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On group differences in the heritability of intelligence: A reply to Giangrande and Turkheimer (2022)
Abstract
Here we reply to Giangrande and Turkheimer's (2022; G&T) recent critique of a meta-analysis we published in Intelligence regarding the Scarr-Rowe Hypothesis and the apparent lack of putative race/ethnic group differences in the heritability of intelligence (Pesta et al., 2020). Our rebuttal is divided into three sections that address ubiquitous misstatements in their critique: Section 1 focuses on conceptual and theoretical points. Section 2 addresses methodological, statistical, and interpretative points. Section 3 provides new analyses suggested by G&T that support our original interpretations. We note that G&T published their critique in Perspectives on Psychological Science (PoPS), which did not invite us to respond before their paper was published and our subsequent submission of a rebuttal was not accepted. Our unsuccessful appeal of these events based on possible ethics violations is detailed here (Appendix E). We recognize that this is a controversial area of research with legitimate disagreements and hope our responses maintain a degree of rigor and professionalism that others can emulate. In 2020, we published a meta-analysis in this journal on the herita-bility of intelligence across different races and ethnicities (i.e., Pesta, Kirkegaard, te Nijenhuis, Lasker, & Fuerst, 2020). There we found no substantial evidence for the existence of Race/Ethnicity x Heritability interactions. These null effects were contrary to predictions stemming from the Scar-Rowe Hypothesis, at least as we interpreted it. Two years later, Giangrande and Turkheimer (2022; G&T) published an article highly critical of our meta-analysis (and ourselves), together with the editors and reviewers at Intelligence who acted on our paper. G&T's critique, however, appeared in "Perspectives in Psychological Science (PoPS), rather than in this journal. Naturally, we initially submitted versions of this rebuttal for publication at PoPS, wherein the Editor (Klaus Fiedler) ultimately desk-rejected us on our second attempt. We appealed the decision and even filed formal ethics complaints with various stakeholders at PoPS, APS, and Sage Publishing. As detailed in Appendix E, neither PoPS nor APS felt we were owed the right to defend ourselves against G&T's scathing critiques, at least not in PoPS (and Sage has yet to come up with a full-fledged response). Instead, our rebuttal finds its home here. Appendix E details the timeline of events with PoPS, and the main text below focuses on point-by-point rebuttals of G&T's article, organized in three sections. Section 1 focuses on conceptual and theoretical misstatements made by G&T. Section 2 addresses methodological, statistical , and interpretative misstatements made by G&T. Finally, Section 3 provides several new analyses of our original, meta-analytic data. Our goal is to constructively address most, if not all of G&T's substantive concerns.
... To allow heritabilities for intelligence to be compared with previously published results (e.g., Pesta et al., 2020Pesta et al., , 2023, for these biometric analyses we defined "Black" as including any non-Hispanic individual identified as being African American. Thus "Black" was defined broadly and includes multi-racial individuals. ...
... More detailed results are provided in Supplementary File 1. Consistent with previously reported results (Pesta et al., 2020(Pesta et al., , 2023, the heritability estimates of the NIHTBX scores were moderate-to-high for the total, the White, and the combined non-White samples (h 2 = .56 to .64). ...
... In this national sample of ten-year-old children, the heritability estimates of general intelligence were moderate-to-high in both the White and the combined non-Whites sample, while the shared environmentality estimates were low. This is in line with the findings of Pesta et al. (2020Pesta et al. ( , 2023, who report that heritabilities are similar across White and non-White groups. Moreover, both brain and intracranial volume were highly heritable in the full sample, the White sample, and the non-White sample. ...
Intelligence tests are excellent predictors of school and job performance, and racial/ethnic differences in mean IQ are common. Based on five lines of evidence, Warne (2021) builds a case for partly genetic causes of differences in general intelligence (g) across American self/parental-identified race or ethnicity (SIRE). Based on a careful reading of Warne (2021) and the authors he cites, we generated 15 predictions flowing from a partial genetic hypothesis. These predictions concern (1) mean cognitive differences and Spearman’s hypothesis, (2) measurement invariance across European genetic ancestry, (3) high within-group heritability and low shared environmentality, (4) admixture regression for g, (5) polygenic scores, (6) brain volume, and (7) results based on the method of correlated vectors. We used the Adolescent Brain Cognitive Development Study sample (N = 10,245) to test these hypotheses using classical and state-of-the-art statistical techniques. Decomposition of variance using twins showed that the heritability of intelligence and of brain/intracranial volume estimates were, respectively, moderate and high for both the White and the non-White subsamples, while the variance attributable to shared environment was low. Within SIRE groups, both genetic ancestry and education-related polygenic scores (eduPGS) predicted both brain volume and g. Moreover, brain volume was weakly but statistically significantly related to g (r = .14 to .25). Path and mediation analysis showed that total brain volume explained approximately 15% of the association between European ancestry and g and also explained approximately 8% of that between eduPGS and g. Finally, based on the method of correlated vectors (MCV), a positive manifold was found for genetic, brain volume, and ancestry/SIRE-related variables. We conclude that the results support the hypotheses tested and are in line with a partial genetic hypothesis.
