Genetic and environmental sources of variance in IQ were estimated from 486 adoptive and biological families
Families include 419 mothers, 201 fathers, 415 adopted and 347 biological fully-adult offspring (Mage = 31.8 years; SD = 2.7)
Proportion of variance in IQ attributable to environmentally mediated effects of parental IQs was estimated at 0.01 [95% CI 0.00, 0.02]
Heritability was estimated to be 0.42 [95% CI 0.21, 0.64]
Parent-offspring correlations for educational attainment polygenic scores show no evidence of adoption placement effect
While adoption studies have provided key insights into the influence of the familial environment on IQ scores of adolescents and children, few have followed adopted offspring long past the time spent living in the family home.
To improve confidence about the extent to which shared environment exerts enduring effects on IQ, we estimated genetic and environmental effects on adulthood IQ in a unique sample of 486 biological and adoptive families. These families, tested previously on measures of IQ when offspring averaged age 15, were assessed a second time nearly 2 decades later (Moffspring age = 32 years).
We estimated the proportions of the variance in IQ attributable to environmentally mediated effects of parental IQs, sibling-specific shared environment, and gene-environment covariance to be 0.01 [95% CI 0.00, 0.02], 0.04 [95% CI 0.00, 0.15], and 0.03 [95% CI 0.00, 0.07] respectively; these components jointly accounted for 8% of the IQ variance in adulthood. The heritability was estimated to be 0.42 [95% CI 0.21, 0.64].
Together, these findings provide further evidence for the predominance of genetic influences on adult intelligence over any other systematic source of variation.
…The question of persistence is perhaps the most important in considering the effects of the rearing environment on IQ, especially since other types of studies have documented a “fadeout” of environmental improvements over time (e.g., Protzko 2015). Kendler and colleagues have used a cosibling control design to examine the effect of the rearing environment on IQ in a sample of 436 adoptive-biological sibships (Kendler et al 2015). These male, 18–20 year old adopted Swedish conscripts showed a mean gain in 4.41 IQ points relative to their biological siblings, who were raised by the original biological family. This finding, which they replicated in a larger sample of half-sibs (with a mean gain of 3.18 IQ points associated with adoption), is a strong indicator that IQ can be, to some extent, affected up to late adolescence by the family environment. These results are consistent with those from the classic cross-fostering study of 14-year-old French children by Capron & Duyme 1989.
Studies such as these do suggest that although this effect is small relative to the genetic effects on IQ, it is not zero; however, the size of this effect diminishes substantially after adolescence. Sandra Scarr, a pioneer of modern IQ adoption studies, was perhaps the first to note this fadeout phenomenon (e.g., Scarr & Weinberg 1978). With respect to the tapering correlations in IQ between children and their adoptive parents as the child matured, observed in the Minnesota Adolescent Adoption Study, Scarr & Weinberg remarked:
“We interpret the results to mean that younger children, regardless of their genetic relatedness, resemble each other intellectually because they share a similar rearing environment. Older adolescents, on the other hand, resemble one another only if they share genes. Our interpretation is that older children escape the influences of the family and are freer to select their own environments. Parental influences are diluted by the more varied mix of adolescent experiences.” (Scarr & Weinberg, 1983, p. 264).
…We tested for placement effects using polygenic scores for educational attainment (PGSEA) derived from the largest genome-wide association study to date (Lee et al 2018)…In an aggregated sample consisting of all white participants (offspring and both parents), an R2 of 0.154 [95% CI 0.113, 0.195] in our prediction of Verbal IQ with a PGS surpasses all previous benchmarks known to us (Allegrini et al 2019; Lee et al 2018; Rietveld et al 2014; Savage et al 2018; Selzam et al 2016; Sniekers et al 2017), and an R2 of 0.114 [95% CI 0.077, 0.151] for Total IQ is near the upper end of previous predictions (SI Table S13). However, we acknowledge that our sample is not large by the standards of PGS validation…These scores also enable a unique test for the so-called “placement effect”, wherein adoptees (typically twins reared apart) are thought by some skeptics to resemble their adoptive parents prior to placement, thus biasing biometrical estimates. By demonstrating a total lack of evidence (p = 0.514) for a correlation between parents and adoptive offspring in polygenic scores, we provide support for the validity of at least some adoption studies in establishing causal inference…the similarity of these correlations to their theoretically predicted values provides evidence that the placement of adoptees in their homes was not strongly purposive or selective, implying that the adoption process may somewhat approximate a true experiment.
…IQ has been subject to a large number of twin and adoption studies, many of which have found a small but statistically-significant effect of parental transmission in adoptive samples up until late adolescencent…Our biometric decomposition of variance is consistent with this figure: the parental environment contributing 4% of the variance in fullscale IQs at age ~15 (Table 3), with a standard deviation of 14.2 for full-scale IQ in adopted offspring, indicates that a 1-SD increase in the quality of the parental environment would increase IQ by approximately 2.83 points (i.e., 14.2 × √0.04; Burks 1938).
