Nature and Nurture in Human Behavior and Development:A View of the Issues
Category : Complex Adaptive Systems, Evidence of Knowledge of Theory, Positive Accounting Theory, Problem Based Learning Scenario, Psychology, Study Leadership
Nature and Nurture
in Human Behavior and Development:
A View of the Issues
In June 2000, a breakthrough announcement was made about the completion of the mapping of the human genome (2001; 2001). Heralded as a major scientific accomplishment on its own, the implications of such knowledge for the creation of genetically based interventions for the amelioration and eradication of disease were immediately postulated.
Although it is quite possible that this scientific breakthrough can have a major influence on treatment of diseases such as diabetes, cancer, heart disease, and other physical ailments that run in families, the effect of identifying particular genes or set of genes implicated in human behavior and development is less clear (2002). What does it mean to find a gene or set of genes that are associated with ADHD, schizophrenia, or autism? Does everybody who has that gene mani-
fest the disease: Why or why not? Could it be easier to alter the environment that triggers the behavioral problem given the presence of that gene? Could we eradicate such diseases from our species through gene therapy? If multiple genes are involved in the manifestation of psychopathology, and if single genes are involved in the manifestations of many behaviors, could gene therapy have many unintended behavioral manifestations?
Perhaps more complicated are the implications of identifying genes that are associated with normal variation resulting in individual differences in, for example, temperament, aggression, shyness, intelligence, or activity level. Could we—and should we—eradicate from our genome, as individuals or as a species, genetic material that predisposes us to be too aggressive or too shy or less intelligent, or not active enough? Who has the political power and/or the moral authority to make those decisions? Who will have access to those interventions?
The premise of this book is that the complexity of the transactions between nature and nurture—between genes and the environment from the cellular to the cultural level—make these questions incredibly complex. Oversimplification of rules of how biology and environment operate in human behavior and development can lead to radically different understanding and implications for public policy.
From such simplistic views arise questions such as: “Is this particular behavioral trait biologically determined and, therefore, not amenable to environmental interventions?” or “How much does “genes versus environment” explain individual differences in a particular behavioral trait or developmental process?” ( 1958; 1997; 1997). Such questions risk splitting nature from nurture (1998), a split that seems illogical when one considers the data on environmental effects that influence human behavior and development. Such splitting can also lead to the misconception that genes are destiny or that of genetic programming is unresponsive to the environment.
In addition, as shown repeatedly by history, the danger of such oversimplificationis its potential impact on public policy and its ethical implications (1981; 1970; 1974;1992; 1984). For example, such simplistic notions of how human beings” behavior and development operate led in the past to eugenic laws that were designed to eradicate particular developmental deviations such as mental retardation or low IQ through selective breeding ( 1981; 1988). Thus, public policy interventions promoting genetic manipulations in certain populations identified as having a particular gene for an undesirable trait, or the lack of a public willingness to intervene if a genetic predisposition rather than environmental etiology has been identified, are two of the possible scenarios derived from this misunderstanding of the complex interplay between genes and the environment.
Fortunately, our current knowledge of biology, developmental systems, and the fused, or synthetic, interplay of environmental and biological influences on behavior and development can illuminate and guide our understanding of such processes
and influence the design of appropriate and useful public policies that are appropriate to derive from them (1997; 2002). Even at the cellular level, genetic codes are expressed within particular environmental circumstances, and alterations on those environments can lead to radically different phenotypic expressions from similar genetic material. Indeed, as explained in several chapters in this volume (), developmental systems theories and the research conducted within this framework suggest that genes and environments work together integratively in a complex and closely intertwined fashion. Consequently, theories of human behavior based entirely on either nature or nurture alone are likely to be counterfactual, and research predicated on such dichotomies will produce incomplete and possibly useless data.
However, though state-of-the-art knowledge is available, recent highly visible works (1998; 1994; 1999/2000) portray pretty simple ideas about the role of genetics in human behavior and development. Such a series of perspectives can have dangerous implications for our understanding of developmental mechanisms and result in public policies and practices that negatively impact society (2002).
Genes and the Promotion
of Positive Human Development: Hereditarian Versus Developmental Systems Perspectives
Many experimental biologists outside of the biomedical-industrial complex are just now coming (back) to grips with the facts of epigenesis; with the profound mystery that developmental biology is, with the poverty of gene programs as an explanatory device; and with a crisis defined by the realization that an increasingly deficient theory of developmental genetics is the only theory currently available. The question remains: if biologists are starting to learn this lesson, will the psychologists be far behind?
Genes are part of the developmental system in the same sense as other components (cell, tissue, organism), so genes must be susceptible to influence from other levels during the process of individual development.
Contemporary theories of human development are predicated on dynamic, relational, and systems perspectives (1998a, 1998b). The complexity of these theories can be daunting to scholars, both in regard to the conceptual difficulties involved in integratively understanding the multiple levels of organization fused
within the developmental system and in respect to the methodological challenges involved in using such theories as a frame for research.
If challenging to scholars, such theories are often seen as virtually impossible to grasp by nonspecialists. for instance, by the “Person in the Street” (to use the term suggested by Horowitz, 2000, p. 8), by media representatives, or by policy makers who influence the allocation of funds to programs aimed at promoting health and human development. These groups may gravitate to “single-variable stories” (2000) about human development—such as “genes cause behavior” (e.g., see Rushton, 1999)—to understand, communicate about, or support policies and programs to improve people's lives, respectively.
Such a simplistic—indeed a distortingly simplistic—alternative to developmental systems theories of human development is embodied in hereditarian views of behavioral development; that is, views that “split” nature from it relation to nurture ( 1998) and that reduce the complexity of the human developmental system to mechanistically acting genetic determinants (1986. 2000: 1994; 1999, 2000). Fields such as human sociobiology and behavior genetics are examples of such hereditarian positions. However, because it is often the case that sociobiologists ( 1999. 2000; 1980) claim that data derived from behavior genetics research pertinent to the concept of heritability provide key evidence in support of the validity of their ideas, behavior genetics constitutes an important sample case for the evaluation of hereditarian thinking. Accordingly, we may note the observations of (2000) in regard to the behavior genetics approach to theory and research about human development. (2000) indicated:
Against the media popularity of single-variable stories, the science itself is moving inexorably toward greater and greater data-driven, integrative theoretical complexity. An exception to this is behavioral genetics. In contrast to the dynamic nonlinear interactive models full of reciprocity between and among levels and variables, behavioral genetics presents a relatively non-dynamic linear additive model that tries to assign percentages of variance in behavior and development that can be attributed to genes. The enterprise rests on the assumption that genetic influence can be expressed as a value accounting for a portion of the variance in a nondynamic linear equation for predicting behavioral functioning and furthermore, that the individual experiences of shared and nonshared environments can be assessed inferentially by the degree of biological relatedness of individuals without empirical observations of experience (1991: 1993).