... The editor eventually accepted the article as is, and apologized for the long delay, which resulted from the fact that the article had to be sent to seven reviewers rather than the usual three in order to get three real reviews of the paper itself (emphasis added). The other four supposed reviews were merely ad hominem diatribes; the editor said it would be too embarrassing to the journal for me to be allowed to see them... Our experience is similar to Jensen's in that we recently submitted a rebuttal article to a prestigious journal in psychology, wherein the editor had to apologize for the lengthy delay in his decision because the first 17 reviewers he invited to review our paper declined (incidentally, the editor ultimately rejected our article, which we claimed was an ethics violation, as detailed in Pesta et al. 2023). ...
Jackson and Winston (“JW;” 2021) recently argued that no real taboos exist regarding the study of potential genetic links between race and IQ test scores. Instead, the authors essentially claimed that researchers in this area have protested too much. JW offered several arguments that presumably supported their claims, which we rebut here first. Empirically, however, we wondered just how “relatively taboo” this topic might be among Americans in general. Via Prolific.com, we surveyed 507 representative Americans on this issue. Our survey comprised 33 “taboo topics” (e.g., whether pedophilia is harmful), wherein each participant subjectively rated “tabooness” on five-point Likert scales. We found that the potential genetic basis of race / IQ gaps was the tabooest item in our survey. In fact, this topic was rated “more taboo” than were items regarding incest and even pedophilia. Further, the rank-ordering of “tabooness” was highly stable across the various demographic groups we looked at in our survey. At least among a (relatively large) representative sample of American adults, research on the genetics of race / IQ gaps is very strongly taboo. We conclude by discussing how our survey results further dampen JW’s claim that the taboo is real rather than mythical.
Gene–environment processes tell us how genetic predispositions and environments work together to influence children in schools. One type of gene–environment process that has been extensively studied using behavioral genetics methods is a gene‐by‐environment interaction. A gene‐by‐environment interaction shows us when the effect of your context on a phenotype differs depending on your genetic predispositions, or vice versa, when the effect of your genetic predispositions on a phenotype differs depending on your context. Developmental behavioral geneticists interested in children's school achievement have examined many different contexts within the gene‐by‐environment interaction model, including contexts measured from within children's home and school environments. However, this work has been overwhelmingly focused on WEIRD samples children, leaving us with non‐inclusive scientific evidence. This can lead to detrimental outcomes when we overgeneralize this non‐inclusive scientific evidence to racialized groups. We conclude with a call to include racialized children in more research samples.
Gene–environment processes tell us how genes and environments work together to influence children in schools. One type of gene–environment process that has been extensively studied using behavioral genetics methods is a gene-by-environment interaction. A gene-by-environment interaction shows us when the effect of your context differs depending on your genes, or vice versa, when the effect of your genes differs depending on your context. Developmental behavioral geneticists interested in children’s school achievement have examined many different contexts within the gene-by-environment interaction model, including contexts measured from within children’s home and school environments. However, this work has been overwhelmingly focused on White children, leaving us with non-inclusive scientific evidence. This can lead to detrimental outcomes when we overgeneralize this non-inclusive scientific evidence to racialized groups. We conclude with a call to include racialized children in more research samples.