The evidence for parenting effects on Wechsler IQ subtests is more equivocal, and biometric decomposition reveals a moderate but statistically-significant effect of gene-environment covariance on Vocabulary in childhood. While a similarly-sized G-E covariance is observed for childhood Total IQ, this effect has completely disappeared in adulthood; the same cannot be said unambiguously for Vocabulary, which retains weak evidence in adulthood for a persistent parenting effect.
This paper investigates whether the impact of children on the labor market outcomes of women relative to men—child penalties—can be explained by the biological links between mother and child. We estimate child penalties in biological and adoptive families using event studies around the arrival of children and almost 40 years of adoption data from Denmark. Short-run child penalties are slightly larger for biological mothers than for adoptive mothers, but their long-run child penalties are virtually identical and precisely estimated. This suggests that biology is not a key driver of child-related gender gaps.
Mental disorders in children decreased continuously with increasing parental income for all mental disorders, except eating disorders.
The parental-income gradient was largest for attention-deficit hyperactivity disorder, followed by anxiety and depression.
Our study suggests that associations between lower parental income and children’s mental disorders were partly, but not fully, attributed to other socio-demographic factors, parents’ own mental disorders and genetic factors.
Background: Children with low-income parents have a higher risk of mental disorders, although it is unclear whether other parental characteristics or genetic confounding explain these associations and whether it is true for all mental disorders.
Methods: In this registry-based study of all children in Norway (n = 1 354 393) aged 5–17 years from 2008 to 2016, we examined whether parental income was associated with childhood diagnoses of mental disorders identified through national registries from primary healthcare, hospitalizations and specialist outpatient services.
Results: There were substantial differences in mental disorders by parental income, except for eating disorders in girls. In the bottom 1% of parental income, 16.9% [95% confidence interval (CI): 15.6, 18.3] of boys had a mental disorder compared with 4.1% (95% CI: 3.3, 4.8) in the top 1%. Among girls, there were 14.2% (95% CI: 12.9, 15.5) in the lowest, compared with 3.2% (95% CI: 2.5, 3.9) in the highest parental-income percentile. Differences were mainly attributable to attention-deficit hyperactivity disorder in boys and anxiety and depression in girls. There were more mental disorders in children whose parents had mental disorders or low education, or lived in separate households. Still, parental income remained associated with children’s mental disorders after accounting for parents’ mental disorders and other factors, and associations were also present among adopted children.
Conclusions: Mental disorders were 3× to 4× more prevalent in children with parents in the lowest compared with the highest income percentiles. Parents’ own mental disorders, other socio-demographic factors and genetic confounding did not fully explain these associations.
We show that family background matters statistically-significantly for children’s accumulation of wealth and investor behavior as adults, even when removing the genetic connection between children and the parents raising them. The analysis is made possible by linking Korean-born children who were adopted at infancy by Norwegian parents to a population panel data set with detailed information on wealth and socioeconomic characteristics. The mechanism by which these Korean-Norwegian adoptees were assigned to adoptive families is known and effectively random. This mechanism allows us to estimate the causal effects from an adoptee being raised in one type of family versus another.
…The linear rank correlations are 0.24 and 0.16 for the samples of non-adoptees and adoptees, respectively. This means that, on average, a 10 percentile increase in parent net wealth is associated with a 2.4 percentile increase in a biological child’s net wealth and a 1.6 percentile increase in an adoptee’s net wealth…On average, the adoptees accrue an extra US$2,250 of wealth if they are assigned to an adoptive family with US$10,000 of additional wealth. The magnitude of this estimate suggests that adoptees raised by parents with a wealth level that is 10% above the mean of the parent generation can expect to obtain a wealth level that is almost 3.7% above the mean of the child generation.
…We find that the indirect effects arising from changes in the observed mediator variables explain about 37% of the average causal effect from assignment to wealthier parents on children’s accumulation of wealth. Direct transfers of wealth are the most important mediator variable, accounting for almost 90% of the indirect effect.
…Columns 1 and 2 in panel A of Table 5 suggest that both family environment and genetics are important in explaining the variation in children’s wealth accumulation. Shared environment accounts for about 16% (10%) of the variation in net (financial) wealth accumulation. Relative to shared environment, the genetic factors explain a larger portion (twice as much or more) of the variation in wealth accumulation (both net and financial wealth). These findings are consistent with the results in Table 3, showing statistically-significant but less wealth transmission from parents to adoptees as compared with non-adoptees.
As shown in column 3 in panel A of Table 5, shared environment is also important for explaining the variation in financial risk-taking, as measured by the risky share. By comparison, genetic factors explain little of the variation in this measure of financial risk-taking. In column 4 of Table 5, we report results for education as measured by years of schooling. These results are close to the American study of Korean adoptees by Sacerdote (2007), who finds that 9% of the variation in years of schooling can be explained by shared environment, while 60% is attributable to genes.