Behavioral genetics involves a relatively simplistic approach when compared with the kinds of dynamic systems theories currently being elaborated. Perhaps that is why. in the mode of wanting simple answers to simple questions, behavior genetic reports are so media attracting.
What then is the view of human development presented by behavior genetics? Why is this view not a viable, nature alternative to dynamic and integrative developmental systems conceptions of human development? What is the frame offered
by behavior genetics for application to public policies and social programs aimed at reducing or preventing the problems of young people or promoting their positive development? And, if behavior genetics fails as a useful model for understanding human development, what potential harm is done to the children, adolescents, and families of our nation if this instance of hereditarian thinking influences policies and programs? Can potential harm be counteracted by forwarding a developmental systems perspective as a frame for applications to policies and programs? To address these questions, it is useful to define the field of behavior genetics.
DEFINITION OF THE FIELD OF BEHAVIOR GENETICS
According to (2000), a prolific contributor to the behavior genetics literature, “Behavioural genetics is the genetic study of behaviour, which includes quantitative genetics (twin and adoption studies) as well as molecular genetics (DNA studies) of human and animal behaviour broadly defined to include responses of the organism from responses measured in the brain such as functional neuroimaging to self-report questionnaires” (1980) indicate that “behavioral genetics lies at the interface between genetics and the behavioral sciences” (p. 12), and Plomin (1986) notes that “behavioral geneticists explore the etiology of individuality, differences among individuals in a population (p. 5). He further explains that “the three basic methods used in human behavioral genetics are family, twin, and adoption studies” (p. 11).
Across all these methods, the goal of behavior genetic analysis is to separate (partition) the variation in a distribution of scores (e.g., for a personality trait, temperamental characteristic, or intelligence) into the proportion due to genes and the proportion due to the environment. Although behavior geneticists admit that genes and environments may be correlated and/or may interact, they most typically seek to compute a score (termed a “heritability coefficient”) that in its most frequently used form denotes the independent contribution of genetic variance to the overall differences in the distribution of scores for a given individual characteristic.
For such heritability scores to be meaningful, the methodologies of behavior genetics rest on a model of gene function that sees as possible genetic contributions that are independent of (not correlated or interactive with) the context within which genes exist. Genes, however, do not work in the way that behavior geneticists imagine.
Fatal Flaws in the Behavior Genetics Model of Gene Function
As illustrated in the epigraphs by (1993a) and (1992), as well as in the writings of other molecular geneticists 1998; 1984; 1988; 2001) and cell biologists (1997, 1998, 1999: 1988) more generally, mo-
lecular biologists do not place credence in the model of genetic function involved in behavioral genetics. In fact. Venter and his colleagues (2001). the group that successfully mapped the sequence of the human genome, emphasize that there are two conceptual errors that should not be made in the face of the advances they and other scientists are making in understanding the structure and functional consequences of the human genome. They stressed:
There are two fallacies to be avoided: determinism, the idea that all characteristics of the person are “hard-wired” by the genome: and reductionism. the view that with complete knowledge of the human genome sequence, it is only a matterof time before our understanding of gene functions and interactions will provide a complete causal description of human variability, ()
Contemporary thought in molecular genetics thus rejects the idea that genes are structures that act on supragenetic levels; instead, these scientists adopt the dynamic, developmental systems view noted in the epigraph by (1992: 1992; 1998b; 1997: . 1990. 1995. 1996, 1999a, 1999b; 1998; 1993: 1994, 1998). This view emphasizes the integration—or fusion—of genes with the other levels of organization that comprise the person and his or her context. In such dynamic systems, the specific features of the interactions of the processes associated with these multiple levels create both the individuality of behavior at any point in time and the integrated character of human functioning that gives behavior its generality and cross-time predictability (1978: 1993; 1998).
In essence, then, we have in the field of behavior genetics (1986. 2000; 1994) the use of a model of genetic structure and function that is specifically rejected by those scientists who study the action of genes directly. This rejection occurs because the field of behavioral genetics not only employs a counterfactual and scientifically atavistic conception of the role of genes in human development (1998; 1984; 1993a. 1993b:2001) but also because behavior genetics is a viewpoint with a conceptually flawed and empirically deficient view of developmental process and. as well, involves the conflation of description and explanation.
For instance, in regard to process, the structural account of genetic action behavior genetics offer suffers from the flaws of all structural accounts of development; that is, as explained by Thelen and Smith (1994. 1998:1993), such conceptions are inherently incomplete. These views do not explain individual behavioral performance (actions), other than to express empirically unsubstantiated confidence that in some way genetic structures translate— through the levels of cells, tissues, organs, the individual, and his or her actual context—into real-time actions.
For example, without any specification of the pathways of influence from genes to behaviors. (1994) asserted:
Genes can produce dispositions, tendencies, and inclinations, because people with subtly different nervous systems are differently motivated … [and] given enough environmental opportunities [for selection of environments], the ones chosen are those most reinforcing for a particular nervous system created by a particular genotype … the direction of the growth curve of development, and the limit ultimately attained, is set in the genes, ()
However, because behavior geneticists believe that genetic structure transcends and is independent of real-time actions, an adequate, empirically verifiable account of actual individual-in-context behavior is beyond theoretical range (1993). Moreover, because of the inability to explain individual performance of actual individual-in-context behavior, behavior genetics, like other structural theories ( 1993), cannot explain the global order of behavior or developmental change itself.
In turn, in regard to the conflation of description and explanation, behavior genetics describes variability in trait distributions in a specific sample and then explains the distribution it has observed by reference to a label it has applied to one (or the other) of the sources of the variability—genes or environment. Not only is this reification an instance of the nominal fallacy, but—to paraphrase the parody of structural explanations presented by (1993)—the cause of the distribution of interindividual differences in a trait distribution is merely an abstract description of the trait distribution itself: Behavior genetics describes the variability in a distribution, labels it with a fancy source term (i.e., heritability), and then imputes that there is a gene, or set of genes, that explains the distribution.
To illustrate, (1994) notes that “understanding the growth and development of a single individual has been confused with understanding the origin of different traits in a population” (). However, this confusion about the distinction between interindividual differences and intraindividual change, as well as the problem of the conflation of description and explanation, exists in behavior genetics. On the basis of heritability data, writers such as Rowe seamlessly slide from talking about descriptive sources of variation within a trait distribution into talking about the genetic basis of individual development, that is, about the “causal influence on such child outcomes as intelligence, personality, and psychopathology” ().