In ecological meta‐analyses, nonindependence among observed effect sizes from the same source paper is common. If not accounted for, nonindependence can seriously undermine inferences. We compared the performance of four meta‐analysis methods that attempt to address such nonindependence and the standard random‐effect model that ignores nonindependence. We simulated data with various types of within‐paper nonindependence, and assessed the standard deviation of the estimated mean effect size and Type I error rate of each method. Although all four methods performed substantially better than the standard random‐effects model that assumes independence, there were differences in performance among the methods. A two‐step method that first summarizes the multiple observed effect sizes per paper using a weighted mean and then analyzes the reduced data in a standard random‐effects model, and a robust variance estimation method performed consistently well. A hierarchical model with both random paper and study effects gave precise estimates but had a higher Type I error rates, possibly reflecting limitations of currently available meta‐analysis software. Overall, we advocate the use of the two‐step method with a weighted paper mean and the robust variance estimation method as reliable ways to handle within‐paper nonindependence in ecological meta‐analyses.
Via meta-analysis, we examined whether the heritability of intelligence varies across racial or ethnic groups. Specifically, we tested a hypothesis predicting an interaction whereby those racial and ethnic groups living in relatively disadvantaged environments display lower heritability and higher environmentality. The reasoning behind this prediction is that people (or groups of people) raised in poor environments may not be able to realize their full genetic potentials. Our sample (k = 16) comprised 84,897 Whites, 37,160 Blacks, and 17,678 Hispanics residing in the United States. We found that White, Black, and Hispanic heritabilities were consistently moderate to high, and that these heritabilities did not differ across groups. At least in the United States, Race/ Ethnicity × Heritability interactions likely do not exist.
To understand the genetic architecture and make inferences about transmissible resemblance of systolic and diastolic blood pressure (SBP and DBP) traits in relatives, the polygenic effect of individual alleles in terms of narrow heritability (h2) is usually assessed. The heritability estimates for BP traits are population specific parameters with a wide range in different studies (6–68%), and there is no comprehensive evidence comparing its source(s) of heterogeneity. To fill the gap, this systematic review and meta-analysis study was carried out. Using MeSH terms, 647 records were detected through searching, “Pubmed,” “Ebsco,” “Web of Science,” and “Scopus” databases. From these, 24 relevant full-text articles with 47 comparisons for final quantitative meta-analysis were included in our review over the five continents. The additive genetic effects of both traits showed a widespread distribution (h2SBP: 17–52%, h2DBP:19–41%). Different categories of transmissible resemblance for BP traits were explained by ethnicity; higher heritability was estimated in Europeans and Mexican Americans, while lower heritability was seen in the Middle Eastern, Asians, Africans, Latinos, Hispanics, and American Indians. Low heterogeneity of polygenic effects was seen for both traits in subgroups of the Middle East, Asians, Africans, and Latinos, Hispanics, American Indians. However, there was a substantial heterogeneity of h2 within European and Mexican American studies. Neither pedigree type nor other covariates explained the variance of additive genetic effects of BP traits in different ethnicities.
Heritability of LPA allele, apolipoprotein(a) [apo(a)] isoform sizes and isoform-associated lipoprotein(a) [Lp(a)] levels was studied in 82 Caucasian and African-American families with two parents and two children (age: 6-74 years). We determined: 1) Lp(a) levels; 2) LPA allele sizes; 3) apo(a) isoform sizes; and 4) isoform-specific apo(a) levels (ISL), the amount of Lp(a) carried by an individual apo(a) isoform. Trait heritability was estimated by midparent-offspring analysis. Ethnicity-adjusted heritability estimate for Lp(a) level was 0.95. Heritability for ISL corresponding to the smaller LPA allele in a given allele-pair was higher than that corresponding to the larger LPA allele (0.91 vs. 0.59, p=0.017). Although not statistically different, heritability for both apo(a) isoforms (0.90 vs. 0.70) and LPA alleles (0.98 vs. 0.82) was higher for the smaller vs. larger sizes. Heritability was generally lower in African-Americans vs. Caucasians with a fourfold difference for the larger LPA allele (0.25 vs. 0.94, p=0.001). In Caucasians, an overall higher heritability pattern was noted for the older (≥47 years) vs. younger (<47 years) families. In conclusions, Lp(a) level and traits associated with the smaller LPA alleles were strongly determined by genetics, although with a varying ethnic influence. Ethnic differences in heritability of the larger LPA allele warrants further investigations.
