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The Genetic and Environmental Effects on Human Intelligence
The use of heritability in determining how genetics and environment affect intelligence, and to what extent.
The extent to which intelligence is determined by one’s genes and environment is a rather debatable topic, as there are studies that prove that both factors play a significant role. Heritability, “the proportion of observed variation in a particular trait that can be attributed to inherited genetic factors in contrast to environmental ones” (Merriam-Webster’s collegiate dictionary, 1999), can be used to determine the role that genetics and environment play in determining an individual’s intellectual aptitude. Phenotypic traits are expressed by genes, which are a unit of heredity that is transferred from a parent to offspring and is held to determine some characteristic of the offspring. Environment is seperate from of one’s genes, as it is “the complex of physical, chemical, and biotic factors that act upon an organism or an ecological community and ultimately determine its form and survival” (Merriam-Webster’s collegiate dictionary, 1999). Environmental and genetic factors may go hand in hand as one’s intelligence may not be dependent not on one of them, but both. Intelligence is the ability to acquire and apply knowledge and skills, and is often expressed as IQ (intellectual quotient). IQ heritability is the portion of a population’s IQ variability attributable to the effects of genes (Devlin). After investigating IQ heritability for almost a century, it has been discovered that covariance between relatives may be due not only to genes, but also to shared environments. Covariance is the measure of the joint variability of two random variables. Throughout this essay, I will be analyzing different studies in order to come to a conclusion on how much intelligence is determined by one’s genetics and environment, and how these two factors affect each other in the process.
How Environmental Factors Affect the Extent to Which Genes Determine Intelligence (Evidence that extent that shared environmental influences vary based on what the environment is)
Turkheimer et al. (2003) was a study conducted to test the genotype-environment interaction in the intelligence of young children. Using a sample of seven year old children from the National Perinatal Collaborative Project, it was concluded that genetic and shared environmental influences on IQ were altered by the socioeconomic status of the children (Harden, 273). For underprivileged children, shared environmental influences were responsible for nearly 60% of the variance, while genetic factors were responsible for minor variance. For privileged children, the results were the opposite, with genetic factors being responsible for a majority of the variance. In a replication of Turkheimer et al (2003) called Genotype by Environment Interaction in Adolescents’ Cognitive Aptitude, participants were sampled from 600,000 American adolescents who had taken the National Merit Scholarship Qualifying Test in 1962 in order to investigate genotype-environment interaction in intelligence (Harden, 274) Of these 600,000 adolescents, almost the entirety of them were in juniors in high school as well as 17 years old. 839 of the participants were twins. The NMSQT is made up of five subtests including English Usage, Mathematics Usage, Social Science Reading, Natural Science Reading, and Word Usage/Vocabulary (Harden, 274). The test is claimed to be highly reliable as “The variance of NMSQT total scores is roughly constant across the range of total scores” (Harden, 274). The test is described as “… a measure of cognitive aptitude, students’ readiness for future and intellectual or educational pursuits” (Harden, 274). The test therefore contrasts with the IQ test used in Turkheimer et. al (2003). Nonetheless, it is suggested that both tests accurately display an individual’s general cognitive ability. “Therefore, we can reasonably expect genotype– environment interactions for NMSQT aptitude scores to be similar to those found for IQ, although differences between cognitive ability and cognitive aptitude may have some implications for replication” (Harden, 274). Mothers described their own and the father’s level of education as well as annual family income by completing a survey. “Parental education was classified on a 6-point ordinal scale, from less than an 8th grade education to a graduate or professional degree. Mid-parent education was calculated as the average of maternal and paternal education (median = 3.5; variance = 1.44). Income was classified on a 7-point ordinal scale (median = 3; variance = 2.37), from less than $5000 per year to over $25,000 per year (roughly equivalent to less than $31,250 to over $156,250 in 2004 dollars)” (Harden, 275). As predicted, the dispersal of parental income was not representative of the United States. 84% of the NMSQT families refused to report incomes less than $5000, as opposed to 58% of the 1960 United States Population. The education and income of parents paralleled with adolescents’ NMSQT scores. Twin pair average NMSQT score for twins pairs without parental income disclosure was substantially less than the average score of twin pairs with parents that agreed to disclose income (Harden, 275). On the other hand, twin pair average scores were not affected by failure to receive parental education disclosure.