Objective: College attainment is one of the few phenotypes to have substantial variance accounted for by environmental factors shared by reared-together relatives. The shared environment is implicated by the consistently strong parent-to-offspring transmission of college attainment. The mechanisms underlying this relationship remain unclear. We use genetically informative methods with a longitudinal, adoption sample to identify possible environmental mechanisms underlying parent-offspring college transmission.
Method: Data were drawn from the Sibling Interaction and Behavior Study (SIBS), which includes 409 adoptive and 208 nonadoptive families, consisting of two offspring followed from adolescence into young adulthood and their rearing parents. Four domains of environmental mechanisms were examined: (a) skill enhancement; (b) academic support; (c) material advantage; and (d) supportive family environment.
Results: Both shared environmental and genetic factors contributed to the parent-offspring transmission of college attainment. However, highly educated parents did not appear to be increasing their adopted offspring’s attainment through skill development. The environmental factors that were associated with increased odds of offspring college attainment were mother’s academic expectations and family income.
Conclusion: While complete mediation of the parent-offspring transmission of college attainment was not identified, the results shed light on some of the mechanisms associated with the common environment variance in the college attainment phenotype.
Sociological research has traditionally emphasized the importance of post-birth factors (ie., social, economic, and cultural capital) in the intergenerational transmission of educational advantages, to the neglect of potentially consequential pre-birth endowments (eg., heritable traits) that are passed from parent to child. In this study, we leverage an experiment of nurture—children who were adopted at birth into nonrelative families—in an effort to simultaneously model the effects associated with both pathways. To do so, we fit a series of simple linear regression models that relate the academic achievement of adopted children to the educational attainments of their adoptive and biological parents, using U.S. data from a recent nationwide sample of birth and adoptive families (the Early Growth and Development Study). Because our dataset includes both “genetic” and “environmental” relatives, but not “genetic-and-environmental” relatives, the separate contributions of each pathway can be identified, as well as possible interactions between the two. Our results show that children’s early achievements are influenced not only by the attainments of their adoptive parents, but also the attainments of their birth parents—suggesting the presence of environmental and genetically mediated effects. Supplementary analyses provide little evidence of effect moderation, using both distal and proximate measures of the childhood environment to model gene-by-environment interactions. These findings are robust to a variety of parameterizations, withstand a series of auxiliary checks, and remain intact even after controlling for intrauterine exposures and other measurable variables that could compromise our design. The implications of our results for theory and research in the stratification literature, and for those interested in educational mobility, are discussed.
Background: Being adopted early in life, an indicator of exposure to early-life adversity, has been consistently associated with poor mental health outcomes in adulthood. Such associations have largely been attributed to stressful environments, eg., exposure to trauma, abuse, or neglect. However, mental health is substantially heritable, and genetic influences may contribute to the exposure to childhood adversity, resulting in potential genetic confounding of such associations.
Methods: Here, we explored associations between childhood adoption and mental health-related outcomes in midlife in 243,797 UK Biobank participants (n adopted = 3151). We used linkage disequilibrium score regression and polygenic risk scores for depressive symptoms, schizophrenia, neuroticism, and subjective well-being to address potential genetic confounding (gene-environment correlations) and gene-environment interactions. As outcomes, we explored depressive symptoms, bipolar disorder, neuroticism, loneliness, and mental health-related socioeconomic and psychosocial measures in adoptees compared with non-adopted participants.
Results: Adoptees were slightly worse off on almost all mental, socioeconomic, and psychosocial measures. Each standard deviation increase in polygenic risk for depressive symptoms, schizophrenia, and neuroticism was associated with 6%, 5%, and 6% increase in the odds of being adopted, respectively. Statistically-significant genetic correlations between adoption status and depressive symptoms, major depression, and schizophrenia were observed. No evidence for gene-environment interaction between genetic risk and adoption on mental health was found.
Conclusions: The association between childhood adoption and mental health cannot fully be attributed to stressful environments but is partly explained by differences in genetic risk between adoptees and those who have not been adopted (ie., gene-environment correlation).
…One of my Facebook friends did not agree. She responded that the big difference between human pet-keeping and this unusual dolphin/whale relationship was that human females never breast-feed members of other species. But she was wrong. The surprising fact is that in many parts of the world, there is a long history of women nursing animals. To modern sensibilities, the idea of a woman suckling an animal is, to say the least, weird, and even perverted.