The relative importance of genes and shared environmental influences on stratification outcomes has recently received much attention in the literature. We focus on education and the gene-environmental interplay. Specifically, we investigate whether—as proposed by the Scarr-Rowe hypothesis—genetic influences are more important in advantaged families. We argue that the social stratification of family environments affects children's chances to actualize their genetic potential. We hypothesize that advantaged families provide more child-specific inputs, which enhance genetic expression, whereas the rearing environments of children in disadvantaged families are less adapted to children's individual abilities, leading to a suppression of genetic potential. We test this relationship in Germany, which represents an interesting case due to its highly selective schooling system characterized by early tracking and the broad coverage of part-time schools. We use novel data from the TwinLife panel, a population-register–based sample of twins and their families. Results of ACE-variance decompositions support the Scarr-Rowe hypothesis: Shared environmental influences on education matter only in disadvantaged families, whereas genetic influences are more important in advantaged families. Our findings support the growing literature on the importance of the gene-environmental interplay and emphasize the role of the family environment as a trigger of differential genetic expression.
Successful cognitive development between childhood and adulthood has important consequences for future mental and physical wellbeing, as well as occupational and financial success. Therefore, delineating the genetic influences underlying changes in cognitive abilities during this developmental period will provide important insights into the biological mechanisms that govern both typical and atypical maturation. Using data from the Philadelphia Neurodevelopmental Cohort (PNC), a large population-based sample of individuals aged 8 to 21 years old (n = 6634), we used an empirical relatedness matrix to establish the heritability of general and specific cognitive functions and determine if genetic factors influence cognitive maturation (i.e., Gene × Age interactions) between childhood and early adulthood. We found that neurocognitive measures across childhood and early adulthood were significantly heritable. Moreover, genetic variance on general cognitive ability, or g, increased significantly between childhood and early adulthood. Finally, we did not find evidence for decay in genetic correlation on neurocognition throughout childhood and adulthood, suggesting that the same genetic factors underlie cognition at different ages throughout this developmental period. Establishing significant Gene × Age interactions in neurocognitive functions across childhood and early adulthood is a necessary first step in identifying genes that influence cognitive development, rather than genes that influence cognition per se. Moreover, since aberrant cognitive development confers risk for several psychiatric disorders, further examination of these Gene × Age interactions may provide important insights into their etiology.
This study investigates three methods to handle dependency among effect size estimates in meta-analysis arising from studies reporting multiple outcome measures taken on the same sample. The three-level approach is compared with the method of robust variance estimation, and with averaging effects within studies. A simulation study is performed, and the fixed and random effect estimates of the three methods are compared with each other. Both the robust variance estimation and three-level approach result in unbiased estimates of the fixed effects, corresponding standard errors and variances. Averaging effect sizes results in overestimated standard errors when the effect sizes within studies are truly independent. Although the robust variance and three-level approach are more complicated to use, they have the advantage that they do not require an estimate of the correlation between outcomes, and they still result in unbiased parameter estimates.
The authors conducted a meta-analysis of interactions between behavioral genetic variance components (ACE) and race/ethnicity for cognitive ability. The differences between the variance components for Black and White Americans were small, despite the large average test score differences. More substantial differences were found between Hispanics and non-Hispanic Whites, though results were based on only two studies. A biometric re-analysis of the CNLSY survey was then conducted and new meta-analytic results were provided. Results were discussed in light of the bio-ecological model which proposes that when the scores of subgroups are environmentally depressed, heritabilities will be likewise.
Although genome-wide association studies have identified over 100 risk loci that explain ∼33% of familial risk for prostate cancer (PrCa), their functional effects on risk remain largely unknown. Here we use genotype data from 59,089 men of European and African American ancestries combined with cell-type-specific epigenetic data to build a genomic atlas of single-nucleotide polymorphism (SNP) heritability in PrCa. We find significant differences in heritability between variants in prostate-relevant epigenetic marks defined in normal versus tumour tissue as well as between tissue and cell lines. The majority of SNP heritability lies in regions marked by H3k27 acetylation in prostate adenoc7arcinoma cell line (LNCaP) or by DNaseI hypersensitive sites in cancer cell lines. We find a high degree of similarity between European and African American ancestries suggesting a similar genetic architecture from common variation underlying PrCa risk. Our findings showcase the power of integrating functional annotation with genetic data to understand the genetic basis of PrCa.