One key basis of the lack of an adequate treatment in behavior genetics of performance, of developmental sequence and process, as well as of the distinction between description and explanation, is that these conceptual problems are coupled in behavior genetics with a lack of an adequate theoretical understanding both of supragenetic intraorganism processes (1991a, 1991b, 1992, 1997;1998) and of extraorganism contextual or ecological processes (1994; 2000;1997; 1999a, 1999b; 1983; 1998). Accordingly, behavior genetics fails to adequately measure the environment, or ecology (Hoffman, 1991) of human development. In short, to paraphrase (1980), in his discussion of (1979) account of the scientific fraud be-
havior geneticist perpetrated regarding the study of the heritability of intelligence, behavior geneticists have methods that give them a lot of numbers but very little sensible or useful data about human development.
BEHAVIOR GENETICS AS THE EMPEROR'S NEW CLOTHES
That these egregious conceptual and methodological problems exist is not news, not even in psychology. ( 1970, 1976a, 1976b. 1990a. 1990b. 1997a. 1997b) has written repeatedly about these problems for about a quarter of a century, and (1956, 1957). (1967, 1970, 1976), (1953. 1970). (1981; 1984; 1968) (1970. 1983, 1992), (1979, 1989; 1994). (2000). (1992). (1993, 2000), (1978, 1984, 1986, 1991). (1997): (1999a, 1999b; 1998), (1998). and(1994, 1998; 1993) have contributed consonant commentaries both prior to and during the period of Hirsch's still ongoing work.
Yet, despite this criticism by theircolleagues in the field of psychology, as well as by the lack of credence given to behavior genetics by molecular geneticists—as well as by eminent population geneticists (1975) and evolutionary biologists (1981, 1996)—many psychologists continue to act as if behavioral genetics provides evidence for the inheritance of behaviors as varied as intelligence (1969, 1998), parenting ( 1992). morality (1975). temperament (1984), television viewing (1990), and even the role in human development of the environment (1998; 1986. 2000; 1987; 1994)! It should be noted that “environment” is the too general, and now outmoded, term used by behavior geneticists to refer to the integrated, multilevel context, or the ecology, involved in the dynamic system of person-context relations that characterizes human development (1979, 1994: 1998; 1998).
The breadth and depth of these continuing criticisms of behavior genetics have been somewhat invisible or, at least, ignored by (2000). who claimed that “The controversy that swirled around behavioural genetics research during the 1970s has largely faded. During the 1980s and especially during the 1990s, the behavioural sciences became much more accepting of genetic influence” ().
This view is wrong in at least two ways. First, the controversy regarding the legitimacy of behavioral genetics—both as a conceptual frame for understanding the role of genes in behavioral development and as a methodology for studying the role of genes in behavioral development—has not diminished at all. One need only note the controversy associated with the publication of The Bell Curve (1994; 1995: 1997a) or the criticisms leveled at the hereditarian views of (1996. 1997a. 1997b. 1999: 1992a, 2002). which rely heavily on information de-
rived from behavior genetics, to recognize that (2000) “declaration of victory” is an inadequate attempt to either ignore or deny the persisting flaws of behavior genetics theory and method identified by scientists from numerous disciplines (e.g., see the critiques published throughout the 1990s and into the twenty-first century by 2000; 1997; 1997a, 1997b; 1993, 2000; 1992; 2000; Peters, 1995; 1993a, 1993b; 1996, 1997a, 1997b).
To illustrate, in a critique of the explanatory model and method associated with behavior genetic analyses of parent behaviors and of the effects of parenting on child and adolescent development, (2000) noted:
Large-scale societal factors, such as ethnicity or poverty, can influence group means in parenting behavior—and in the effects of parenting behaviors—in ways that are not revealed by studies of within group variability. In addition, highly heritable traits also can be highly malleable. Like traditional correlational research on parenting, therefore, commonly used behavior-genetic methods have provided an incomplete analysis of differences among individuals,
Accordingly, (2000) concluded:
Whereas researchers using behavior-genetic paradigms imply determinism by heredity and correspondingly little parental influence (1994), contemporary evidence confirms that the expression of heritable traits depends, often strongly, on experience, including specific parental behaviors, as well as predispositions and age-related factors in the child,
Second, Plomin rewrites history by stating that it was not until the 1990s that behavioral science accepted the role of genes in behavioral development. For well more than a half century (1958; 1935; 1945a, 1945b; 1956, 1957), genes have been accepted as part of the developmental system that propels human life across time. The issue is not the one that Plomin points to, then, that of accepting that genes are involved in development. Instead, the issue is how do genes contribute to development. (2000) approach and that of other behavior geneticists (1994) involves a split, nature-reductionist treatment of this issue (1998). Most contemporary developmental scientists take an integrated, relational developmental systems approach to the issue (1998a, 1998b; 1998).
In fact, (2000) conceptually approaches the vacuity of the behavior genetics approach, at least as it has been pursued through the twentieth century. Although he maintains that “twin and adoption research and genetic research using nonhuman animal models will continue to thrive” in the twenty-first century ( perhaps admits to the serious flaws in this approach to understanding the role of genes in behavioral development when he acknowledges that “the greatest need is for quantitative genetic research that goes beyond heritability, that is.
beyond asking whether and how much genetic factors are important in behavioral development (p. 31). Moreover, he then goes on to ask a series of important questions about the role of genes in behavioral development: “How do genetic effects unfold developmentally? What are the biological pathways between genes and behaviour? How do nature and nurture interact and correlate?” (p. 31). Unfortunately, he seeks answers to these questions through the flawed model and methods of behavior genetics and never explores the potential usefulness of developmental systems approaches. Nevertheless, such exploration would be very useful because Plomin admits that it would be a major mistake:
To think that genes determine outcomes in a hard-wired, there's-nothing-we-cando-about-it way. For thousands of rare single-gene disorders, such as the gene on chromosome 4 that causes Huntington's disease, genes do determine outcomes in this hard-wired way. However, behavioral disorders and dimensions are complex traits influenced by many genes as well as many environmental factors. For complex traits, genetic factors operate in a probabilistic fashion like risk factors rather than predetermined programming, (p. 33)
Thus, ultimately, (2000) admits that a probabilistic, nature-nurture relation is involved in accounting for the role of genes in behavioral development. Still, his views about single-gene disorders reflect an ahistorical conception of such problems of human development. That is, in respect to other such single-gene disorders, for example, as involved with phenylketonuria (PKU), genetic research has found means to counteract the problems produced by the genetic inheritance and has thus shown that a hard-wired genetic influence is not that hard-wired after all ( I980a, 1980b). As such. Plomin maintains a narrow view of the probabilistic developmental system; it apparently does not include the ingenuity of scholars who capitalize on the plasticity within the developmental system to demonstrate that what might seem to be hard-wired is in reality amenable to change as a consequence of the embeddedness of genes within a dynamic system. Nevertheless, in admitting to the importance of a probabilistic system in behavioral development, (2000) is in actuality defeating his own split approach to the nature and nurture of behavioral development.