The first step towards finding the results was to perform an exploratory factor analysis using the twin’s subtest scores. The EFA randomly picked a twin from each pair in attempt to eliminate bias as a result of non-independent observations. For this reason, it was decided to consider genotype-environment interactions for overall cognitive aptitude, as a common factor of the NMSQT subtests (Harden, 275). Through the use of the cognitive aptitude factor, two series of interaction models were used for each measure of SES. Both interaction models broke down the variance of cognitive aptitude into four parts, “variance accounted for by the measured environment (income or education), variance due to other environmental influences shared by twins (C), variance due to additive genetic influences (A), and variance unique to each twin (E; due to environmental influences not shared by twins and measurement error)” (Harden, 275). The principle effect of nonshared environment was estimated due to the strong monozygotic twin correlations for NMSQT proposing that shared influences are insignificant. “Inclusion of the main effects of parental income and education is necessary both because it was hypothesized there are such main effects and because of the possibility of genotype–environment correlation (rGE)” (Harden, 276). Parent’s cognitive aptitude correspond with their levels of income and education which means that the genetic impacts on intellectual aptitude that teenagers inherit parallel with their socioeconomic status. Purcell (2000) was a study that that proved that including the most significant impact of the measured environment disallows bias when estimating genotype-environment correlation. However, in this study, genotype-environment correlation could not be examined because a within-twin pair variation would have been necessary to include in the analysis. Twin pairs were required to be monozygotic for the parental variables used in order to indicate socioeconomic status.
Tables were used to record the common factor model of NMSQT subtest estimates for education and income models. There are slight differences between the two tables with the reason being that they are built upon two vaguely different subsets of the sample. It may also be feasible that that these slight differences between education and income in their accordance to NMSQT subtests are indicated in the measurement segment of the model. The results of the investigation supported the theory that the extent of genetic impacts on intellectual aptitude differs based on socioeconomic status. These results partly reproduce the results found by Turkheimer et al. (2003). Although, no shared environmental interaction impacts were confirmed in the present study. Genetic influences were responsible for close to 55% of the variance in adolescents’ cognitive aptitude while shared environmental influences were responsible for about 35% of the variance amid families of higher income (Holden 280). Amid families of lower income, the proportions were quite the opposite, with genetics influences being responsible for around 39% of the variance and shared environment being responsible for nearly 45% of the variance. This pattern is is similar to the one presented by Turkheimer et al. (2003), but is less pronounced. “We were unable to demonstrate directly that parental income and parental education differ in their interaction with genetic influences on cognitive aptitude; however, income and education models had different patterns of results, with a significant genetic interaction detected only for income” (Holden, 280). This statement suggest that not all aspects of socioeconomic status equally aid the expression of genetic potential. “Overall, these results mirror findings in other areas of behavior genetic research demonstrating that the magnitude of genetic variance is not a static characteristic of a trait but a population statistic that may be moderated by other predictors” (Holden, 280).
Despite the credibility of this replication of Turkheimer et al., there are limitations present throughout the study. The first limitation involves the difficulty with interpreting interaction between genotype and socioeconomic status. The difficulty lies in the idea that socioeconomic status most likely reflects genetic difference between parents as well as differences in the the condition of the environment provided for the children. “The observed increase in heritability with parental income, therefore, may reflect an interaction with genetic differences between more and less affluent families, rather than an interaction with environmental quality. Income, however, is loaded with genetic variance to a lesser extent than parental education or occupational status and is less closely related to parental IQ” (Holden, 281). In addition, there were some issues with using an even distribution of types of participants used in the study. “The National Collaborative Perinatal Project sample over-represented children from extremely disadvantaged environments, with 33% of families on public assistance and 25% of mothers having less than a 9th grade education. In contrast, the adolescents composing the NMSQT sample are relatively advantaged in terms of intellectual ability” (Holden, 281).This uneven representation may have skewed the results of the study. It is then explained that the socioeconomic advantage of NMSQT adolescents may be due to factors including, (a) for this cohort, only adolescents with a certain level of academic achievement took the NMSQT; (b) of twins identified as potential participants, non-response may have been associated with environmental disadvantage” (Holden, 281). Overall, the results of the study are valid due to the extensive precision and accuracy of observed data within. While limitations are present, they do not affect the results of the data extensively.