A core hypothesis in developmental theory predicts that genetic influences on intelligence and academic achievement are suppressed under conditions of socioeconomic privation and more fully realized under conditions of socioeconomic advantage: a Gene × Childhood Socioeconomic Status (SES) interaction. Tests of this hypothesis have produced apparently inconsistent results. We performed a meta-analysis of tests of Gene × SES interaction on intelligence and academic-achievement test scores, allowing for stratification by nation (United States vs. non-United States), and we conducted rigorous tests for publication bias and between-studies heterogeneity. In U.S. studies, we found clear support for moderately sized Gene × SES effects. In studies from Western Europe and Australia, where social policies ensure more uniform access to high-quality education and health care, Gene × SES effects were zero or reversed.
We examine updated Wechsler IQ data in 7-year old twins from the Louisville Twin Study for evidence of an interaction between the heritability of IQ and socioeconomic status. Data records that had never been entered were recovered, allowing us to increase previously reported sample sizes by more than 20 %. Twin families were assigned socioeconomic status scores using a Hollingshead index based on parental education and occupation. A structural equation model in which genetic and environmental variances were modeled as squared linear functions of SES provided ambiguous replication of earlier findings from the National Collaborative Perinatal Project: relations between SES and heritability for performance and full scale IQ were in the same direction as the previous report, but at p < 0.07. As was the case in Turkheimer et al. (Psychol Sci 14(6):623-628, 2003), no interaction was found for VIQ. These results cannot yet be taken as a definitive replication of Turkheimer et al. (Psychol Sci 14(6):623-628, 2003). Many more measurement occasions, subtests and environmental moderators remain to be analyzed.
The relationship between IQ and completed fertility among a sample of 3520 Americans from MIDUS II (1960's birth cohorts) is examined using a common factor comprised of eight cognitive ability measures, in order to determine the rate of phenotypic IQ loss due to genetic selection. Negative correlations are present in both the male and female subsamples, and are associated with a predicted loss in heritable g (g.h) of − .262 points per decade, increasing to − 1.072 points when the additive effect of mutation accumulation is considered. The ability–fertility associations showed Jensen effects at the level of the whole sample (.167), and also separately for each sex (.185 and .147 for the females and males respectively). The magnitude of the expected g.h loss in this cohort due to selection is comparable to that derived from a meta-analysis of disattenuated decadal g.h declines from eight US studies (− .44 points per decade; N = 127,389). There is a Flynn effect in the US amounting to gains of 3.6 points per decade, which are concentrated on more environmentally plastic and specialized sources of ability variance (s.e) suggesting co-occurrent socio-ecological specialization with respect to narrower cognitive abilities in the present cohort.
Much of sociological analysis is devoted to assessing
the relative importance of ascribed and achieved characteristics for
social mobility. In this article, we extend this line of sociological
work by focusing on children's differential opportunity to achieve their
genetic potential for intellectual development. We hypothesize that the
extent to which a child realizes his or her genetic potential depends on
socioeconomic environment. Using a large sibling sample collected by the
National Longitudinal Study of Adolescent Health, we test this hypothesis
with a variant of the Peabody Picture Vocabulary Test (PPVT) as the
dependent variable. When measures of social environment are considered
simultaneously, parental unemployment and ethnicity have a significant
effect on the extent to which genetic potential for intellectual
development is realized. Our findings suggest that policymakers can help
children in disadvantaged environments realize full genetic potential
for intellectual development by altering their social circumstances.
The poor performance of Black children on IQ tests and in school has been hypothesized to arise from (a) genetic racial differences or (b) cultural/environmental disadvantages. To separate genetic factors from rearing conditions, 130 Black and interracial children adopted by advantaged White families were studied. The socially classified Black adoptees, whose natural parents were educationally average, scored above the IQ and the school achievement mean of the White population. Biological children of the adoptive parents scored even higher. Genetic and environmental determinants of differences among the Black and interracial adoptees were largely confounded. The high IQ scores of the socially classified Black adoptees indicate malleability for IQ under rearing conditions that are relevant to the tests and the schools.
Developed to offer researchers an informative account of which methods are most useful in integrating research findings across studies, this book will enable ...