And yet, both of the two most important books on the evolution of pets, James Serpell’s In the Company of Animals and Psychology Today blogger John Bradshaw’s The Animals Among Us, discuss the role of wet-nursing animals by women in the origins of pet-keeping. Indeed, Bradshaw writes, “Far from an aberration confined to one tribe, breast-feeding of pets used to occur all over the world…” The most extensive academic treatise on the geography and functions of women breastfeeding animals is a fascinating but little known 1982 article by Fredrick Simoons and James Baldwin titled “Breast-Feeding of Animals: Its Socio-Cultural Context and Geographic Occurrence.” The authors were particularly interested in regional differences in the suckling of animals…Why Do Women Breast-feed Animals? Simoons and Baldwin reported that wet-nursing of young animals occurred in different societies for four reasons:
Affectionate Breast-feeding: In affectionate breast-feeding, women elected to nurse baby animals out of “compassion, warmth, love.” These creatures were essentially pets treated like human babies. This form of nursing was most common among the hunter-gatherers of the Amazon and the Malay Peninsula.
Economic Breast-feeding: In economic breast-feeding, young animals were nursed primarily for utilitarian purposes, for example, the rearing of a hunting dog. On Polynesian islands where dogs were on the menu, puppies were breastfed in order to improve the flavor of their flesh when they were consumed as adults.
Ceremonial Breast-feeding: This rare form of animal nursing was practiced by the Ainu in Japan who raised bear cubs for sacrificial slaughter.
Human Welfare Breast-feeding: In these cases, animals were nursed for the benefit of the humans. The most common examples were in cultures in which lactating women breast-fed animals to relieve breast pain. And as Carys Williams and her colleagues pointed out, breast-feeding puppies in Polynesia may even have been used as a form of contraception by extending lactation.
…Animal Breastfeeding and the Origins of Pet-keeping: Simoons and Baldwin argue that breast-feeding was an important step on the path to pet-keeping and the domestication of animals. John Bradshaw is not so sure. He writes, “Just because women in other cultures interacted with animals in ways that seen unfathomably intense to us does not mean they automatically considered them”pet" in the sense that we do." His point is well-taken. However, I still don’t see much difference between the adoption of a baby melon-headed whale by a nurturing mother dolphin, and the modern penchant for adopting puppies and kittens, showering them with love, and calling them “our babies.”
An extensive body of research has examined the role that genetic influences play in the development of antisocial behavior. Even so, there remains much that is unknown regarding the intersections among antisocial behavior, environments, and genetic influences. The current study is designed to shed some light on this issue by examining whether gene-environment correlations are present in the lives of adopted adolescents. More specifically, this article seeks to contribute to scholarship efforts aimed at understanding whether biological parents’ antisocial behavioral phenotypes—behaviors often attributed to an increased likelihood of receiving a genetic propensity for antisocial behaviors—predict variation in environments that are experienced by their adopted-away offspring. To do so, the biological parents of adoptees were assessed and used to identify ways in which children elicit certain responses from their adoptive parents based, in part, on their genotype. Correlational analyses were calculated on a sample of adoptees (the final analytic sample ranged between n = 229 and n = 293) drawn from the National Longitudinal Study of Adolescent to Adult Health (Add Health). The results of the study revealed very little evidence of gene–environment correlations. The implications of these findings are considered.
Virtual twins (VTs) are defined as same-age unrelated siblings raised together from early infancy. This special class of adoptive siblings replays the rearing situation of twins, absent genetic relatedness. The first such pair was identified and studied in 1990 at the University of Minnesota, leading to the creation of the Fullerton Virtual Twin Study (FVTS) at California State University, Fullerton(CSUF) the following year. The registry currently includes 169 VT pairs, mostly children, with new pairs identified on a regular basis. These sibling sets provide a direct estimate of environmental influences on developmental traits and, as such, offer informative comparisons with ordinary monozygotic and dizygotic twins, full siblings and adoptive brothers and sisters. The sample characteristics, assessment battery and findings to date are summarized in this 2019 update.
We used classical and extended adoption designs in Swedish registries to disentangle genetic and rearing-environment influences on the intergenerational transmission of divorce. In classical adoption analyses, adoptees (n = 19,715) resembled their biological parents, rather than their adoptive parents, in their history of divorce. In extended adoption analyses, offspring (n = 82,698) resembled their not-lived-with fathers and their lived-with mothers. There was stronger resemblance to lived-with mothers, providing indirect evidence of rearing-environment influences on the intergenerational transmission of divorce. The heritability of divorce assessed across generations was 0.13. We attempted to replicate our findings using within-generation data from adoptive and biological siblings (ns = 8,523–53,097). Adoptees resembled their biological, not adoptive, siblings in their history of divorce. Thus, there was consistent evidence that genetic factors contributed to the intergenerational transmission of divorce but weaker evidence for a rearing-environment effect of divorce. Within-generation data from siblings supported these conclusions.
Teenagers face some serious issues: drugs, bullying, sexual violence, depression, gangs. They don’t always like to talk about these things with adults. One way that researchers and educators can get around that is to give teens a survey—a simple, anonymous questionnaire they can fill out by themselves without any grown-ups hovering over them. Hundreds of thousands of students take such surveys every year. School districts use them to gather data; so do the federal government, states and independent researchers.