How Genes Directly Influence Intelligence (Evidence of Direct Genetic Effects on Intelligence making specific references to genetic defects)
While the previous study’s results suggest that the extent of genetic impacts on cognitive aptitude differs based on socioeconomic status, the next studies that will be referenced will focus on direct genetic effects on mental ability. Genetic factors can directly impact mental ability just like how environmental factors can directly influence the extent to which genetics impact intelligence. The author of “Genes for Intelligence”: A Review of Recent Progress, Gerhard Meisenberg, states, “Some of the genetic effects on mental ability appear to be mediated by the speed of neural information processing (Luciano et al., 2004), and others by brain size (Posthuma et al., 2002) or brain structure (Toga and Thompson, 2005). Brain size and the speed of information processing are independently related to intelligence (Walhovd et al., 2005)” (Meisenberg, 139-140). General intelligence, usually determined by IQ tests, is a good applicant for molecular genetic studies because it is known that this trait has quite a high heritability. Meisenburg believes that while there is not much known about the heritability of episodic memory, social skills, common sense and several other cognitive abilities that are not normally included in mental tests, there is no reason to think that these abilities are free from genetic influences (Meisenburg, 140). Molecular genetic studies may uncover genetic variants that impact these abilities selectively and with the abilities incorporated into mental tests.
Mental deficiency is a symptom of several uncommon genetic diseases that are the outcome of significant single-gene defects. “According to a recent search of the Online Mendelian Inheritance in Man database, at least 282 genes are known in which serious mutations can cause mental retardation (Inlow and Restifo, 2004)” (Meisenberg, 140). Meisenburg claims that these mental retardation syndromes are uncommon because the responsible mutations are often removed from the gene pool through natural selection. “We do not know to what extent subtle genetic variants in these mental retardation genes contribute to variations of intelligence in the ‘normal’ range” (Meisenberg, 140). Meisenburg goes on to explain that while mental retardation syndromes are caused by serious genetic defects, IQ variation in the normal range in believed to be contributed to genetic variants with smaller effects (Meisenburg, 140). These variations occur in genes called quantitative trait loci. “As pointed out in an earlier review (Meisenberg, 2003), we can expect two types of genetic variation in these quantitative trait loci. One type consists of damaging mutations that are not sufficiently severe to cause clinically recognized mental retardation syndromes. Most of these mutations are expected to be pleiotropic, having other unfavorable effects in addition to reduced intelligence” (Meisenberg, 140). These undesirable mutations are often eliminated by natural selection throughout the course of several generations and for this reason it is believed that they could never rise to high rates in the population. According to Meisenburg, this is called purifying selection. The majority of genetic forms of mental retardation are the product of mutations that started in the patient or emerged rather recently. “The hypothesis that new mutations are also an important cause of low intelligence in the “normal” population is hard to test directly, but it does make a testable prediction: IQ declines with advanced paternal age” (141-142). New mutations that lead to dominantly inherited diseases are known to be more frequent in kids with fathers on the older side of the age spectrum, and polygenic conditions have also been claimed to grow with paternal age (Meisenburg, 142) “For example, the risk of schizophrenia increases with increased paternal age, presumably as a result of new mutations (El-Saadi et al., 2004). Since low IQ predisposes to schizophrenia (Zammit et al., 2004), it is possible that some mutations have a dual effect, lowering the IQ while raising the schizophrenia risk” (Meisenberg, 142).
