits, as well as somatic, behavioral, and psychiatric disorders—have not exhibited clear Mendelian patterns of inheritance. For those traits, an extension of Mendel's work to quantitative traits that was first developed by Sir Ronald Fisher, has been used extensively. Beginning in the 1990s, an additional, more molecular, set of techniques was developed to examine possible influences of genetics on human behavior. These two broad approaches to studying the influences of nature and nurture in psychiatry are termed quantitative (or epidemiological) and molecular. A brief summary of the two approaches is presented here, including some examples of their results and their problems (an overview of them can be found in Neiderhiser and in Schaffner , and a systematic analysis is presented in Behavioral Genetics by Plomin et al.).
QUANTITATIVE METHODS. Quantitative, or epidemiological, methods are utilized to distinguish genetic and environmental contributions to quantitative traits or features of an organism, as well as to assess correlations and interactions between genetic and environmental factors that account for differences between individuals. These methods do not examine individual genes, but report on proportions of differences in traits due to heredity or environment, or to their interactions, broadly conceived. The methods include family, twin, and adoption studies. Adoption studies examine genetically related individuals in different familial environments, and thus can prima facie disentangle contributions of nature and nurture. Twin studies compare identical and fraternal twins, both within the same familial environment and (in adoption studies) in different familial circumstances.
Twin studies have been used extensively in psychiatry to indicate whether a disorder is genetic or environmentally influenced, and to what extent. Twin studies make several assumptions to analyze gathered data, including that the familial environment is the same for twins raised together but different for twins raised apart, an assumption called the equal environments assumption. Though critics of genetic influence often question this assumption empirical studies have confirmed it (Kendler et al.). The example of schizophrenia may help make some twin results clearer. Employing what are termed concordance studies of twins, Gottesman and his associates have reported over many years that the risk of developing schizophrenia if a twin or sibling has been diagnosed with the condition is about 45 percent for monozygotic (MZ) twins, 17 percent for dizygotic (DZ) twins, and 9 percent for siblings (Gottesman and Erlenmeyer-Kimling). This concordance pattern supports what is called a non-Mendelian polygenic (many genes) quantitative trait etiology for schizophrenia with a major environmental effect (> 50%), i.e., more than half of the differences in liability to schizophrenia among individuals is due to environmental factors. Twin studies can also be used to estimate the heritability of a trait or a disorder, which for schizophrenia is about 80 percent. Heritability is a technical term, one that is often confusing even to experts, and one which only loosely points toward the existence of underlying genetic factors influencing a trait. Investigators note that "it does not describe the quantitative contribution of genes to … any … phenotype of interest; it describes the quantitative contribution of genes to interindividual differences in a phenotype studied in a particular population" (Benjamin et al., p. 334). If there are no interindividual differences in a trait, then the heritability of that trait is zero—leading to the paradoxical result that the heritability of a human having a brain is virtually zero. Heritability is also conditional on the environment in which the population is studied, and the heritability value can significantly change if the environment changes.
Keeping these caveats in mind, heritability estimates for many major psychiatric disorders appear to be in the 70 to 80 percent range, and personality studies indicate heritabilities of about 30 to 60 percent for traits such as emotional stability and extraversion, suggesting that these differences among humans are importantly genetically influenced. But even with a heritability of schizophrenia of about 80 percent, it is also wise to keep in mind that approximately 63 percent of all persons suffering from schizophrenia will have neither first- nor second-degree relatives diagnosed with schizophrenia, reinforcing the complex genetic-environmental patterns found in this disorder.
Twin studies were also the basis of a distinction between shared and nonshared environments. The meaning of environment in quantitative genetics is extremely broad, denoting everything that is not genetic (thus environment would include in utero effects). The shared environment comprises all the nongenetic factors that cause family members to be similar, and the nonshared environment is what makes family members different. Remarkably, quantitative genetics studies of normal personality factors, as well as of mental disorders, indicate that of all environmental factors, it is the nonshared ones that have the major effect. A meta-analysis of forty-three studies undertaken by psychologists Eric Turkheimer and Mary Waldron in 2000 indicated that though the nonshared environment is responsible for 50 percent of the total variation of behavioral outcomes, identified and measured nonshared environmental factors accounted for only 2 percent of the total variance. Turkheimer infers that these nonshared differences are nonsystematic and largely accidental, and thus have been, and will continue to be, very difficult to study (Turkheimer, 2000). This possibility had been considered in 1987 by Robert Plomin and Denise Daniels but dismissed as a "gloomy prospect"—though it looks more plausible.