But a new research paper points out one huge potential flaw in all this research: kids who skew the results by making stuff up for a giggle. “Mischievous Responders”, they’re called.
They may say they’re 7 feet tall, or weigh 400 pounds, or have three children. They may exaggerate their sexual experiences, or lie about their supposed criminal activities…For example, 41% of the students who claimed they were transgender also claimed to be extremely tall or short, and the same percentage also claimed they were in a gang…In other words, kids will be kids, especially when you ask them about sensitive issues.
Jackson Terry, 14, says he answered honestly when he took one of these surveys last year, but he knows kids who didn’t. “They handed out the sheet, I believe it was in language class”, says Terry, who’s from Granville, Ohio. “The teacher was in the room. It was anonymous. I think they asked us about bullying, do you feel safe in school, some questions about drugs, the learning environment.” Some kids “would joke through the entire thing and have a cocky attitude about it”, Terry says. “Afterwards some would say, yeah, No. 5, that’s totally not true; I just made something up.”
…This is important because researchers are often the most interested in minority groups, and so the undetected presence of a small number of jokesters can seriously mess up results. In a 2003 study, 19% of teens who claimed to be adopted actually weren’t, according to follow-up interviews with their parents. When you excluded these kids (who also gave extreme responses on other items), the study no longer found a statistically-significant difference between adopted children and those who weren’t on behaviors like drug use, drinking and skipping school. The paper had to be retracted. In yet another survey, fully 99% of 253 students who claimed to use an artificial limb were just kidding.
“Part of you laughs about it, and the researcher side is terrified”, says Robinson-Cimpian. “We have to do something about this. We can’t base research and policy and beliefs about these kids on faulty data.”
This article introduces novel sensitivity-analysis procedures for investigating and reducing the bias that mischievous responders (ie., youths who provide extreme, and potentially untruthful, responses to multiple questions) often introduce in adolescent disparity estimates based on data from self-administered questionnaires (SAQs). Mischievous responders affect a wide range of disparity estimates, including those between adoptees and non-adoptees, sexual minorities and non-minorities, and individuals with and without disabilities. Thus, the procedures introduced here have broad relevance to research and can be widely, and easily, implemented. The sensitivity-analysis procedures are illustrated with SAQ data from youths in Grades 9–12 (n = 11,829) to examine between-group disparities based on sexual identity, gender identity, and physical disability. Sensitivity analyses revealed that each disparity estimated with these data was extremely sensitive to the presence of potentially mischievous responders. Patterns were similar across multiple approaches to dealing with mischievous responders, across various outcomes, and across different between-group comparisons. Mischievous responders are ubiquitous in adolescent research using SAQs and can, even in small numbers, lead to inaccurate conclusions that substantively affect research, policy, and public discourse regarding a variety of disparities. This article calls attention to this widespread problem and provides practical suggestions for assessing it, even when data are already collected.
The longitudinal rank-order stability of cognitive ability increases dramatically over the lifespan. Multiple theoretical perspectives have proposed that genetic and/or environmental mechanisms underlie the longitudinal stability of cognition, and developmental trends therein. However, the patterns of stability of genetic and environmental influences on cognition over the lifespan largely remain poorly understood.
We searched for longitudinal studies of cognition that reported raw genetically-informative longitudinal correlations or parameter estimates from longitudinal behavior genetic models. We identified 150 combinations of time points and measures from 15 independent longitudinal samples. In total, longitudinal data came from 4,538 monozygotic twin pairs raised together, 7,777 dizygotic twin pairs raised together, 34 monozygotic twin pairs raised apart, 78 dizygotic twin pairs raised apart, 141 adoptive sibling pairs, and 143 non-adoptive sibling pairs, ranging in age from infancy through late adulthood.
At all ages, cross-time genetic correlations and shared environmental correlations were substantially larger than cross-time nonshared environmental correlations. Cross-time correlations for genetic and shared environmental components were low during early childhood, increased sharply over child development, and remained relatively high from adolescence through late adulthood. Cross-time correlations for nonshared environmental components were low across childhood and increased gradually to moderate magnitudes in adulthood. Increasing phenotypic stability over child development was almost entirely mediated by genetic factors. Time-based decay of genetic and shared environmental stability was more pronounced earlier in child development.
Results: are interpreted in reference to theories of gene-environment interaction and correlation.
In 1998, Robert Plomin and his Colorado Adoption Project (CAP) colleagues published the results of a longitudinal adoption study of personality. They found an average personality test score correlation of only 0.01 between birth-parents and their 240 adopted-away 16-year-old biological offspring, suggesting no genetic influences on personality. However, the researchers interpreted their results in the context of previous twin studies, produced an average 14% heritability estimate, and concluded that nonadditive genetic factors underlie personality traits. The author challenges these conclusions and notes that the near-zero correlation stands in contrast to other types of behavioral genetic methods, such as twin studies, that are more vulnerable to environmental confounds and other biases. The author shows that authoritative psychology texts frequently fail to mention this 1998 CAP study. When it is mentioned, the original researchers’ conclusions are usually accepted without critical analysis. The author also assesses the results in the context of the 20-year failure to discover the genes that behavioral geneticists believe underlie personality traits. He concludes that this 1998 investigation is a “lost study” in the sense that, although it is one of the most methodologically sound behavioral genetic studies ever performed, its results are largely unknown.