The past 30 years of research in intelligence has produced a wealth of knowledge about the causes and consequences of differences in intelligence between individuals, and today mainstream opinion is that individual differences in intelligence are caused by both genetic and environmental influences. Much more contentious is the discussion over the cause of mean intelligence differences between racial or ethnic groups. In contrast to the general consensus that interindividual differences are both genetic and environmental in origin, some claim that mean intelligence differences between racial groups are completely environmental in origin, whereas others postulate a mix of genetic and environmental causes. In this article I discuss 5 lines of research that provide evidence that mean differences in intelligence between racial and ethnic groups are partially genetic. These lines of evidence are findings in support of Spearman’s hypothesis, consistent results from tests of measurement invariance across American racial groups, the mathematical relationship that exists for between-group and within-group sources of heritability, genomic data derived from genome-wide association studies of intelligence and polygenic scores applied to diverse samples, and admixture studies. I also discuss future potential lines of evidence regarding the causes of average group differences across racial groups. However, the data are not fully conclusive, and the exact degree to which genes influence intergroup mean differences in intelligence is not known. This discussion applies only to native English speakers born in the United States and not necessarily to any other human populations.
In 2020, Pesta et al. published an article entitled “Racial and Ethnic Group Differences in the Heritability of Intelligence: A Systematic Review and Meta-Analysis” in the journal Intelligence. The authors framed their analysis as an examination of the Scarr-Rowe hypothesis, which holds that the heritability of intelligence varies as a function of socioeconomic status. Pesta et al. concluded that the heritability of intelligence does not differ across racial and ethnic groups in the United States. They claimed their results challenge the Scarr-Rowe hypothesis and support the hereditarian position that mean differences in IQ among racial and ethnic groups are attributable to genetic differences rather than environmental disparities. In this commentary, we outline severe theoretical, methodological, and rhetorical flaws in every step of Pesta et al.’s meta-analysis. The most reliable finding from Pesta et al. is consistent with the Scarr-Rowe hypothesis and directly contradicts a hereditarian understanding of group differences in intelligence. Finally, we suggest that Pesta et al. serves as an example of how racially motivated and poorly executed work can find its way into a mainstream scientific journal, underscoring the importance of robust peer review and rigorous editorial judgment in the open-science era.
Background
The atopic march has been studied mostly in White populations, biasing our current paradigms.
Objective
To define the atopic march in Black and White children and explore mechanisms for racial differences.
Methods
Utilizing the Mechanisms of Progression of Atopic Dermatitis to Asthma in Children (MPAACH) cohort (N=601), we assessed longitudinal sensitization, food allergy, allergic rhinitis, risk of asthma development (through the Pediatric Asthma Risk Score), SCORAD, transepidermal water loss (TEWL), skin filaggrin (FLG) expression, exposures and genetic heritability to define AD progression endotypes in Black and White children.
Results
White MPAACH children were more likely to be sensitized to aero and food allergens (p=0.0001) and over 3-times more likely to develop food allergy (FA) and/or allergic rhinitis (AR) without asthma risk (p<0.0001). In contrast, Black children were over 6-times more likely to proceed to high asthma risk without FA, sensitization, or AR (p<0.0001). White children had higher lesional and non-lesional TEWL (both p<0.001) and decreased non-lesional keratinocyte FLG expression (p=0.02). Black children had increased genetic heritability for asthma risk and higher rates of exposures to secondhand smoke and traffic-related air pollution.
Conclusions
Black and White children with AD have distinct allergic trajectories defined by different longitudinal endotypes. Black children exhibit higher asthma risk despite a more intact skin barrier, and less sensitization, FA and AR. White children have less asthma risk, despite a more dysfunctional skin barrier, and more FA, AR and sensitization. The observed racial differences are likely due, in part, to increased genetic heritability for asthma risk and harmful environmental exposures in the Black children. Collectively, our findings provide a new paradigm for the atopic march that is inclusive of Black children.
There is much evidence to suggest that family background and the context of secondary education both contribute to the formation of educational inequalities. Meanwhile, our knowledge about the role of ability in generating class differences in educational outcomes is still limited. By deploying genetic data that allow us to measure at least part of “innate” ability inherited through biological mechanisms from parents, this study examines how such abilities are associated with educational tracking outcomes among U.S. high schoolers. This study also details our understanding of the role of nature and nurture in the educational attainment processes by testing for gene-environment interactions—that is, a joint, mutually moderating effect of one’s genetic potential and one’s environment (e.g., family background or school context) on phenotypic outcomes (educational tracking). Using the National Longitudinal Study of Adolescent to Adult Health that collects a unique set of demographic, educational, and genetic characteristics of students, we report the following results: First, a positive association between the genetic potential for educational attainment and taking advanced courses holds even after controlling for previous course tracking measures. Second, results provide suggestive evidence that parental SES amplifies the association between one’s genetic potential for educational attainment and mathematics tracking. In contrast to the argument by some stratification scholars that places primary emphasis on the role of social background for the reproduction of educational stratification, the present findings imply that we need to fully consider the role of genetic inheritance for educational stratification in addition to social origin.