Epidemiological investigations have also identified two important features of how genetic and environmental contributions work together. The first, genotype-environment correlation (G E), represents possible effects of an individual's genetics on the environment (e.g., via that individual's evoking different responses or selecting environments). Such effects were found for both normal and pathological traits in the large Nonshared Environmental Adolescent Development (NEAD) study, described in detail in the 2000 book The Relationship Code, written by David Reiss and colleagues. Secondly, different genotypes have different sensitivities to environments, collectively called genotype×environmental interaction (G×E). Differential sensitivity is important in many genetic disorders, including the neurodevelopmental models of schizophrenia genetics and in a recent study on the cycle of violence in maltreated children (discussed later).
MOLECULAR METHODS. Classical quantitative or epidemiological studies can indicate the genetic contributions to psychiatric disorders at the population level, but they do not identify any specific genes or how genes might contribute (patho) physiologically to behavioral outcomes. According to psychiatric geneticist Peter McGuffin and his colleagues, "quantitative approaches can no longer be seen as ends in themselves," and the field must move to the study of specific genes, assisted by the completed draft versions of the human genome sequence (McGuffin et al., p. 1232). In point of fact, a review of the recent literature indicates that most research in behavioral genetics, and especially in psychiatric genetics, has taken a "molecular turn."
It is widely acknowledged that most genes playing etiological and/or pathophysiological roles in human behaviors, as well as in psychiatric disorders, will not be single locus genes of large effect following Mendelian patterns of the Huntington's and PKU type discussed earlier. The neurogeneticist Steven Hyman notes that mental disorders will typically be heterogeneous and have multiple contributing genes, and likely have different sets of overlapping genes affecting them. Mental disorders will thus be what are called complex traits, technically defined as conforming to non-Mendelian inheritance patterns.
There are two general methods that are widely used by molecular behavioral and molecular psychiatric geneticists in their search for genes related to mental disorders: (1) linkage analysis, and (2) alleleic association. Linkage analysis is the traditional approach to gene identification, but it only works well when genes have reasonably large effects, which does not appear to be the case in normal human behavior or in psychiatry. Allelic association studies are more sensitive, but they require "candidate genes" to examine familial data. An influential 1996 paper by statisticians Neil Risch and Kethleen Merikangas urged this strategy.
Studies in schizophrenia are again illustrative of these approaches, as are the Alzheimer's disease genetic studies reviewed later. Though there was an erroneous 1988 report of an autosomal dominant gene for schizophrenia on chromosome 5 that is seen as a false positive, evidence has been accumulating for genes or gene regions of small effect related to schizophrenia on many chromosomes, including 1q, 2, 3p, 5q, 6p, 8p, 11q, 13q, 20p, and 22q (Harrison and Owen). Replication difficulties with these results in different populations of schizophrenics and their families have been a recurring problem, however.
Environmental Research and the Envirome
It is clear from epidemiological studies that more than half the variance of typical behavioral traits, as well as half of the liability for psychiatric disorders (including schizophrenia), is environmental. This has fueled major searches for various environmental causes. In schizophrenia, this work has been reviewed by Ming Tsuang and his colleagues, who note that the major environmental risk factors in schizophrenia are due to the nonshared environment. These include problems in pregnancy (e.g., pre-eclampsia) and obstetric complications, urban birth, winter birth, and maternal communicational deviance. Thus far, identified predisposing environmental factors have small values in comparison with genetic risk factors. Using a term coined in 1995 by James C. Anthony, Tsuang et al. have proposed that the entire envirome needs to be searched for extragenetic causes of disorders, including schizophrenia. These factors are believed to affect susceptible genotypes, involving G×E interactions.
