Because of this palpable meshing together of two variables, it is then plausible to establish what aspects of personality are linked to genes, and what aspects most likely exist due to environmental leverage. It has been said that heredity and the environment both contribute 50% to the makeup of an entire human being, but much debate exists about specific percentages and the existence of higher percentages of one factor in different age groups than others (Petrill et al., 2004). Some tactics that have been used in attempts to figure out the many characteristics of human beings include adoption studies, family studies, and twin studies. A review of different topics in human behavior and psychopathology, from human attitudes to the mental disorder schizophrenia, is a beneficial way to broadly explore the argument. Loose conclusions may be derived from these studies, but much more investigation needs to be done, both in creating new research projects and in analyzing previous methodologies and results, before this argument has any potential of being resolved.
Fraternal twins, or dizygotic twins, share exactly half their genes with each other. They are not as optimal as identical twins for deciphering the degrees of genetic influence, but they are a very good basis for comparison for identical twins. Fraternal twins are similar to first-degree relatives, except they are sure to share the exact same age, as do identical twins. Twin studies usually rely on samples of identical and fraternal twins; if biology has a greater hand than environment, then identical twins should behave or possess psychopathology similar to each other more so than fraternal twins (Plomin et al., 1997). This is an example of the heritability coefficient coming into play: the estimate of how much someone's specific trait in comparison to other people's traits under one characteristic is attributable to genes (Olson, Vernon, Harris, Aitken, & Jang, 2001). This coefficient ought to be higher in identical twins than in fraternal twins. Then again, it is possible for identical twins to express different phenotypes (external expression of genetics) for the same genotypes (genetic makeup). This is representative of their nonshared environments; even though identical twins possess the same genetic makeup, they may go through different experiences throughout their lives that shape their personality, behavior, and psychopathology in ways that make them unique relative to each other (Hughes et al., 2005).
AttitudesOne particular study sought to determine the heritability of attitudes among twins, as well as the genetic variables, such as intelligence, that could affect attitudes among pairs of twins. A questionnaire was provided to the participants, in which they were asked to rate their personality traits, physical abilities, and physical attractiveness. They were also asked to note their academic achievements (Olson et al., 2001).
The results of the study showed that differences between attitudes of the participants were at least partially correlated to genetic factors. It also showed that attitudes related to self-reported perspectives or to activities were often correlated. For instance, the survey asked subjects to rate themselves on the trait of sociability. That trait was correlated with 5 out of 6 attitude factors subjects had toward sociability. Attitudes toward athleticism highly correlated with findings on self-reported athletic abilities.
The causal model was expressly supported in these findings, because athletic skill (the mediator), for example, seemed to be linked with attitudes toward athleticism. Of course, this model is not without its problems: one cannot assume that X is the cause of Y in every single situation. Case in point: attitudes toward leadership seemed to be related to high self-ratings of physical attractiveness, sociability, and aggressiveness. Because of these numerous factors, it is still not possible to always accurately assume direct, singular relations between genetic traits and attitudes (Olson et al., 2001).
Interestingly, nonshared environment experiences between pairs of twins seemed to be the strongest cause of attitude variances, overshadowing genetic predispositions as well as shared environment experiences (Olson et al., 2001). Nonshared environment is a term used to refer to something in the environment that directly affects one twin but does not impact the other at all (Van den Oord, Boomsma, & Verhulst, 2000). The study did indicate that some nonshared environment experiences were very much connected to attitudes and self-reports of physical characteristics and intelligence (Olson et al.). This study leads to further questions about nonshared environments: why is it that different environments have so much effect on twins' behaviors and personalities? And why are some attitudes apparently rooted in genetics, while others are not? As previously stated, it is clear that much more research must be conducted on twins before any solid answers can be found.
Theory of MindMental states are made up of beliefs, intents, and desires. A child usually acquires a theory of mind, which is the understanding that objects and situations can be falsely interpreted or represented by their own mental states, by the age of four. The question for research here is: between biology and environment, what accounts the most for the differences in how much individual children vary in false-belief comprehension? It has been shown that children from large families experience accelerated acquisition of theory of mind, but deaf children born to hearing adults experience decelerated acquisition of theory of mind. This points to cultural influences, and thus, to environmental influences. Inversely, children with the highly transmissible disorder autism have also been found to possess impaired theory of minds, as do girls with the chromosomal disorder Turner's syndrome. This points to genetic influences (Hughes et al., 2005).