We review new findings and new theoretical developments in the field of intelligence. New findings include the following: (a) Heritability of IQ varies statistically-significantly by social class. (b) Almost no genetic polymorphisms have been discovered that are consistently associated with variation in IQ in the normal range. (c) Much has been learned about the biological underpinnings of intelligence. (d) “Crystallized” and “fluid” IQ are quite different aspects of intelligence at both the behavioral and biological levels. (e) The importance of the environment for IQ is established by the 12-point to 18-point increase in IQ when children are adopted from working-class to middle-class homes. (f) Even when improvements in IQ produced by the most effective early childhood interventions fail to persist, there can be very marked effects on academic achievement and life outcomes. (g) In most developed countries studied, gains on IQ tests have continued, and they are beginning in the developing world. (h) Sex differences in aspects of intelligence are due partly to identifiable biological factors and partly to socialization factors. (1) The IQ gap between Blacks and Whites has been reduced by 0.33 SD in recent years. We report theorizing concerning (a) the relationship between working memory and intelligence, (b) the apparent contradiction between strong heritability effects on IQ and strong secular effects on IQ, (c) whether a general intelligence factor could arise from initially largely independent cognitive skills, (d) the relation between self-regulation and cognitive skills, and (e) the effects of stress on intelligence.
Context: Prior research suggests that drug abuse (DA) is strongly influenced by both genetic and familial environmental factors. No large-scale adoption study has previously attempted to verify and integrate these findings.
Objective: To determine how genetic and environmental factors contribute to the risk for DA.
Design: Follow-up in 9 public databases (1961-2009) of adopted children and their biological and adoptive relatives.
Participants: The study included 18 115 adopted children born between 1950 and 1993; 78,079 biological parents and siblings; and 51,208 adoptive parents and siblings.
Main Outcome Measures: Drug abuse recorded in medical, legal, or pharmacy registry records.
Results: Risk for DA was significantly elevated in the adopted offspring of biological parents with DA (odds ratio, 2.09; 95% CI, 1.66-2.62), in biological full and half siblings of adopted children with DA (odds ratio, 1.84; 95% CI, 1.28-2.64; and odds ratio, 1.41; 95% CI, 1.19-1.67, respectively), and in adoptive siblings of adopted children with DA (odds ratio, 1.95; 95% CI, 1.43-2.65). A genetic risk index (including biological parental or sibling history of DA, criminal activity, and psychiatric or alcohol problems) and an environmental risk index (including adoptive parental history of divorce, death, criminal activity, and alcohol problems, as well as an adoptive sibling history of DA and psychiatric or alcohol problems) both strongly predicted the risk for DA. Including both indices along with sex and age at adoption in a predictive model revealed a significant positive interaction between the genetic and environmental risk indices.
Conclusions: Drug abuse is an etiologically complex syndrome strongly influenced by a diverse set of genetic risk factors reflecting a specific liability to DA, by a vulnerability to other externalizing disorders, and by a range of environmental factors reflecting marital instability, as well as psychopathology and criminal behavior in the adoptive home. Adverse environmental effects on DA are more pathogenic in individuals with high levels of genetic risk. These results should be interpreted in the context of limitations of the diagnosis of DA from registries.
This chapter reviews the recent evidence of genetic and environmental influences on human aggression. Findings from a large selection of the twin and adoption studies that have investigated the genetic and environmental architecture of aggressive behavior are summarized. These studies together show that about half (50%) of the variance in aggressive behavior is explained by genetic influences in both males and females, with the remaining 50% of the variance being explained by environmental factors not shared by family members. Form of aggression (reactive, proactive, direct/physical, indirect/relational), method of assessment (laboratory observation, self-report, ratings by parents and teachers), and age of the subjects-all seem to be significant moderators of the magnitude of genetic and environmental influences on aggressive behavior. Neither study design (twin vs. sibling adoption design) nor sex (male vs. female) seems to impact the magnitude of the genetic and environmental influences on aggression. There is also some evidence of gene-environment interaction (G × E) from both twin/adoption studies and molecular genetic studies. Various measures of family adversity and social disadvantage have been found to moderate genetic influences on aggressive behavior. Findings from these G × E studies suggest that not all individuals will be affected to the same degree by experiences and exposures, and that genetic predispositions may have different effects depending on the environment.