Though evidence for susceptibility genes for major mental disorders continues to accumulate, there has been no strongly replicated result that might be used in diagnosis or in early detection and prevention interventions. Of all the psychiatric disorders that have been investigated to date by genetic strategies, only Alzheimer's disease (AD) provides both a classical Mendelian etiological picture and complex trait patterns, and thus can function as a concrete prototype for psychiatric genetics and for research on genetic influences on human behavior in general. There are three Mendelian forms of early-onset AD, due to dominant mutations in genes APP, PS1, and PS2. The strongly replicated APOE4 locus associated with late-onset Alzheimer's disease (LOAD), in contrast, is a susceptibility gene, neither necessary nor sufficient for the disease. The APOE4 and APOE2/3 alleleic forms also interact with other genes and with the environment. APOE alleles 2 and 3 appear to protect individuals with the APP mutation (Roses). Other susceptibility genes for LOAD continue to be investigated. a possible locus on chromosome 12 has been identified, and one was reported in 2000 on chromosome 9 (Pericak-Vance et al.; Roses).
Cognitive Abilities and Intelligence
Though there are more data about the inheritance of intelligence than about any other complex behavioral characteristic of humans, the word intelligence is viewed even by the proponents of IQ testing as misleading because it has too many different meanings. IQ researchers seem to prefer to use the expression "general cognitive ability," represented by the letter g (Jensen; Plomin, DeFries, et al., 2001). The notion of substantial genetic influences on individual variation in g or "intelligence" remains controversial even after almost a century of investigation.
Most investigators in behavioral genetics view the level of intellectual functioning (abstract reasoning, ability to perform complex cognitive tasks, score on tests of general intelligence, IQ) as a strongly heritable trait. In 1963, psychologists Nikki Erlenmeyer-Kimling and Lissy Jarvik summarized the literature dealing with correlations between the measured intelligence of various relatives. After eliminating studies based on specialized samples or employing unusual tests or statistics, they reviewed eighty-one investigations. Included were data from eight countries on four continents spanning more than two generations and containing over 30,000 correlational pairings. The overview that emerged from that mass of data was unequivocal. Intelligence appeared to be a quantitative polygenic trait; that is, a trait influenced by many genes, as are such physical characteristics as height and weight.
The results did not suggest that environmental factors were unimportant, but that genetic variation was quite important. The less sensitive trait of height (or weight) can be used to illustrate this distinction. It is well known that an individual's height can be influenced by nutrition, and inadequate diets during development can result in reduced height. The average height of whole populations has changed along with changes in public health and nutrition. Yet at the same time, individual differences in height (or weight) among the members of a population are strongly influenced by heredity. In general, taller people tend to have taller children across the population as a whole, and the relative height of different people is strongly influenced by their genes. This also appears to be the case with intelligence. The Erlenmeyer-Kimling and Jarvik survey data suggest that about 70 percent of the variation among individuals in measured intelligence is due to genetic differences. The remaining 30 percent of the variation is due to unspecified (and still unknown) environmental effects.
Two decades later, in 1981, Thomas Bouchard and Matt McGue at the University of Minnesota also compiled a summary of the world literature on intelligence correlations between relatives. They summarized 111 studies, 59 of which had been reported during the seventeen years since the Erlenmeyer-Kimling and Jarvik review. Bouchard and McGue summarized 526 familial correlations from 113,942 pairings. The general picture remained the same, with roughly 70 percent of normal-range variation attributable to genetic differences and about 30 percent due to environmental effects.
However, researchers examining the behavioral genetics of cognitive ability estimate the heritability of g (or IQ) as substantially lower, about 30 to 35 percent. Statisticians Bernie Devlin, Michael Daniels, and Kathryn Roeder argue that the much of the difference between the high and low heritabilities can be accounted for by a substantial maternal environmental component. As in the height and weight example above, there is also a substantial general environmental component that increased IQ scores by about 30 points between 1950 and 2000. This is known as the Flynn effect (see Flynn).
Robert Plomin and colleagues have attempted to identify specific genes or gene regions, also known as quantitative trait loci (QTLs), that influence IQ. Though there has been one publication reporting an IQ-related gene (see Plomin, Hill, et al.), replication has not yet been forthcoming.