A study was created to investigate this topic, using both identical and fraternal twins. It measured socioeconomic status, verbal ability, and more importantly, the theory of mind of each participant. The first part of the test given to the subjects contained questions that examined their abilities to connect a mistaken belief about a character in stories provided. The second part tested the subjects' abilities to make inferences and their tendencies to attribute a false belief to a belief about characters within the provided stories (Hughes et al., 2005).
Most of the variation between theory of minds of the pairs of twins resulted from nonshared environments. The percentages of influence in decreasing order were attributed to shared environments, verbal abilities, and then genetics. Families with twins are often highly charged with competitiveness, and the more the families discuss conflicts, the more accelerated theory of minds tend to be. This emphasis on environmental influences does outweigh genetic influences on the development of theory of minds in children, but it does not outweigh genes' existence and role entirely (Hughes et al., 2005).
Genotype-Environment InteractionA study was performed using a portion of the identical twins that participated in the Swedish Adoption/Twin Study of Aging (Bergeman, Plomin, McClearn, Pederson, & Friberg, 1988). These researchers were interested in the relations between phenotypes and genotypes of twins reared apart, which was the experience of all the participants in the Swedish study. One twin's phenotype should be the biggest indicator of the other twin's genotype, because the study examined the experiences of pairs of twins who had been separated their whole lives (Bergeman et al., 1988). If anything was similar about the pair, it ought to be correlated to their shared genes, because they certainly did not share the same environment.
The study was designed to measure personality traits of extraversion and neuroticism among the twin pairs, traits of impulsivity and monotony avoidance, and family environment and socioeconomic status. Using this information, and taking into consideration that a study like this had never been done before, the researchers came to three different conclusions in regards to genotype-environment interaction. Genotype-environment interaction is a term used by many researchers in relation to twin studies, referring to the potential for people with different genetic makeup to respond differently toward the same external situation (Bergeman et al., 1988). This is an important concept in twin studies because genotype-environment interaction can also be applied to how people with the same genotypes might respond to the same environment.
One particular genotype-environment, labeled Type I, indicates that the environment has more of an impact on individuals with a genotype for low scores on a specific personality trait. Individuals who had low genotypes for extraversion would also score low on extraversion if they perceived their families as high in control or organization, as opposed to individuals who had high genotypes for extraversion. The latter individuals expressed that high extraversion trait regardless of the perceived level of control or organization of their respective families (Bergeman et al., 1988).
Type II genotype-environment interaction was essentially the opposite of Type I. Individuals who have genotypes that cause them to score high on a specific trait were affected by their environments, while individuals with genotypes that caused them to score lower were not affected by their environments. For example, an individual who possesses a high genotype for impulsivity will have that trait increased if she or he lives in a conflict-filled environment (Bergeman et al., 1988).
Finally, Type III genotype-environment interaction was a category only derived from the researchers' study on mice; it was not derived from the Swedish twins. Type III genotype-environment interaction occurs when the environment influences individuals with genotypes that cause them to score higher on traits as well as individuals who have genotypes that cause them to score lower on traits. An environment high in parental control, for example, will restrict the expression of a genotype, while a permissive environment will allow a genotype to emerge as a strong phenotype (Bergeman et al., 1988).
SchizophreniaThe first adoption study performed on schizophrenia showed that family environment contributes little to a child's risk for a disorder such as schizophrenia. This study was performed through interviews of adopted-away children of biological mothers who suffered from schizophrenia, and interviews of adopted children whose birth parents did not suffer from any mental disorders. Several of the adopted away children of schizophrenic mothers suffered from schizophrenia themselves, while the adoptees whose parents didn't have schizophrenia also did not have schizophrenia themselves. This supports the theory that it doesn't matter what specific environment a child is raised in; if its parent or parents suffer from a mental disorder, the risk for suffering from the same disorder will be equal regardless of if the child was raised with its biological parents or with its adoptive parents (Plomin et al., 1997).