Moreover, other scholars are not as convinced as is (2000) that the various methodologies he associates with behavior genetics will generate useful data. For example (2000) noted:
One criticism is that the assumptions, methods, and truncated samples used in behavior-genetic studies maximize the effects of heredity and features of the environment that are different for different children and minimize the effects of shared family environments … A second criticism is that estimates of the relative contributions of environment and heredity vary greatly depending on the source of data … heritability estimates vary considerably depending on the measures used to assess similarity between children or between parents and children … The sizable variability in estimates of genetic and environmental contributions depending on the
paradigms and measures used means that no firm conclusions can be drawn about the relative strength of these influences on development,
Similarly, and again counter to (2000) assertion that the controversy surrounding behavior genetics faded by the 1990s, in 2000, noted:
One sees increasing skepticism about what is to be learned from assigning variance percentages to genes … The skepticism is informed by approaches that see genes, the central nervous system and other biological functions and variables as contributors to reciprocal, dynamic processes which can only be fully understood in relation to sociocultural environmental contexts. It is a perspective that is influenced by the impressive recent methodological and substantive advances in the neurosciences. (p. 3)
The cutting-edge study of the neurosciences within the developmental systems perspective noted by (2000) is exemplified by the work of (1997, 2000; ) who sought to identify how genes and context fuse within the developmental system. Because of the close genetic similarity of rhesus moneys to humans, he studied such organisms as a means to provide a model for the investigation of this system. In one recent instance of this long-term research program, (2000; ) found that young rhesus monkeys show individual differences in their emotional reactivity (or “temperament”). Some young monkeys are highly reactive; for example, they become quite excited and agitated when they experience environmental stress, for instance, separation from their mothers; other monkeys show low reactivity in such situations, for instance, they behave calmly in the face of such separation. (2000;) discovered that these individual differences in behavior are associated with different genetic inheritances related to the functioning of serotonin, a brain chemical involved in neurotransmission and linked to individual differences in such conditions as anxiety, depression, and impulsive violence.
Accordingly, to study the interrelation of serotonergic system genes and environmental influences on behavioral development, (2000; ) placed high or low reactivity rhesus young with foster rhesus monkeys that were also either high or low in emotional reactivity. When young monkeys with the genetic inheritance marking high reactivity were reared for the first six months of life with a low reactivity mother, they developed normally and, despite their genes, did not show high reactivity even when removed from their foster mothers and placed in a group of peers and unknown adults. In fact, these monkeys showed a high level of social skill; for example, they took leadership positions in their group. However, when young monkeys with this same genetic marker for high reactivity were raised by high reactivity foster mothers, they did not fare well under stressful conditions and proved socially inept when placed in a new social group.
Moreover, (2000; ) found that the interaction between the serotonin transporter genotype and early experience not only influences rhesus monkey behavior but, as well, brain chemistry regarding the use of seroto-
nin. Despite have a high reactivity genotype, the monkeys whose early life experiences were with the low reactivity foster mothers had brain chemistry that corresponded to monkeys with a low reactivity genotype. Accordingly.(2000) concluded:
The recent findings that specific polymorphisms in the serotonin transporter gene are associated with different behavioral and biological outcomes for rhesus monkeys as a function of their early social rearing histories suggest that more complex geneenvironment interactions actually are responsible for the phenomenon. It is hard to imagine that the situation would be any less complex for humans.
THE CONCEPTUAL FRAMES
PROVIDED BY BEHAVIOR
GENETICS AND DEVELOPMENTAL SYSTEMS FOR HUMAN
The purported uses for applications to policies and programs pertinent to human development of behavior genetics rest on the secondary (or even epiphenomenal) role assigned within this perspective to the ecology of human development in contributing to the causal bases of individual functioning. If context is not of primary significance in the determination of behavior and development, then any policies or programs aimed at enhancing the context of human development (e.g., prevention programs pertinent to youth risk behaviors or policies aimed at changing the family, school, or community experiences of poor children to promote their positive life chances) would be at best of only secondary importance. If context is, however, not at all causal—or if purported contextual influences on human development are seen as only illusory or epiphenomenal influences that can be reduced completely to genetic influences (1994; 1999, 2000)—then attempts to change the context to enhance human development are irrelevant, misguided, and wasteful exercises. They could be construed, in fact, as inhumane exercises that falsely elevated the hopes of people whose problematic plights were due not to their social circumstances (e.g., social injustice or the absence of opportunity, equity, or democracy) but rather to their fixed and immutable genetic inheritances.
Such a view of the impotence of the ecology of human development as a source of plasticity in behavior would result then in applications directed to the only causal source of variance in human development, that is, genetic ones. If the genes that caused the problems afflicting the human condition could not be changed through antenatal repair, then the only policies and programs that would make scientific and societal sense would be ones aimed at, in the short term, diminishing the chances of possessors of the problematic genes from reproducing and thus passing their affliction onto another generation (1940a.
1940b, 1943a, 1943b;cf. 1981, 1996; 1992a; 1988). The long-term, or final, policy or program solution would be the elimination of the genes from the human genetic pool. The view of context associated with hereditarian conceptions (1994: 1999. 2000) contrast significantly with the fused conception of person and context variables found in developmental systems perspectives about the bases of human development (2002).
The Dynamic, Developmental Systems “Alternative” to Behavior Genetics
The developmental process envisioned in the dynamic developmental systems perspective stands in marked contrast to the hereditarian view of developmental process found in behavior genetics. As (1992) explained, in a developmental systems view of process, the key “conception is one of a totally interrelated, fully coactional system in which the activity of genes themselves can be affected through the cytoplasm of the cell by events originating at any other level in the system, including the external environment” (). As such. (1992, 1997) and other developmental systems theorists (1998) emphasized that neither genes nor context by themselves cause development. The fusion among levels within the integrated developmental system means that relations among variables—not splits between nature and nurture—constitute the core of the developmental process.
Accordingly, although hereditarians argue that biological contributions are isomorphic with genetic influences (1999), this equivalence is not seen as veridical with reality from the perspective of developmental systems theory. For instance, although some hereditarians see constitutional variables (e.g. relating to brain volume, head size, size of reproductive organs, and stature) as all based on heredity (1999), within developmental systems:
“Constitutional” is not equivalent to “genetic. ” and purposely so. Constitutional includes the expressed functions of genes—which, in themselves require some environmental input—but constitutional includes the operations of the central nervous system and all the biological and environmental experiences that impact organismic functioning and that make constitutional variables part of the dynamic change across the life span as they affect the development of and the decline of behavior. (2000)
In short, developmental science and developmental scientists should stop engaging in the pursuit of theoretically anachronistic and counterfactual conceptions of gene function. Indeed, significant advances in the science of human development will rest upon embedding the study of genes within the multiple, integrated levels of organization comprising the dynamic developmental system of person-context relations.