Much is known about the genetics of mental retardation and learning disabilities. The most common single causes of severe general learning disabilities are chromosomal anomalies (having too many or too few copies of one of the many genes that occur together on a chromosome). These genes may reside on additional chromosomes, for example trisomy 21 (an extra chromosome 21, or three instead of the normal two) is the cause of Down's syndrome, and the "fragile X" condition may by itself account for most, if not all, of the excess of males among people with severe learning disabilities (Plomin, DeFries, et al., 2001). A large number of rare single-gene mutations, many of them recessive, induce metabolic abnormalities that severely affect nervous system function and thus lead to mental retardation. Because the specific alleles involved are individually rare and recessive, such metabolic abnormalities can cause learning-disabled individuals to appear sporadically in otherwise unaffected families. The new field of molecular genetic technology holds a promise of future therapeutic regimens for many learning disabilities.
Dimensions of personality tend to be familial (Benjamin et al.). Modern studies of twins and adoptees suggest that for adults, some major dimensions are influenced by differences in family environments, while some are not. For the dimension of extroversion, which encompasses such tendencies as sociability and impulsivity, genetic factors account for about 30 to 60 percent of the variation among adults, with about 50 percent of the variation being environmental in origin.
But, surprisingly, none of the variation among adults appears to be related to environmental differences within families.
For neuroticism, which taps such traits as anxiousness (a characteristic state of anxiety), emotional instability, and anxious arousability (a tendency to react with anxiety to events), about 40 percent of the adult variation appears to be caused by genetic differences, and again none of the variation is from environmental differences that are shared by members of the same family. In contrast, social desirability, which measures a tendency to answer questions in socially approved ways and to want to appear accepted by and acceptable to society, does not show evidence of genetic causation. Essentially all of the measurable variation in social desirability appears to be environmental, with about 20 percent due to family environment.
Some authors, including Robert Plomin and colleagues, the authors of Behavioral Genetics (2001), suggest that because extroversion and neuroticism are general factors involved in many other personality scales or dimensions, most of the others also show moderate genetic variation. For example, a twin study involving eleven personality scales found genetic influence of various degrees for them all (Tellegen et al.). On average, across the eleven personality scales, 54 percent of the variation was attributable to genetic differences among the people, and 46 percent to environmental differences.
Tendencies toward affective (mood) disorders, including psychotic depression and bipolar disorder type I (manic depression), also are clearly influenced by genetics. A lack of familial co-occurrence has established the separateness of schizophrenia from the affective psychoses. Unipolar depression and bipolar affective disorder do co-occur, and there may be a genetically influenced major depressive syndrome distinct from manic depression. The affective disorders probably include a diversity of genetic conditions.
Although data are sparse for many traits, modern studies are revealing genetic involvement in many conditions of importance to society. Plomin and colleagues point out that, for males, the best single predictor of alcoholism is alcoholism in a first-degree biological relative. Alcoholism clearly runs in biological families. Severe alcoholism affects about 5 percent of males in the general population, but among male relatives of alcoholics the incidence is about 25 percent. The incidence remains about the same for adopted-away sons of male alcoholics. However, biological children of nonalcoholics are not at increased risk for alcoholism when raised by alcoholic adoptive parents.
Behavioral and psychiatric geneticists have studied genetic influence on antisocial behavior and adult criminality. Studies tend to report that shared environment is more important as a cause in juveniles and that genetics plays more of a role in adults (Lyons et al.). These studies have been extremely contentious, however (Wasserman and Wachbroit). Since the early 1990s several molecular studies of genetics and violence have also emerged, two of which are cited here. In 1993 Hans Brünner and his group reported on a Dutch family with a missing gene on the X chromosome which governed the monoamine oxidase A (MAOA) enzyme, an enzyme that metabolizes some key neurotransmitters (Brünner et al.). The Dutch families' males exhibited an unusual number of antisocial behaviors of varied sorts (assaults, rape, arson, etc.). Males, lacking a second X chromosome, were more vulnerable to the effects of this mutation. The mutation was subsequently determined to be extremely rare, and behavioral geneticists largely lost interest in the MAOA gene. In August 2002, however, a major study involving about 1000 New Zealand families found that a less severe MAOA gene mutation had a significant effect on males' display of antisocial behaviors, including their being convicted for violent offenses (Caspi et al.). But the antisocial behaviors only appeared in those subjects (in as much as 85% of them) who had experienced abuse during childhood, indicating an important G × E interaction effect of gene with environment. This carefully designed study is yet to be replicated, but it has received widespread attention.