Another adoption study showed that a high percentage of proband adoptees, or adoptees whose birth parents had schizophrenia, also suffered from chronic schizophrenia or displayed schizophrenic-like behaviors. None of the control adoptees, or adoptees whose biological parents did not suffer from schizophrenia, had schizophrenia themselves, and only a small percentage of them displayed schizophrenic-type symptoms. A current study is also supporting these results, because a significant percentage of proband adoptees displayed some psychotic symptoms, while only a small percentage of control adoptees displayed these types of symptoms. This study also showed that the adoptees whose biological parents suffered from schizophrenia had a higher likelihood of schizophrenia or other related disorders when the adoptive families were low functioning. This speaks volumes for the genotype-environment interaction theory, because of the expression of a genotype being linked to the type of rearing environment (Plomin et al., 1997).
Despite all of this information, it is still very much uncharted territory as to what explicitly causes schizophrenia, and how it may or may not be expressed among adopted children. One of the main difficulties subsists in the deficiency of knowledge on a gene that carries the disorder schizophrenia. It is unknown whether such a gene exists, and doubly unknown to what degree this possible gene influences these types of adoption studies (Loehlin, Willerman, & Horn, 1988).
Infant ShynessAn adoption study was conducted to disentangle the reasons behind why some infants are open and responsive to attention right away, some take time to open up, and still yet, some others are fearful and withdrawn. It is difficult to tell whether babies are shy because their mothers are shy and thus do not take them out very much, or because the shy mothers pass down their shyness traits. Measures of this study attempted to clarify the relationship between the infants and adoptive and biological parental shyness, parental sociability, and parental introversion-extraversion (Daniels & Plomin, 1985).
Adoptive parents were given questionnaires that asked them to rate their infants' shyness levels, and then to rate themselves on the traits listed previously. It must be noted that the self-reported ratings of the biological were performed before the birth of the infants, and the scoring of the infants' shyness were performed by the adoptive parents when the babies were two years old. The results showed that in nonadoptive families, the parents who reported high rates of shyness, low rates of sociability, and high rates of introversion also had shy infants. This was also seen in adoptive families whose parents rated similarly, indicating that a combination of home environment and genetics must come into play. One significant conclusion was made in this study that was based on the fact that biological mothers rated high in shyness, and their adopted-away babies were also shy. This strengthens the possibility of a genetic link overshadowing family environment, but of course further research must be done (Daniels & Plomin, 1985).
Children's Adjustment to DivorceA study was performed to investigate the possible connection between genetic factors and children's adjustment to parental divorce. Interviews, questionnaires, and standardized tests were administered to probands and their parents. Interviewers also rated the social behavior of the probands at the time of their interviews (O'Connor, Plomin, Caspi, & DeFries, 2000).
Measures of the study included age of the probands at the time of separation and/ or divorce, self concept (self-esteem) of the probands, social ability, academic ability, behavioral and/or emotional problems, loneliness, and substance use. Of course, the type of adjustment processes that children from biological families went through could be attributed to biology or environment, while adjustment for probands would have had to be linked to environmental processes. The results showed that probands' adjustment to divorce in terms of social ability, self-concept, and academic accomplishments were at least partially genetically influenced, but that their psychopathology could be attributed to environmental factors (O'Connor et al., 2000).
Antisocial Personality DisorderMany studies have been composed to attempt to discover if children who are at risk for antisocial personality disorder are more likely to develop symptoms in an adoptive family environment, or if that environment will protect them from the disorder's development. It has been shown through these various studies that antisocial personality disorder is, indeed, more likely to present itself in adoptees that already have biological risk factors (at least one biological parent had a background of criminality or antisocial personality disorder). The adoptees that are born with no risk of developing the disorder do not usually develop it while living in an adoptive environment. The adoptive family environment combining with the preexisting biological risk seems to make antisocial personality disorder quite prevalent among adoptees (Roth & Finley, 1998).
It was also found that adoptees experienced an even higher risk for antisocial personality disorder if both their biological parents and their adoptive parents came from criminal backgrounds. However, methodological problems exist with these kinds of studies because there are so many factors to consider. For example, it has yet to be clarified whether this disorder is more likely to be carried through the biological mother, or the biological father. Most of these adoption studies were conducted using only information from the biological mother, and not the other half of the equation: the biological father. Information is also vague regarding a criminal background as an instant checkmark for antisocial personality disorder in biological and adoptive parents. It is often assumed that the existence of a biological parent's criminal background immediately means that that parent has antisocial personality disorder, and also has definitely passed it down to the adopted-away offspring. The problem is, it also cannot be assumed that the lack of a criminal background points to a lack of the disorder itself (Roth & Finley, 1998).