As (1994, 1998; 1993) noted, pursuing this dynamic interactionist. developmental systems perspective will surely be an ardu-
ous path, one likely filled with conceptual and empirical difficulties, mistakes, and uncertainties. Nevertheless, there is more than sufficient reason to continue to pursue this approach to behavioral development.
First, the nature-mechanistic approach of behavior genetics fails completely as an adequate theoretical or empirical approach to understanding human development. Second, and to paraphrase the epigraph by (1993) that opened this paper, we have no better option available than to pursue a dynamic developmental systems approach. And third, great progress is being made. To appraise this progress it is useful to return again to the ideas of (2000).
The Contributions of
Horowitz to Understanding the Importance
of Developmental Systems Theories
Summarizing the status at the beginning of the twenty-first century of theory and research pertinent to developmental systems perspectives, Horowitz (2000) noted that there exists:
extremely important information about structural plasticity in neuro-psychological function. Most critically, this structural and functional plasticity across developmental time is being tied directly to the amplifications and constraints of the social/cultural contexts that determine the opportunities that children and adults have to experience and to learn, (p. 3)
To help frame these data, (2000) introduced a model of the dynamic developmental system that she notes corresponds to those of other developmental systems theorists (e.g., 1998; 1998a, 1998b). As such, indicated:
In this model, as in some of the others, the assumption is made (supported by data) that from the moment of conception development is influenced by constitutional, social, economic and cultural factors and that these factors, furthermore, continue in linear and nonlinear relationships, to affect development across the life span, with development broadly defined to accommodate both the increase and decrease in ability and function, (p. 4)
Moreover, in the context of presenting her model of the human developmental system, (2000) compared the approach to developmental analysis represented by hereditarian approaches to behavior development, such as behavior genetics, with the approach pursued in the sorts of theories represented in her model. While recognizing the attractiveness to the “average person” and the media of the simplistic answers provided by nature-oriented theorists, (2000) observed:
The conundrum for many is to explain the regularities of the postnatal emergence of the normal universal species-typical behaviors in each individual child despite the
seeming variations in the gross nature of environments. The nativists answer is recourse to instincts, to predetermined, architecturally and genetically driven explanations both for the species as a whole and for the individuals in particular (1965; 1994; 1992: 1998). To the Person in the Street these explanations seem to provide the simple answers to simple questions though the nativist position is by no means simplistic and the position is often supported by very interesting data.
The alternative view and, I believe, the more compelling view is to consider that within all the gross environmental variations there is present the essential minimal experience necessary for the acquisition—the learning—of the basic universal behaviors of our species. There is a growing agreement that universal behaviors and physical structures are not built into the organism but that humans are. at the very least, evolutionary primed to take advantage of the transactional opportunities provided by what (1998) sees as the universal physical and social ecologies available to all normal human organisms—the kinds of transactional opportunities so beautifully analyzed by Thelen and her colleagues with respect to early motor development (1991). As a result of these transactional experiences, the forms and function of the universal developmental domains are constructed, whether as described in dynamic systems approach to motor development (1994; 1991). or in (1996) powerful analysis and synthesis of the role of language in cognitive development, or in notion of the ” constructive web” and his attempts to document the linear and nonlinear mechanisms involved in the construction and development of the hierarchies of skills (1980: 1998).
In short, given the myriad theoretical and methodological problems associated with behavior genetics, little can be gained either for advancing the science of human development orfor adequately informing or serving (2000) “Person in the Street” by continuing to invest resources in the behavior genetics approach. There seem to be compelling reasons to make human and financial investments elsewhere given, on one hand, the counterfactual view of genetic activity inherent in behavior genetics and the several insurmountable conceptual and computational problems involved in the derivation of heritability estimates and. on the other hand, the availability of the theoretically rich and empirically productive developmental systems alternative to hereditarian approaches such as behavior genetics.
I believe, then, that both science and society may be well served by embarking on the scholarly path envisioned by (2000). To both enhance understanding of human development, and to best promote its healthy progression across ontogeny, we should begin to devote our theoretical and research efforts to the exploration of the dynamic developmental system depicted by her and others (2000; 1992; 1991, 1996. 1998. 1998a. 1998b, 2002; 1992; 1997; 1983; 1993; 1994.1998). Such an initiative would be important because the hereditarian and the developmental systems viewpoints have quite different implications for policies and programs pertinent to the promotion of positive human development.
Environmental and Behavioral
Influences on Gene Activity:
From Central Dogma to
The new discipline of the genetics of behaviour, to judge by some recent books, is caught in the dogmas of Mendelian genetics without regard to developments in modern genetics during the last ten years, and to modern experimental approaches to the genetic roots of behaviour. Books on the subject usually begin with an account of the principles of Mendelian genetics. The material on behaviour deals mainly with mutated animals and their observed changes in behaviour. That is exactly what genetic principles predict. If an important mutation should not be followed by a change in behaviour—then geneticists would have to worry about the validity of the principles.
What these books fail to pay attention to is the trend in modern genetics which deals with the activation of gene areas, with the influence of external factors on the actualization of gene-potentials and their biochemical correlates in behaviour. I would venture to guess that, apart from the dogma, the main reason for this silence is the fear of even the slightest suspicion that one might misinterpret such facts to mean that a Lamarckian mechanism were at work. (1969)
In the ensuing decades since Hyden made the above observation, things have not changed very much. A virtual revolution has taken place in our knowledge of environmental influences on gene expression that has not yet seeped into the social sciences in general and the behavioral sciences in particular. Aside from the feared
misinterpretation of Lamarckian mechanisms at work, there is an explicit dogma, formulated as such, that does not permit environmental influences on gene activity: The Central Dogma of Molecular Biology, first enunciated by in 1958.
Though the central dogma may seem quite remote from psychology. I think it lies behind some psychological and behavioral theories that emphasize the sheerly endogenous construction of the nervous system and early behavior (e.g., Elman et al., 1996; Spelke & Newport, 1998), and the “innate foundation of the psyche” (e.g., Tooby & Cosmides, 1990), independent of experience or functional considerations: The essentially dichotomous view that genes and other endogenous factors construct part of the organism and environment determines other features of the organism. The present chapter attempts to show how genes and environment necessarily cooperate in the construction of organisms; specifically, how genes require environmental and behavioral inputs to function appropriately during the normal course of individual development.