Both twin and adoption studies that indicate obesity is highly heritable, probably about 70 percent (Grilo and Pogue-Geile). In addition, a large adoption study of obesity among adults found that family environment by itself had no apparent effect—in adulthood, the body mass index of the adoptees showed a strong relationship to that of their biological parents, but there was no relationship between weight classification of adoptive parents and the adoptees. The relation between biological parent and adoptee weight extended across the spectrum, from very thin to very obese. Once again, cumulative effects of the rearing home environment were not important determinants of individual differences among adults (Stunkard et al.).
Philosophical and Theoretical Perspectives
Biologists, psychologists, and philosophers have engaged in high-level theorizing about the effects of genes on traits in general and on human behavior in particular. Perhaps the most vigorous and ongoing discussion has been generated by a variety of papers and books that can be loosely characterized as a "developmentalist challenge" to the separability of genetic and environmental contributions to an organism's features (Schaffner, 1998). Over the years, the biologist Richard Lewontin's views have been particularly influential in this regard. Similar views critical of an overemphasis of genetic influence on traits have been articulated by several other scholars (see Cycles of Contingency , by Susan Oyama, Paul Griffiths, and Russell Gray, which presents a number of contributions to "developmental systems theory" [DST]). Thus far, DST has largely been directed at critiquing DNA priority in molecular developmental and evolutionary claims, and at recommending more epigenetic-driven research. It is conceivable that as DST develops further, it will be applied more specifically to the relation of nature and nurture in a number of psychiatric disorders.
Some recent articles suggest that research integrating quantitative and molecular approaches with neuroscientific strategies will be the most fruitful way to provide a framework for genetic and environmental effects on organisms. Reiss and Neiderhiser recommend an "integrated" approach. In their 1991 book Schizophrenia Genesis, Irving Gottesman and Dorothea Wolfgram envision the future promise of neuroscience programs to assist progress in schizophrenia. The increasingly important neurodevelopmental perspective approach to schizophrenia has been championed by Tsuang and colleagues and implemented in recent papers from the Pittsburgh group (Mirnics et al.). In addition, a series of ethical issues have arisen in neuroscience that mirror many of those first generated by behavioral genetics, including issues of reduction, determinism, and responsibility. A new term, neuroethics, has been coined to describe these issues (Marcus).
The completion of the draft mapping of the human genome has led to a realization that the next stage of inquiry into examining human behavioral traits, and both somatic and mental disorders, will need to be very complex, involving functional genomics, proteomics (the study of proteins and their effects) (Pandey and Mann), and enviromics (Anthony). These will be difficult and complex projects that will also need to attend carefully to developmental issues, since most human diseases, including psychiatric disorders, probably represent the culmination of "lifelong interactions between our genome and the environment" (Peltonen and McKusick, p. 1228). Animal models will be helpful here, as will new technologies using DNA genetic chips, also known as microarrays.
There are diverse methodological approaches to studying the effects of genetics on human behavior and in relation to psychiatric disorders. The working out of the partitioning of genetic and environmental causes and their interactions at multiple levels of aggregation in complex systems, as humans are, will require many research programs extending over many years, hopefully producing a number of useful interim results such as those discussed above. These results, however, will not silence the continuing debates over the roles that genes and environments play in the complex choreography of organism development and behaviors.
glayde whitney (1995)
revised by kenneth f. schaffner
SEE ALSO: Genetic Counseling, Ethical Issues in; Genetic Counseling, Practice of; Genetic Engineering, Human; Genetics and Environment in Human Health; Genetics and Human Self-Understanding; Genetics and Racial Minorities; Genetics and the Law; Human Dignity; Human Nature;Privacy and Confidentiality in Research; and other Genetics and Human Behavior subentries
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