Meisenburg is then lead to the idea that if new mutations are a cause of lower intelligence in the standard population, then the children of older fathers are predicted to have lower IQs than those of younger fathers. A recent study exhibited that a paternal age over 45 corresponds with lower IQ in the child. Although, particularly young fathers have children with below-average IQ as well. “The paternal age effect persisted when statistical controls for maternal age, parental education, social class, sex and birth order were included (Malaspina et al., 2005). The IQ decline with advanced paternal age is compatible with a role of new mutations, but it can also be explained by genomic imprinting or by psychosocial factors that were not controlled in Malaspina et al.’s study” (Meisenburg, 142). Though the evidence for a role of new mutations variability is weak, it still makes sense logically. Meisenburg claims that the hypothesis of genetic load, which is the presence of unfavorable genetic material in the genes of a population, is still very plausible despite the lack of evidence. He then goes on to discuss the direct association general intelligence with functional polymorphisms, where he claims that the human genome contains 20,000 to 30,000 protein-coding genes. A substantial portion of these are expressed in the brain, either during early development of later on in life. “One strategy for the identification of ‘IQ genes’ is to focus on genes that are known to play roles either in brain development or in the functioning of the mature brain. Plausible ‘candidate genes’ include, for example, genes encoding neurotransmitter receptors, enzymes of neurotransmitter metabolism, ion channels, intracellular signal transducers, nuclear transcription factors, growth factors, growth factor receptors, or cell adhesion proteins” (Meisenberg, 142-143). It had been found that at least seven candidate genes have corresponded with general intelligence so far. “A group led by David Comings of the City of Hope Medical Center in California reported the association of general intelligence with a polymorphism in the CHRM2 (cholinergic receptor, muscarinic type 2) gene (Comings et al., 2003). The gene product is a brain-expressed receptor for acetylcholine, a neurotransmitter that is known to be involved in cognition” (Meisenberg, 143). In a sample of 828 white Americans, participants homozygous for one of the alleles outperformed participants homozygous for the alternative allele by around 4 IQ points on a composite of four WAIS-R subtests. Heterozygotes scored halfway between the two types of homozygotes and around 1% of the total variability in IQ scores was backed up by this polymorphism. The results of this study lead him to say, “The polymorphism in question is located in the 3′ untranslated region of the gene. Although this mutation does not change the structure of the encoded protein, it may well participate in the regulation of transcription or influence the stability of the messenger RNA, thereby changing the rate at which the encoded protein is synthesized. Alternatively, it may be genetically linked to an as yet unidentified polymorphism nearby, either in the same gene or a neighboring gene” (Meisenberger, 143). He then claims that linkage disequilibrium, which is the non-random co-occurrence of genetic variants should be anticipated whenever two polymorphic sites are near each other on the same chromosome.
Overall, the studies throughout this essay demonstrate that while environmental factors such as socioeconomic status can influence the extent to which genes affect intelligence, genes can also have a direct impact of intelligence, independent of environmental factors. In the replication of Turkheimer et al. called Genotype by Environment Interaction in Adolescents’ Cognitive Aptitude, the adolescent’s results on the National Merit Scholarship Qualifying Test was evidence of correlation between socioeconomic status and how much genes affected the participant’s intelligence. The results of the study were valid due to the extensive precision and accuracy of observed data within. While limitations were present, they did not affect the results of the data extensively. Next, several references to molecular genetic studies were made in order to determine how general intelligence, as assessed by IQ tests, can be affected by defects in genes. It was discussed that while there is not yet sufficient evidence that genetic load is a cause of low intelligence, it is highly plausible. Lastly, it was discussed how polymorphisms have been found to explain variability in IQ scores. Both environmental and genetic factors are integral in the process of determining one’s intelligence, but genetics seem to have a more direct impact than environment.