PREDETERMINED AND PROBABILISTIC EPIGENESIS
In earlier articles, I described two concepts of epigenetic development: predetermined and probabilistic epigenesis ( 1970, 1976). In these early formulations, the difference between the two points of view hinged largely on how they conceived of the structure-function relationship. In predeterminism. it was unidirectional (S -> F), whereas in probabilism, it was bidirectional (S <-> F). Subsequently, I (1983) extended the uni-and bidirectionality to include genetic activity:
Predetermined Epigenesis Unidirectional Structure-Function Development Genetic activity (DNA -> RNA -> Protein) -> structural maturation -> function, activity, or experience
Probabilistic Epigenesis Bidirectional Structure-Functional Development Genetic activity (DNA <-> RNA <-> Protein) <-> structural maturation <-> function, activity, or experience
As applied to the nervous system, structural maturation refers to neurophysiological and neuroanatomical development, principally the structure and function of nerve cells and their synaptic interconnections. The unidirectional structure-function view assumes that genetic activity gives rise to structural maturation that then leads to function in a nonreciprocal fashion, whereas the bidirectional view holds that there are reciprocal influences among genetic activity, structural maturation, and function. In the unidirectional view, the activitv of
genes and the maturational process are pictured as relatively encapsulated or insulated, so that they are uninfluenced by feedback from the maturation process or function, whereas the bidirectional view assumes that genetic activity and maturation are affected by function, activity, or experience. The bidirectional or probabilistic view applied to the usual unidirectional formula calls for arrows going back to genetic activity to indicate feedback serving as signals for the turning on and turning off of genetic activity. The usual view, as we shall see below in the central dogma of molecular biology, calls for genetic activity to be regulated by the genetic system itself in a strictly feed-forward manner. In this chapter, I (a) present the central dogma as a version of predetermined epigenesis and (b) elaborate on the prior description of probabilistic epigenesis to bring it up to date on what we now know about the details of the bidirectional effects among genetic activity, structural maturation, neural and behavioral function, and experience.
THE CENTRAL DOGMA
The central dogma asserts that “information” flows in only one direction from the genes to the structure of the proteins that the genes bring about through the formula DNA -> RNA -> Protein. (Messenger RNA [mRNA] is the intermediary in the process of protein synthesis. In the lingo of molecular biology, the DNA -> RNA is called transcription, and the RNA -> Protein is called translation. ) After retroviruses were discovered in the 1960s—in which RNA reversely transcribes DNA through the enzyme reverse transcriptase— wrote a postscript to his 1958 paper in which he congratulated himself for not claiming that reverse transcription was impossible: “In looking back I am struck not only by the brashness which allowed us to venture powerful statements of a very general nature, but also by the rather delicate discrimination used in selecting what statements to make” (1970). He then went on to consider the central dogma formula, DNA -> RNA -> Protein, in much more explicit detail than in his earlier paper. In particular, he wrote: ” These are the three [information] transfers which the central dogma postulates never occur:
Protein -> Protein Protein -> DNA Protein -> RNA. ” ()
I suppose if one is going to be brash about making proposals in largely unchartered waters, it stands to reason one might err, even given the otherwise acknowledged insight of the author regarding other scientific issues. In the present case, Crick was wrong in two of the three central-dogmatic postulates described above. Regarding protein-protein interactions, it is now known that in neurodegenerative disorders such as Creutzfeldt-Jakob disease, prions (abnormally conformed proteins) can transfer their abnormal conformation to other proteins
(=Protein -> Protein transfer of information), without the benefit of nucleic acid participation (1996). The strength of the dogma that nucleic acids are required for information transfer is so compelling that some people believe there must be something like an RNA transforming virus that brings about the changed protein conformation, even though there is no evidence for such a virus (1998; 1996).
Regarding Protein -> DNA transfer, there has long been recognized a class of regulative proteins that bind to DNA, serving to activiate or inhibit DNA expression (i.e., turning genes on or off; reviews in Davidson, 1986, and Pritchard. 1986).
With respect to the third prohibited information transfer (Protein -> RNA). which would amount to reverse translation, to my knowledge that phenomenon has not yet been observed.
Any ambiguity about the controlling factors in gene expression in the central dogma was removed in a later article by , in which he specifically says that the genes of higher organisms are turned on and off by other genes ( 1982). Figure 5.1 shows the central dogma of molecular biology in the form of a diagram.
The Genome According to Central Dogma
The picture of the genome that emerges from the central dogma is (a) one of encapsulation, setting the genome off from supragenetic influences, and (b) a largely feedforward informational process in which the genes contain a blueprint or master plan for the construction and determination of the organism. In this view, the genome is not seen as part of the developmental-physiological system of the organism, responsive to signals from internal cellular sources such as the cytoplasm of the cell, cellular adhesion molecules (CAMs). or to extracellular influences such as hormones, and certainly not to extraorganismic influences such as stimuli or signals from the external environment. Witness the well-known biologist (1982) view “that the DNA of the genotype does not itself enter into the developmental pathway but simply serves as a set of instructions” (). (1984) characterized this view of the genes
FIG. 5.1. Central dogma of molecular biology. The right-going arrows represent the central dogma. The discovery of retroviruses (represented by the left-going arrow from RNA to DNA) was not part of the dogma but, after the discovery, was said by (1970) not to be prohibited in the original formulation of the
as the unmoved movers of development and the masters of the cellular slave machinery of the organism. Ho's own work on the transgenerational effects of altered cytoplasmic influences seriously faults this view, as does the research reviewed by (1995).
Genes are conserved during evolution so some of the same genes are found in many different species. What this has shown us is that there is not an invariable association between the activity of a specific gene and the part of the body in which it is active. One of the nicest demonstrations is the activity of the so-called Hox genes that are found in a number of species (1997). As shown in Fig. 5.2, in fruit flies the Hox genes are active only in the abdominal segment of the body, whereas in centipedes the same Hox genes are active in all segments of the body except the head. And, in a related worm-like creature, Onychophora, the Hox genes are active only in a single segment of the organism, in its hindmost region. Because these are not homologous parts of these three species, this demonstrates that the specific developmental contribution of the same genes varies as a consequence of the developmental system in which they find themselves. Genes that play a role in the abdominal segment of fruit flies are active in virtually all the bodily segments of centipedes but only in a single segment in Onychophora.
The main point of the present chapter is to extend the normally occurring influences on genetic activity to the external environment, thereby further demonstrating that the genome is not encapsulated and is, in fact, a part of the organism's general developmental-physiological adaptation to environmental stresses and signals: Genes express themselves appropriately only in responding to internally and externally generated stimulation. Further, in this view, while genes participate in the making of protein, protein is also subject to other influences (1986;1986), and protein must be further stimulated and elaborated to become part of the nervous system (or other systems) of the organism, so genes operate at the lowest level of organismic organization and they do not, in and of themselves, produce finished traits or features of the organism. 1 Thus, there is no correlation between genome size and the structural complexity of organisms (1992), nor is there a correlation between numbers of genes and numbers of neurons in the brains of a variety of organisms (Table 5.1). The organism is a product of epigenetic development, which includes the genes as well as many other supragenetic influences. Because this latter point has been the subject of numerous contributions (1992, 1997), I will not deal with it further here but, rather, restrict this chapter to documenting that the activity of genes is regulated in just the same way as the rest of the organism, being called forth by signals from the normally occurring external environment, as well as the internal environment (1990; 1986). Though this fact is not well known in the social and behavioral sciences, it is surprising to find that it is also not widely appreciated in biology proper (1997). In biology, the external environment is seen as the agent of natural selection in promoting evolution, not as a crucial feature of individual development (1995). Many biologists subscribe to the notion that “the genes are safely sequestered inside the nucleus of the cell and out of reach of ordinary environmental effects” (1989).