Interpreting the results of adoption studies is very difficult for the aforementioned reasons, and it is also challenging to make valid conclusions due to the fact that adoptees already display a higher rate of antisocial personality disorder as compared to the general population. Ironically, the adoptive family environment is often better in terms of care, education, stability, and health in comparison to families in the rest of the population. Adopted-away children, however, are often placed in adoptive family environments similar to their original, biological family environments. Genetic factors are thus "simulated" when the adoptive family environment is similar to the biological environment (Rhee & Waldman, 2002). With all of these discrepancies and uncertainties, it is undoubtedly a complex process to try to figure out what factor has the most effect on the development of antisocial personality disorder.
These kinds of studies are most often used to determine the risk of passing down mental disorders to offspring within families. It must also be taken into consideration that these types of studies do not tangibly express outside factors, such as family environment and culture. These studies are performed using molecular genetic studies, where DNA is extracted from participants' blood samples and the correlation between the DNA and the observed behavior is projected. The most common molecular genetic study is called linkage analysis. This type of study tries to locate a specific gene on a chromosome in the human body. If a gene for a particular mental illness is being searched for, researchers identify an already-recognized gene on the chromosome and label that as a marker. That marker's location, and the location of the actual diseased gene, is very important: the closer the two are, the higher the likelihood that the disease and marker genes will be passed on together, or linked together (Jang, 2005).
Bipolar Disorder and SchizophreniaBipolar disorder and schizophrenia share many similarities, from the average age of onset to the courses of the illnesses. Family studies, including molecular genetic studies, were conducted to decipher how much overlap exists for the genetic risks for both these disorders (Berrettini, 2000).
Studies carried out on bipolar disorder showed that first-degree relatives of people with bipolar disorder suffered a higher risk for some related mental disorders including bipolar I disorder, bipolar II disorder, schizoaffective disorder, and recurrent unipolar disorder. However, there was not an increased risk for schizophrenia itself (Berrettini, 2000).
Studies carried out using first-degree relatives of people who suffered from schizophrenia showed similar results. Those relatives were at higher risk for schizophrenia, schizoaffective disorder, and recurrent unipolar disorder, but not for bipolar disorder. Interestingly enough, first-degree relatives of people who suffered from both bipolar disorder and schizophrenia did experience higher risk for schizoaffective and recurrent unipolar disorders. This indicates an overlap and suggests a possible partial overlap in familial risk for bipolar disorder and schizophrenia (Berrettini, 2000). A larger-scaled study needs to be conducted before this can be fully determined.
SuicideSuicidal behavior is increased among relatives of suicide victims, but the singular cause of this is unclear. A study was conducted to figure out if the cause for this increased risky behavior was due to family heritability. It compared relatives of suicide victims with relatives of demographically similar adolescents; both groups were examined for Axis I and II disorders, histories of aggression, and histories of suicidal behavior (Brent, Bridge, Johnson, & Connolly, 1996).
First-degree relatives of suicide victims, also called suicide probands, had a greater likelihood of suicide attempts, but it also has to be taken into consideration that they also had an increased risk of other psychological disorders. The suicide probands who had high rates of aggression also had higher risk for attempts at suicide. The increased risk for suicidal behavior in suicide probands, it was concluded from this study, is probably a trait independent of Axis I and II psychiatric disorders (Brent et al., 1996).
Eating DisordersAnorexia nervosa and bulimia often exist comorbid with other psychiatric disorders, such as depression, anxiety, and obsessive-compulsive disorder. A study was performed to attempt to figure out if eating disorders were comorbid through family genetics. Interviews of relatives of eating disorder victims and best-estimate conclusions were conducted throughout the study. Interviews of a control group, or a group of relatives whose family members did not suffer from any eating disorders, were also carried out. The interviews determined whether the eating disorder probands themselves had eating disorders, and whether they suffered from mood, anxiety, substance abuse, and specific personality disorders (Lilenfield et al., 1998).
This study's results showed that eating disorder probands experienced a higher risk of eating disorders, major depressive disorder, and obsessive-compulsive disorder. Substance abuse disorder was placed at higher risk for bulimia probands than for anorexia probands, and obsessive-compulsive disorder was placed at higher risk for anorexia probands than bulimia probands (Lilenfield et al., 1998).