While the previous study focused on how socioeconomic status affects the shared genetic and environmental effects on IQ, the next study that will be discussed will focus on the varying IQs of monozygotic twins raised together as opposed to apart. This study, in addition to the first, supports the idea that genetics have a significant impact on one’s genetics as researchers discovered that monozygotic twins raised together had equal probabilities of having the same level of intelligence as monozygotic twins raised apart. Monozygotic twins are identical twins as opposed to dizygotic twins which are not identical. “Often, twins are a subject of interest to scientists because identical or monozygotic twins share all of their genes , which allows for the control of genetic differences that is otherwise difficult to achieve with non-identical individuals.” The researchers studied identical twins that were raised apart to create an opportunity to separate the environmental and genetic factors that may have an influence on human features such as intelligence. Author says, “According to the Genetic Science Learning Center of the University of Utah in Salt Lake City, Utah, the strength of twin studies arises from the fact that monozygotic twins share all of their genes, while dizygotic twins on average share about 50 percent of them.” It is this fact that leads to the idea that environmental factors should be entirely to blame for the behavioral differences between monozygotic twins who were separated at birth. “The occurrence of twins being reared apart is rare, but provides an effective way to compare the genetic and environmental influences on human characteristics.” These influences are investigated in what is known as the Minnesota Twin Study.
The Minnesota Twin Study is discussed in the paper, “Sources of Human Psychological Differences: the Minnesota Study of Twins Reared Apart.” For this study, a hundred sets of twins were used from several countries around the globe, including the United States, United Kingdom, China, Germany and Canada. This wide range of origins allows for less cultural bias and results that are a more global representative. The study sample was made up of adult twins who were separated shortly after being born and then reunited as adults. Both monozygotic twins and dizygotic twins were gathered and their zygosities were determined by serological or body fluid comparisons, fingerprint ridge count, and anthropometric measurements. The twin pair proceeded to participate in 50 hours of medical and psychological testing including intellectual aptitude tests. Testing was also executed in order to determine the effect of infancy to adulthood environments on the mental development of the twins pairs. The Twins completed three different IQ tests including the Wechsler Adult Intelligence Scale, the Raven Mill Hill Composite Measurement and the first principle component measurement. These tests were executed in order to determine whether the twins had substantially different IQ scores or if they were about the same. Using heritability, it was found that the IQ scores of the monozygotic twins raised apart were very similar. It was also found that the variation of IQ between monozygotic twins was not only low between those raised apart, but also between those raised together. “Based on that comparison, Bouchard and his colleagues conclude that monozygotic twins reared apart were just as similar as monozygotic twins”
These results led that authors of “” to two possible reasons that the IQs between monozygotic twins were raised apart were so similar. “First, the authors state that the genetic factors strongly influence the behavior and general intelligence of individuals and accounts for about 70 percent of the variation in IQ.” This means that although the twins were raised in two different environments, the genetics impacts outweighed the environmental impacts on their intelligence. “Finally, the authors state that genetic factors control the effects of environmental factors.” This means that no matter how large of an influence environmental factors may have, the genetic similarities between the twins may also cause them to receive the same influence from different environments.
- Devlin, B., Daniels, M., & Roeder, K. (1997). The heritability of IQ. Nature, 388(6641), 468-71. doi:http://dx.doi.org/10.1038/41319
- Meisenberg, G. (2005). “Genes for intelligence”: A review of recent progress.Mankind Quarterly, 46(2), 139-164.
- Eric Turkheimer, A. H., Waldron, M., D’Onofrio, B., & Gottesman, I. I. (2003). Socioeconomic status modifies heritability of IQ in young children. Psychological Science, 14(6), 623-628.
- Bouchard,Thomas J.,,Jr. (1998). Genetic and environmental influences on adult intelligence and special mental abilities. Human Biology, 70(2), 257-79.
- Capron, C., Vetta, A. R., & Vetta, A. (1998). Genetic model fitting in IQ, assortative mating & components of IQ variance. Race, Gender & Class, 5(3), 51.
- Bahjat, Mudhaffar. “‘Sources of Human Psychological Differences: The Minnesota Study of Twins Reared Apart’ (1990), by Thomas J. Bouchard Jr, David T. Lykken, Matthew McGue, Nancy L. Segal and Auke Tellegen.” Semantic Scholar, Arizona State University. School of Life Sciences. Center for Biology and Society. Embryo Project Encyclopedia., 19 Oct. 2017.
- “Dictionary by Merriam-Webster: America’s Most-Trusted Online Dictionary.” Merriam-Webster, Merriam-Webster, www.merriam-webster.com/.
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