One of the most important findings that has emerged from human behavioral genetics involves the environment rather than heredity, providing the best available evidence for the importance of environmental influences on personality, psychopathology, and cognition. The research also converges on the remarkable conclusion that these environmental influences make two children in the same family as different from one another as are pairs of children selected randomly from the population. The theme of the target article is that environmental differences between children in the same family (called “nonshared environment”) represent the major source of environmental variance for personality, psychopathology, and cognitive abilities. One example of the evidence that supports this conclusion involves correlations for pairs of adopted children reared in the same family from early in life. Because these children share family environment but not heredity, their correlation directly estimates the importance of shared family environment. For most psychological characteristics, correlations for adoptive “siblings” hover near zero, which implies that the relevant environmental influences are not shared by children in the same family. Although it has been thought that cognitive abilities represent an exception to this rule, recent data suggest that environmental variance that affects IQ is also of the nonshared variety after adolescence. The article has three goals: (1) To describe quantitative genetic methods and research that lead to the conclusion that nonshared environment is responsible for most environmental variation relevant to psychological development, (2) to discuss specific nonshared environmental influences that have been studied to date, and (3) to consider relationships between nonshared environmental influences and behavioral differences between children in the same family. The reason for presenting this article in BBS is to draw attention to the far-reaching implications of finding that psychologically relevant environmental influences make children in a family different from, not similar to, one another.
I analyze a new set of data on Korean American adoptees who were quasi-randomly assigned to adoptive families.
I find large effects on adoptees’ education, income, and health from assignment to parents with more education and from assignment to smaller families. Parental education and family size are statistically-significantly more correlated with adoptee outcomes than are parental income or neighborhood characteristics. Outcomes such as drinking, smoking, and the selectivity of college attended are more determined by nurture than is educational attainment.
Using the standard behavioral genetics variance decomposition, I find that shared family environment explains 14% of the variation in educational attainment, 35% of the variation in college selectivity, and 33% of the variation in drinking behavior.
This article notes 5 reasons why a correlation between a risk (or protective) factor and some specified outcome might not reflect environmental causation. In keeping with numerous other writers, it is noted that a causal effect is usually composed of a constellation of components acting in concert. The study of causation, therefore, will necessarily be informative on only one or more subsets of such components. There is no such thing as a single basic necessary and sufficient cause. Attention is drawn to the need (albeit unobservable) to consider the counterfactual (ie., what would have happened if the individual had not had the supposed risk experience). 15 possible types of natural experiments that may be used to test causal inferences with respect to naturally occurring prior causes (rather than planned interventions) are described. These comprise 5 types of genetically sensitive designs intended to control for possible genetic mediation (as well as dealing with other issues), 6 uses of twin or adoptee strategies to deal with other issues such as selection bias or the contrasts between different environmental risks, 2 designs to deal with selection bias, regression discontinuity designs to take into account unmeasured confounders, and the study of contextual effects. It is concluded that, taken in conjunction, natural experiments can be very helpful in both strengthening and weakening causal inferences.
Some polygenic traits—eg. stature, IQ, harm avoidance, negative emotionality, interest in sports—are polygenic-additive, so pairs of relatives resemble one another on the given trait in proportion to their genetic similarity.
But the existence and the intensity of other important psychological traits seem to be emergent properties of gene configurations (or configurations of independent and partially genetic traits) that interact multiplicatively rather than additively. Monozygotic (MZ) twins may be strongly correlated on such emergenic traits, while the similarity of dizygotic (DZ) twins, sibs or parent-offspring pairs may be much less than half that of MZ pairs. Some emergenic traits, although strongly genetic, do not appear to run in families.
MISTRA has provided at least two examples of traits for which MZAtwins are strongly correlated, and DZA pairs correlate near zero,while DZ pairs reared together (DZTs) are about half as similar asMZTs.
These findings suggest that even more traits may be emergenic than those already identified. Studies of adoptees reared together (who are perhaps more common than twins reared apart) may help to identify traits that are emergenic, but that also are influenced by a common rearing environment.
Group and individual-difference adoption designs lead to opposite conclusions concerning the importance of shared environment (SE) for the child outcomes of IQ and antisocial behavior. This paradox could be due to the range restriction (RR) of family environments (FE) that goes with adoption studies. Measures of FE from 2 of the most recent adoption studies indicate that RR is substantial, about 67%, which corresponds to the top half of a normal FE distribution. FE of 57% cuts effect sizes and R2 statistics by factors of 3 and 2–2.5, respectively. Because selection into an option study is inherently a between-family process and assuming that comparable restriction of genetic (G) influences are absent, estimates of SE, G, and nonshared influences will be substantially biased, respectively, down, up, and up by RR. Corrections for RR applied to adoption studies indicate that SE could account for as much as 50% of the variance in IQ.