It was concluded that there was definitely a link between people who suffered from eating disorders and their relatives' risk for suffering from the same problems. A plausible connection between the probands' risk for major depressive disorder, substance abuse disorder, and obsessive-compulsive disorder, however, could not be proven. The only theory that could be somewhat supported was that the traits for obsessive-compulsive disorder could cause a familial risk for anorexia (Lilenfield et al., 1998).
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It is often difficult to separate the relative influences of heredity and environment on human characteristics. People who have similar genetic makeup (e.g., brothers and sisters, parents and their children) typically live in similar environments as well. So when we see similarities in IQ among members of the same family, it is hard to know whether those similarities are due to the genes or to the environments that family members share. Nevertheless, a significant body of research tells us that both heredity and environment affect intelligence.
Evidence for Hereditary Influences
Earlier we mentioned that measures of information processing speed correlate with IQ scores. Speed of processing depends on neurological efficiency and maturation, which are genetically controlled. From this standpoint, then, we have some support for a hereditary basis for intelligence (Perkins, 1995). The fact that children with certain genetic defects (e.g., Down syndrome) have, on average, significantly lower IQ scores than their nondisabled peers (Keogh & MacMillan, 1996) provides further evidence of heredity’s influence. But perhaps the most convincing evidence comes from twin studies and adoption studies.
Numerous studies have used monozygotic (identical) twins and dizygotic (fraternal) twins to get a sense of how strongly heredity affects IQ. Because monozygotic twins begin as a single fertilized egg which then separates, they are genetically equivalent human beings. In contrast, dizygotic twins are conceived as two separate fertilized eggs. They share about 50 percent of their genetic makeup, with the other 50 percent being unique to each twin. If identical twins have more similar IQ scores than fraternal twins, we can reasonably conclude that heredity influences intelligence.
Most twins are raised together by the same parent(s) and in the same home, and so they share similar environments as well as similar genes. Yet even when twins are raised separately (perhaps because they have been adopted and raised by different parents), they typically have similar IQ scores (Bouchard & McGue, 1981; N. Brody, 1992; Mackintosh, 1998; Plomin & Petrill, 1997). In a review of many twin studies, Bouchard and McGue (1981) found these average (median) correlations:
|Correlations of Twins’ IQs:|
|Identical twins raised in the same home||.86|
|Identical twins raised in different homes||.72|
|Fraternal twins raised in the same home||.60|
The correlation of .72 indicates that identical twins raised in different environments tend to have very similar IQ scores. In fact, these twins are more similar to each other than are fraternal twins raised in the same home.4
Another way to separate the effects of heredity and environment is to compare adopted children with both their biological and adoptive parents. Adopted children tend to be similar to their biological parents in genetic makeup. Their environment, of course, more closely matches that of their adoptive parents. Researchers have found that adopted children’s IQ scores are more highly correlated with their biological parents’ IQs than with their adoptive parents’ IQs. In other words, in a group of people who place their infants up for adoption, those with the highest IQs tend to have offspring who, despite being raised by other people, also have the highest IQs. Furthermore, the IQ correlations between adopted children and their biological parents become stronger, and those between the children and their adoptive parents become weaker, as the children grow older, especially during late adolescence (Bouchard, 1997; McGue, Bouchard, Iacono, & Lykken, 1993; Plomin, Fulker, Corley, & DeFries, 1997; Plomin & Petrill, 1997). (If you find this last research result puzzling, we’ll offer an explanation shortly.)
Keep in mind that twin studies and adoption studies do not completely separate the effects of heredity and environment (W. A. Collins, Maccoby, Steinberg, Hetherington, & Bornstein, 2000; Wahlsten & Gottlieb, 1997). For example, adopted children have shared a common environment for at least 9 months—the 9 months of prenatal development—with their biological mothers. Likewise, monozygotic twins who are raised in separate homes have shared a common prenatal environment and often have similar, if not identical, postnatal environments as well. Furthermore, twin studies and adoption studies do not allow researchers to examine the ways in which heredity and environment might interact in their effects on measured intelligence. Any interactive effects are often added to the “heredity” side of the scoreboard (A. Collins et al., 2000; Turkheimer, 2000). Despite such glitches, twin and adoption studies point convincingly to a genetic component in intelligence (Bouchard, 1997; N. Brody, 1992; E. Hunt, 1997; Neisser, 1998a; Petrill & Wilkerson, 2000).