ON GENE ACTIVITY
As can be seen in Table 5.2, a number of different naturally occurring environmental signals can stimulate gene expression in a large variety of organisms from nematodes to humans. The earliest demonstration of this regularly occurring phenomenon that I could find in intact organisms is the work of H. Hyden (1962). In this rarely cited study, hungry rats had to learn to traverse a narrow rod from an elevated start platform to an elevated feeding platform—a veritable balancing act. The nuclear base ratios in their vestibular nerve cells were then compared with an untrained control group and a control group given passive vestibular stimulation. The RNA base ratios in the experimental groups differed from both the control groups, and there was no difference between the control groups.
IMPORTANCE OF BEHAVIORAL
AND NEURAL ACTIVITY
IN DETERMINING GENE EXPRESSION, ANATOMICAL
STRUCTURE, AND PHYSIOLOGICAL FUNCTION
Many, if not all, of the normally occurring environmental influences on genetic activity summarized in Table 5.2 involve behavioral and neural mediation. In the spirit of this chapter, I want to emphasize the contribution of events above the genetic level (the whole organism and environmental context) by way of redressing the balance to the way many think about the overriding importance of molecular biology. The earliest synaptic connections in the embryonic and fetal nervous system are created by spontaneous activity of nerve cells (1994, 1996). This early, exuberant phase produces a very large array of circuits which is then pared down by the organism's encounters with its prenatal and postnatal environment. In the absence of behavioral and neural activity (e. g., experimentally induced paralysis), cells do not die and circuits do not become pruned in an adaptive way that fits the organism to the demands of its physical, social, and cultural environments (1979). A recent review of the development and evolution of brain plasticity may be found in (1998).
Sometimes one reads the perfectly reasonable-sounding suggestion that, though genes don't make anatomical, physiological, or behavioral traits, they constrain the outer limits of variation in such traits. It is of course the developmental system, of which the genes are a part ( Fig. 5.3 ), and not solely the genes that constrain development. It is not possible to predict in advance what the outcome of development will be when the developing organism is faced with novel environmental or behavioral challenges never before faced by the species or strain of animal. This has been known since 1909, when Woltereck did the first experiments that resulted in the open-ended concept of the norm of reaction, an idea that has been misunderstood by some behavior geneticists who think of genes as setting up a too-narrow range of reaction (1995; 1988).
A very striking example of the role of novel behavior bringing about an entirely new anatomical structure can be seen in Fig. 5.7 : (1942) goat. This animal was born with undeveloped forelimbs and adopted a kangaroo-like form of locomotion. As a result, its skeleton and musculature became modified, with a pelvis and lower spinal column like that of a biped instead of a quadruped ( Fig. 5.7 ). Thus, while there can be no doubt that genes and other factors place constraints on development, Slijper's goat shows that it is not possible to know the limits of these constraints in advance, though it might seem quite reasonable to assume, in advance of empirical inquiry, that a quadruped is not capable of bipedality. While an open-ended, empirically based norm of reaction can accommodate Slijper's goat.
Heredity vs. Environment – Beyond Heritability
As illustrated so far, most psychology researchers are in agreement that heredity and environment both play significant roles in the development of various human traits. Researchers may disagree, however, on the extent to which heredity and environment contribute to the development of a particular dimension, and on how various factors may affect each other to create a certain human characteristic. Neither heritability estimates nor concordance rates provide useful information on the latter type of disagreement: how various hereditary and environmental factors interact with each other to result in a particular characteristic. Mental health, education, and applied psychology researchers are especially concerned about optimizing the developmental outcomes among people from all backgrounds. To this end, knowing that there is a .86 heritability estimate for IQ scores among identical twins, for example, is not particularly helpful in terms of establishing ways of maximizing the life choices and opportunities for individuals. In attaining such goals, it is crucial to understand how various factors relate to each other. Naturally, in order to do so, one must first identify which factors are involved in the development of a given trait. Unfortunately, researchers have had very limited success in identifying specific genetic patterns that influence particular psychological and behavioral characteristics.
Nevertheless, this is not to suggest that one should ignore the role of heredity as reflected in heritability estimates altogether and focus on optimizing the environmental factors for every child. Heredity, as has been examined, undoubtedly contributes to the development of various human traits. Also, researchers exploring environmental influences have found that contrary to what most theorists expected, environmental factors that are shared by reared-together twins do not appear to be relevant in explaining the development of particular traits. It is therefore unlikely that exposing every child to a "one size fits all" environment designed to foster a particular trait, would benefit everyone equally. Some may react favorably to such an environment, while others may not react to it at all; there may be yet others who react negatively to the same environment. The notion of "range of reaction" helps us conceptualize the complex relationship between heredity and environment; people with varying genetically influenced predispositions respond differently to environments. As suggested by Douglas Wahlsten in a 1994 article in Canadian Psychology, an identical environment can elicit different reactions in different individuals, due to variations in their genetic predispositions. In a hypothetical scenario, Wahlsten suggested that increasing intellectual stimulation should help increase cognitive performances of some children. Moderate, rather than high, levels of intellectual stimulation may, however, induce optimal cognitive performances in others. By contrast, the same moderate levels of stimulation may actually cause some children to display cognitive performances that are even worse than how they performed in a minimally stimulating environment. In addition, the "optimal" or "minimal" performance levels may be different for various individuals, depending on their genetic makeup and other factors in their lives. This example illustrates the individual differences in ranges of reaction; there is no "recipe" for creating environments that facilitate the development of particular characteristics in everyone. Heredity via environment, rather than heredity versus environment, therefore, may better characterize this perspective.
These views are consistent with the 1990s' backlash against the view that was prevalent in the mid- to late twentieth century among many clinical psychologists, social workers, and educators, who focused solely on environmental factors while discounting the contributions of hereditary factors. Among the theories they advocated were that gay males decidedly come from families with domineering mothers and no prominent masculine figures, that poor academic performances result from lack of intellectual stimulation in early childhood, and that autism stems from poor parenting practices. Not surprisingly, empirical data do not support these theories. Still, people often continue to believe, to some extent, that proper environments can prevent and "cure" these non-normative characteristics, not realizing that heredity may play significant roles in the development of these traits.