[Keywords: restricted range of family environments, estimates of heritability & nonshared environment for child outcomes of IQ & antisocial behavior in behavior-genetic adoption studies]
Annals Of Science about a case of child abuse in which a child named Genie was kept isolated from the world, locked in a restraining harness in a silent bedroom in her parent’s house in Temple City, California. She was either harnessed to an infant’s potty chair, unable to move anything except her fingers and hands, feet and toes, she was left to sit, tied-up, hour after hour, often into the night, day after day, month after month, year after year. At night, when Genie was not forgotten, she was placed into another restraining garment—a sleeping bag which her father had fashioned to hold Genie’s arms stationary. In effect, it was a straight jacket. Describes her environment, and the “toys” she was given to “play” with. Because of two plastic raincoats that were sometimes hung in the room, she had an inordinate fondness for anything plastic. She was incarcerated by her father for 11 1⁄2 of the first 13 years of her life in a silent room. She could not speak when she was rescued, and only learned to talk when she reached the hospital. Tells about the fallout, both in human terms and legally, surrounding the research into her linguistic abilities. Investigations of Genie’s brain unveiled the utter dominance of her “spatial” right hemisphere over her “linguistic” left…This may have been why she was unable to grasp grammar—because she was using the wrong equipment…From the misfortunes of brain-damaged people, it is clear that language tasks are dispersed within their left-hemisphere home. Someone whose brain is injured above the left ear will still be able to speak, but there will be no idea behind the word strings…Tells about a suit her mother, Irene, brought against the hospital when her therapy sessions with hospital staff were included in research results by Susan Curtiss, a graduate student studying Genie. The results of Curtiss’s doctorate study seemed to both confirm and deny linguist Noam Chomsky’s theory about language acquisition. Genie was shuttled from foster home to foster home after the scientists at the hospital (including the head of research, David Rigler, who adopted her for four years) ran out of grant money. She is currently institutionalized in an adult home for the mentally retarded, and in the words of one scientist, Jay Shurley, filled with a soul-sickness, and sinking into an apparent’ replica of an organic dementia.
An important question in studies of mental ability concerns the effect of parental socio-economic status (SES) on the IQ of their offspring. Only a full cross-fostering study, including children born to biological parents from the most highly contrasting SES and adopted by parents with equally contrasting SES, can answer this question.
Previous adoption studies using incomplete cross-fostering designs1–3 have indicated an effect of postnatal environment on the IQ of children born to low-SESbackgrounds and adopted by high-SES parents. They have not shown whether a low SES reduces the IQ of children born to high-SES parents or whether the SES of biological parents has an effect on IQ, or whether the effect of the SES of adoptive parents is independent of the SES of biological parents.
We present a full cross-fostering study dealing with IQ, and find that children adopted by high-SES parents score higher than children adopted by low-SES parents; children born to high-SES parents score higher than children born to low-SES parents; and that there is no evidence for an interaction between these 2 factors on children’s IQ.
The well-known study by Skodak & Skeels 1949, in which 100 infants who were born to unwed mothers of below-average IQ and were adopted into superior foster homes and grew up to obtain Stanford-Binet IQs averaging 20 points higher than the IQs of their biological mothers, has frequently been interpreted as a contradiction of the evidence for the high heritability of intelligence.
It is here shown that this is a misinterpretation of the Skodak and Skeels results, based on failure to consider the prediction made from a simple polygenic model of parent-offspring resemblance.
The Skodak and Skeels data, when analyzed properly in terms of a quantitative-genetic model, are found to be not all improbable or contradictory of a broad heritability for IQ in the range of 0.70 to 0.80. Also, the common fallacy of generalizing the results of Skodak and Skeels as an environmental explanation of the cause of the approximately 1 σ mean white-Negro IQ difference is explicated from the standpoint of genetic theory.
“The present study approaches the problem by a comparison of two groups of children living in approximately identical environments.” One group consists of adopted children and the other of “own” children. After surveying the records of 2449 children, 194 adopted children between the ages 5 and 14 (white, non-Jewish, north-European, and placed in their adoptive homes at the age of 6 months or younger) were matched with 194 own children whose sex was the same, whose age was within 6 months, whose fathers’ occupations belonged to the same group on the Minnesota Occupational Scale, whose fathers’ school attainments agreed within one school grade (mothers’ also), whose parents were white, non-Jewish, and north-European, and whose residence had been in communities of 1000 or more. The children of both groups were given the Stanford-Binet and the Woodworth-Mathews Personal Data Sheet; the parents were given the Otis Self-Administering Test and the Stanford-Binet vocabulary.
“Variation in IQ is accounted for by variation in home environment to the extent of not more than 4%; 96% of the variation is accounted for by other factors… . Measurable environment does not shift the IQ by more than 3 to 5 points above or below the value it would have had under normal environmental conditions… . The nature or hereditary component in intelligence causes greater variation than does environment. When nature and nurture are operative, shifts in IQ as great as 20 points are observed with shifts in the cultural level of the home and neighborhood… . Variation in personality traits other than intelligence may be accounted for less by variation in heredity than by variation in environment.”
Earlier studies are reviewed and 8 references are cited.