This is not to say that children are predestined to have an intelligence level similar to that of their biological parents. In fact, most children with high intelligence are conceived by parents of average intelligence rather than by parents with high IQ scores (Plomin & Petrill, 1997). Children’s genetic ancestry, then, is hardly a surefire predictor of what their own potential is likely to be. Environment also makes an appreciable difference, as we shall now see.
Evidence for Environmental Influences
Numerous sources of evidence converge to indicate that environment has a significant impact on IQ scores. We find some of this evidence in twin studies and adoption studies. Studies of the effects of nutrition, toxic substances, home environment, early intervention, and formal schooling provide additional support for the influence of environment. Also, a steady increase in performance on intelligence tests over the past several decades—known as the Flynn effect—is almost certainly attributable to environmental factors.
Twin studies and adoption studies revisited
Let’s look once again at the IQ correlations for identical twins raised in the same home versus in different homes. The median correlation for twins raised in different homes is .72, whereas that for twins raised in the same home is .86. In other words, twins raised in different homes have less similar IQs than twins raised in the same home. The distinct environments that different families provide do have some influence on intellectual development.
Adoption studies, too, indicate that intelligence is not determined entirely by heredity (Capron & Duyme, 1989; Devlin, Fienberg, Resnick, & Roeder, 1995; Waldman, Weinberg, & Scarr, 1994). For instance, in one study (Scarr & Weinberg, 1976), some children of poor parents (with unknown IQs) were adopted by middle-class parents with IQs averaging 118–121. Other children remained with their biological parents. IQ averages of the children in the two groups were as follows:
Although the adopted children’s IQ scores were, on average, lower than those of their adoptive parents, they were about 15 points higher than the scores for the control group children, who were raised by their biological parents.
Effects of early nutrition
Severe malnutrition, either before birth or during the early years of life, can limit neurological development and have a long-term impact on cognitive development and intelligence (Ricciuti, 1993; S. A. Rose, 1994; Sigman & Whaley, 1998). Attention, memory, abstract reasoning, and general school achievement are all likely to suffer from inadequate nutrition. Children sometimes recover from short periods of poor nourishment (due, perhaps, to war or illness), but the adverse effects of long-term deprivation are more enduring (Sigman & Whaley, 1998).
Some research studies have examined the effects of providing medically approved food supplements and vitamins to infants and young children who would not otherwise have adequate nutrition. Such interventions are most likely to enhance children’s development of motor skills, but in some instances cognitive development is enhanced as well (Pollitt & Oh, 1994; Sigman & Whaley, 1998).
Effects of toxic substances
A variety of toxic substances, or teratogens, in children’s prenatal or early postnatal environments—for instance, alcohol, drugs, radiation, lead-based paint dust—affect neurological development and thus also affect children’s later IQ scores (e.g., Michel, 1989; Neisser et al., 1996; Streissguth, Barr, Sampson, & Bookstein, 1994; Vogel, 1997; Vorhees & Mollnow, 1987). An example of such effects is fetal alcohol syndrome, in which children whose mothers consumed large amounts of alcohol during pregnancy show poor motor coordination, delayed language, and mental retardation (Dorris, 1989).
Effects of home environment
One likely explanation for the beneficial effects of adoption is that adoptive parents, who typically have adequate financial resources and high levels of education, can provide a more stimulating home environment than the biological parents might have been able to offer. Correlational studies indicate that stimulating home environments—those in which parents interact frequently with their children, make numerous learning and reading materials available, encourage the development of new skills, use complex sentence structures in conversation, and so on—are associated with higher IQ scores in children (Bradley & Caldwell, 1984; Brooks-Gunn et al., 1996; McGowan & Johnson, 1984). Furthermore, when two biologically unrelated children of the same age are raised by the same parents (typically because one or both children are adopted), the children’s IQs tend to be more similar than we would expect by chance alone—a relationship that can be attributed only to the influence of a common home environment (N. L. Segal, 2000).