Some scholars believe that this "radical environ-mentalist" view found its popularity in the 1950s as a reaction to racist Nazi thinking, which held that some groups of individuals are genetically inferior to others and that the undesirable traits they are perceived to possess cannot be prevented or modified. These assumptions are harmful, as they limit the opportunities for advancement of some people, strictly because of their membership in a stigmatized group. It is nevertheless important to reiterate that individual differences, as opposed to group differences, in genetic predispositions are evident in the development of most emotional, behavioral, and cognitive traits. With this in mind, it is also important to realize that focusing on optimizing environmental influences while ignoring hereditary influences may lead to the neglect of the developmental needs of some individuals, and it may be just as harmful in some cases as focusing exclusively on hereditary influences.
Heredity and Environment
The causes of individual variation are to be sought in the individual’s hereditary background and in the environmental conditions to which he has been exposed. Every trait or behavior manifestation of the individual depends both on his heredity and on his environment. Traits and activities cannot be classified into those which are inherited and those which are acquired. The problem thus resolves itself into a determination of the relative contribution of hereditary and environmental factors in the development of the individual. To what extent can the development of any given characteristic be altered by the control of environmental influences, and to what extent is such modification limited by hereditary conditions? Individual variations found under similar hereditary conditions may be attributed to the operation of different environmental factors. Similarly, when the environments are sufficiently similar, any dissimilarity of behavior may be regarded as indicative of a difference in heredity. We may speak, therefore, of hereditary and environmental determiners or factors in the development of a given characteristic, although such a dichotomy cannot be applied to traits.
How does heredity operate in the development of the individual? The understanding of the mechanism of heredity has been greatly furthered by the concept of the gene. The individual begins life at conception with the union of one germ cell from each parent, the ovum of the female and the spermatozoon of the male. Each of these cells contains hundreds of thousands of very minute particles, called genes. A gene is the carrier of a “unit character”, ie an hereditary factor or influence which always operates as a unit, or in an all-or-none fashion. These unit characters of the geneticists are not be confused with traits as ordinarily conceived, but are of a much more elementary nature.
It is obvious that any attempt to identify psychosocial characteristics, and especially such a manifold and ill-defined phenomenon as “intelligence”, with unit characters is entirely inconsistent with the concepts and data of genetics.
The hereditary basis of individual differences is to be found in the almost unlimited variety of possible gene combinations which presents itself, especially in the case of such a complex organism as man. – often times producing diversity
The only exception to this individual diversity of gene constitution is that of identical twins, which develop from a single fertilized ovum. Such twins are always of the same sex and identical in appearance. Fraternal twins, do not reveal such close resemblance and may be either of the same or opposite sex. The hereditary similarity of fraternal twins is no greater than that of ordinary siblings, since they result from the simultaneous development of two different cells. Fraternal twins are however, exposed to the same prenatal environment, which may be an important factor in rendering them similar in their subsequent development.
Hereditary factors may influence the development of the individual long after birth, and in fact throughout the life span. Even the onset of death itself may be determined partly by hereditary factors, as suggested by the observation that longevity or “long life” tends to run in families. Hereditary influences may become manifest for the first time at any age. Similarly, environmental influences begin to operate upon the individual from the moment of conception. The importance of temperature, chemical, and other types of stimulation in the prenatal surroundings of the developing embryo is rapidly coming to be recognized. Birth is not to be regarded as either a beginning or an end in the life of the organism, but as a relatively minor occurrence in a developmental continuum which begins at conception and ends at death.
Prenatal Environment: IN general, it may be said that the earlier an environmental condition operates in the life of the individual, the more pronounced will be its effects. After an advanced state of growth has been reached, the organism becomes much less modifiable. For this reason, the stimuli to which the individual is exposed during the embryonic stage exert a pronounced and lasting influence upon its future development. Variations in diet and nutrition, glandular secretion, and other conditions of the mother which are manifested in the chemical condtion of the blood have a marked effect upon the characteristics of the embryo. The structureal development of the individual is definitely influenced by such environmental factors. It is also possible that a certain amount of rudimentary learning may occur during prenatal life. The presence of certain reflexes and other simple movements in young embryos has been definitely established. Such responses may early become conditioned in various ways to changes of temperatures, pressure, and other stimuli furnished by the intra-uterine environment.
*Even a clearly demonstrable “inherited effect” is actually only a tendency to develop in a given way under certain environmental conditions.
Experimentally Produced Variations in Behavior: Numerous experiments have shown the possibility of pronounced alteration in behavior as a result of environmental differences. Animals reared in isolation from other members of the species or from individuals of the opposite sex, or in close association with a human child, have developed curious modifications of behavior. Activites which are commonly assumed to be unlearned and fixed by hereditary constitution have proved susceptible to marked change. Universal characteristics in behavior, as in structure, have been shown to result as much from common environments and similar opportunities for learning as from common heredity.
The songs of different birds, generally considered to characteristic of the species, have been found to contain much that is learned in their specific manifestations. A group of newly hatched orioles were segregated from all older members of the species and brought up by themselves. When the birds reached a certain age, they began to sing. Their song, however, was not the characteristic oriole song, but a new one. When other newly hatched orioles were reared with the group that had grown up in the laboratory, the young birds in turn learned the new song developed by the first group.
Sexual behavior has also proved to be dependent upon learning in its specific manifestations. Some form of sexual activity will occur at a definite developmental stage, because of the presence of glandular secretions in the blood and other physiological factors. The particular way in which such activity is expressed and the object towards which it is directed, however, will vary according to environmental circumstances.
Lack of association with adults during a certain critical period of early childhood produces in some or all normal children marks like those of congenital defect. The evidence seems against the romantic view that a civilized community is a chief obstacle to the development of personality. On the contrary, the higher forms of personality become possible only in and through such a community. By our biological endowment alone, or by this as developed by maturing and learning in an infrahuman environment, we remain man-beasts. We become human only by active intercourse in a society of those who already have become human.
Psychology - 2007 -
Human Behavior Genetics
Vehement discussion continues regarding the role of genetic determinants in behavior, IQ, and personality. Some scientists entirely deny genetic influences on normal behavior or social characteristics such as personality and intellect. This attitude toward genetics is shared by some psychologists and social scientists and even a few geneticists who are concerned about the possible future political and social misuse of studies in human behavioral genetics and sociobiology that claim to show strong genetic determinants of intelligence and social behavior.
We do not agree with those who deny any genetic influence on behavior or social traits in humans. However, we also caution against a too ready acceptance of results from biometric comparison of twins and other relatives, which claim high heritabilities for many of these traits. Genetic data and pseudodata may be seriously misused by political bodies. However, as biologists and physicians impressed by biological variation under genetic control, we would be surprised if the brain did not also show significant variation in structure and function. Such variation is expected to affect intellect, personality, behavior, and social interactions. The extent to which genetic variation contributes to such traits, and especially the biological nature of such variation, will have to await further studies.