We find especially compelling evidence for the beneficial effects of stimulating home environments in an ongoing project in Romania (C. A. Nelson, 2005). As a result of previous government policies, most Romanian orphans were at one time placed in large institutions to be raised. After a change in government and the intervention of a team of developmental psychologists, some institutionalized infants (randomly selected) were placed with adults willing to serve as foster parents. (Sadly, the intervention team could not find foster families for all of the infants.) As researchers periodically assessed the children’s physical and cognitive development, they found dramatic differences between the two groups. Despite adequate nutrition, children remaining in an institution throughout infancy and the preschool years had smaller head circumferences and less brain activity than the foster children. When intelligence was assessed, the institutionalized children had an average IQ of 64 (indicating mental retardation), whereas the foster children, on average, had IQs in the normal range.
Effects of early intervention
Unfortunately, not all children live in homes that provide ongoing stimulation and nurturance. When children live in impoverished or neglectful home environments, enriching preschool programs and other forms of early intervention can make an appreciable difference. For instance, high-quality child care and preschool programs (e.g., Head Start) frequently lead to short-term IQ gains and other cognitive and academic benefits (Bronfenbrenner, 1999; NICHD Early Child Care Research Network, 2002b; Zigler, 2003). The effects of such programs don’t continue indefinitely, however. Without follow-up interventions during the elementary school years, cognitive advantages (e.g., higher IQ scores and academic achievement) often diminish over time and in some cases disappear altogether (Brooks-Gunn, 2003; Farran, 2001).
We must not be disheartened by such results. Publicly funded preschool programs such as Head Start often enroll the most economically disadvantaged children in the community. To study the long-term effects of these programs, researchers sometimes have difficulty finding an appropriate control group. For instance, they may compare children who attended the programs with children who, though not attending preschool, grew up in more advantaged circumstances (Schnur, Brooks-Gunn, & Shipman, 1992). Furthermore, early intervention often leads to long-term improvements in areas not reflected in IQ test scores. For instance, children who attend intensive, developmentally appropriate academic preschool programs are, later on, more likely to have high achievement motivation and self-esteem, less likely to exhibit serious behavior problems or need special education services, and more likely to graduate from high school (F. A. Campbell & Ramey, 1995; McCall & Plemons, 2001; Spencer et al., 2001; Washington & Bailey, 1995).
Early intervention is most effective in fostering intellectual development when it is tailored to children’s existing abilities and interests. But bombarding infants and small children with constant or intense stimulation is not effective. Children seem to have a natural desire to learn about their environment, and most eagerly explore their surroundings. But they can handle only so much information—and certainly only so much new information—at any one time. Furthermore, pushing young children into exceptionally challenging (perhaps age-inappropriate) activities can cause stress, depression and, in some cases, physical harm (Elkind, 1987). And ultimately, a secure, supportive relationship with one or more caregivers or teachers is just as important as age-appropriate toys and activities (S. Loeb, Fuller, Kagan, & Carrol, 2004; NICHD Early Child Care Research Network, 2002b).
Effects of formal schooling
The very act of attending school leads to small increases in IQ. In Western societies, children who begin their educational careers early and attend school regularly have higher IQ scores than children who do not. When children must start school later than they would otherwise for reasons beyond their families’ control, their IQs are at least 5 points lower for every year of delay. Furthermore, children’s IQ scores decline slightly (usually only temporarily) over the course of the summer months, when children are not attending school. And other things being equal, children who drop out have lower IQ scores than children who remain in school, losing an average of almost 2 IQ points for every year of high school not completed (Ceci, 2003; Ceci & Williams, 1997).
The benefits of schooling for intellectual growth are seen in a wide variety of cultures. One probable reason why school attendance affects IQ is that it encourages acquisition of more advanced cognitive processes—rehearsal, organization, metacognition, and so on (M. Cole, 2006). And as Vygotsky pointed out, school provides a systematic means through which children can acquire many concepts and perspectives that previous generations have developed to tackle day-to-day tasks and problems effectively.
The Flynn effect
The last few decades have seen a slow, steady increase in people’s average performance on IQ tests throughout the industrialized world (Flynn, 1987, 1999, 2003; Neisser, 1998b). This trend is commonly known as the Flynn effect. A similar change has been observed in children’s performance on traditional Piagetian tasks (Flieller, 1999). Such improvements are difficult to attribute to heredity because the same gene pool (albeit with an occasional mutation) is passed along from one generation to the next, and so the cause is almost certainly environmental. Theorists disagree as to the likely explanations, however. Better nutrition, smaller family sizes, higher quality home environments, better schooling (for parents as well as children), and more enriching and informative stimulation (increased access to television, reading materials, etc.) are all possibilities (Daley, Whaley, Sigman, Espinosa, & Neumann, 2003; Flynn, 2003; Neisser, 1998b).
How Nature and Nurture Interact in Their Influence on Intelligence
Clearly both nature and nurture influence intelligence. What is less clear is how much influence each of these factors has. A few theorists have tried to estimate nature’s contribution (the heritability of IQ) from the correlations obtained in twin and adoption studies (e.g., McGue et al., 1993; Plomin et al., 1997). But most psychologists now believe that it may ultimately be impossible to separate the relative effects of heredity and environment. They suggest that the two combine to influence children’s cognitive development and measured IQ in ways that we can probably never disentangle (e.g., W. A. Collins et al., 2000; Flynn, 2003; Rogoff, 2003; Turkheimer, 2000). Theorists have made the following general points about how nature and nurture interact as they affect intellectual development:
Heredity establishes a range rather than a precise figure. Heredity does not dictate that a child will have a particular IQ score. Instead, it appears to set a range of abilities within which children will eventually fall, with the actual ability level each one achieves depending on his or her specific environmental experiences (Weinberg, 1989). Heredity may also affect how susceptible or impervious a child is to particular environmental influences (Rutter, 1997). For example, high-quality instruction may be more important for some children than for others. In the opening case study, Gina learned how to read before she attended school, and with only minimal help from her mother. Yet other, equally intelligent children may learn to read only when they have systematic reading instruction tailored to their individual needs.
Genetic expression is influenced by environmental conditions. Genes are not entirely self-contained, independent “carriers” of developmental instructions. Rather, the particular instructions they transmit are influenced by the supportive or nonsupportive nature of children’s environments. In an extremely impoverished environment—one with a lack of adequate nutrition and little if any stimulation—heredity may have little to say about the extent to which children develop intellectually. In an ideal environment—one in which nutrition, parenting practices, and educational opportunities are optimal and age-appropriate—heredity can have a significant influence on children’s IQ scores (Ceci, 2003; D. C. Rowe et al., 1999; Turkheimer, Haley, Waldron, D’Onofrio, & Gottesman, 2003).
Intelligence is almost certainly the result of many genes, each contributing a small amount to measured IQ (Sattler, 2001). These genes may “kick in” at different points in development, and their expression will be influenced by particular environmental conditions at those times. Thus we do not have a single heredity-environment interaction, but rather a number of heredity-environment interactions all contributing to intellectual growth (Simonton, 2001).
Especially as they get older, children choose their environments and experiences. Children may actively seek out environmental conditions that match their inherited abilities—a phenomenon known as niche-picking (Flynn, 2003; Halpern & LaMay, 2000; Scarr & McCartney, 1983). For example, children who, genetically speaking, have exceptional quantitative reasoning ability may enroll in advanced mathematics courses, delight in tackling mathematical brainteasers, and in other ways nurture their inherited talents. Children with average quantitative ability are less likely to take on such challenges and so have fewer opportunities to develop their mathematical skills. In such circumstances the relative effects of heredity and environment are difficult to tease apart.
Earlier we mentioned that the IQ correlations between adopted children and their biological parents become stronger over time. We now have a possible explanation for this finding. Children gain increasing independence as they get older. Especially as they reach adolescence, they spend less time in their home environments, and they make more of their own decisions about the kinds of opportunities to pursue—decisions undoubtedly based, in part, on their natural talents and tendencies (McGue et al., 1993; Petrill & Wilkerson, 2000).
You might think of intelligence as being the result of four factors (Gottlieb, 1991, 1992). Genetic activity affects neural activity (i.e., the operation of neurons in the brain), which in turn affects behavior, which in turn affects the environment. But influence moves in the opposite direction as well: The environment affects behavior, and these two (through stimulation, nutritional intake, physical activity, etc.) affect neural activity and genetic expression.
4In our teaching experiences, we have found that some students erroneously interpret the higher correlations as indicating that identical twins have higher intelligence. This is, of course, not the case. The size of each correlation indicates the strength of the relationship between twins’ IQs, not the level of twins’ intelligence per se.
Excerpt from Child Development and Education, by T.M McDevitt, J.E. Ormrod, 2007 edition, p. 291-296.
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