We consider the problem of interpreting negative maximum likelihood estimates of heritability that sometimes arise from popular statistical models of additive genetic variation. These may result from random noise acting on estimates of genuinely positive heritability, but we argue that they may also arise from misspecification of the standard additive mechanism that is supposed to justify the statistical procedure. Researchers should be open to the possibility that negative heritability estimates could reflect a real physical feature of the biological process from which the data were sampled.
Sociological research has traditionally emphasized the importance of post-birth factors (i.e., social, economic, and cultural capital) in the intergenerational transmission of educational advantages, to the neglect of potentially consequential pre-birth endowments (e.g., 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.
Experts (Nmax = 102 answering) on intelligence completed a survey about IQ research, controversies, and the media. The survey was conducted in 2013 and 2014 using the Internet-based Expert Questionnaire on Cognitive Ability (EQCA). In the current study, we examined the background of the experts (e.g., nationality, gender, religion, and political orientation) and their positions on intelligence research, controversial issues, and the media. Most experts were male (83%) and from Western countries (90%). Political affiliations ranged from the left (liberal, 54%) to the right (conservative, 24%), with more extreme responses within the left-liberal spectrum. Experts rated the media and public debates as far below adequate. Experts with a left (liberal, progressive) political orientation were more likely to have positive views of the media (around r = |.30|). In contrast, compared to female and left (liberal) experts, male and right (conservative) experts were more likely to endorse the validity of IQ testing (correlations with gender, politics: r = .55, .41), the g factor theory of intelligence (r = .18, .34), and the impact of genes on US Black-White differences (r = .50, .48). The paper compares the results to those of prior expert surveys and discusses the role of experts' backgrounds, with a focus on political orientation and gender. An underrepresentation of viewpoints associated with experts' background characteristics (i.e., political views, gender) may distort research findings and should be addressed in higher education policy.
The revised edition of the Handbook offers the only guide on how to conduct, report and maintain a Cochrane Review ? The second edition of The Cochrane Handbook for Systematic Reviews of Interventions contains essential guidance for preparing and maintaining Cochrane Reviews of the effects of health interventions. Designed to be an accessible resource, the Handbook will also be of interest to anyone undertaking systematic reviews of interventions outside Cochrane, and many of the principles and methods presented are appropriate for systematic reviews addressing research questions other than effects of interventions. This fully updated edition contains extensive new material on systematic review methods addressing a wide-range of topics including network meta-analysis, equity, complex interventions, narrative synthesis, and automation. Also new to this edition, integrated throughout the Handbook, is the set of standards Cochrane expects its reviews to meet. Written for review authors, editors, trainers and others with an interest in Cochrane Reviews, the second edition of The Cochrane Handbook for Systematic Reviews of Interventions continues to offer an invaluable resource for understanding the role of systematic reviews, critically appraising health research studies and conducting reviews.
Behavioral and molecular genetic research has established that child cognitive ability and academic performance are substantially heritable, but genetic variation does not account for all of the stratification of cognitive and academic outcomes across families. Which specific contexts and experiences contribute to these shared environmental influences on cognitive ability and academic achievement? Using an ethnically and socioeconomically diverse sample of N = 1728 twins ages 7–20 from the Texas Twin Project, we identified specific measured family, school, and neighborhood socioecological contexts that statistically accounted for latent shared environmental variance in cognitive abilities and academic skills. Composite measures of parent socioeconomic status (SES), school demographic composition, and neighborhood SES accounted for moderate proportions of variation in IQ and achievement. Total variance explained by the multilevel contexts ranged from 15% to 22%. The influence of family SES on IQ and achievement overlapped substantially with the influence of school and neighborhood predictors. Together with race, the measured socioecological contexts explained 100% of shared environmental influences on IQ and approximately 79% of shared environmental influences on both verbal comprehension and reading ability. In contrast, nontrivial proportions of shared environmental variation in math performance were left unexplained. We highlight the potential utility of constructing “polyenvironmental risk scores” in an effort to better predict developmental outcomes and to quantify children's and adolescents’ interrelated networks of experiences. A video abstract of this article can be viewed at: https://youtu.be/77E_DctFsr0
Background:
Indices of cardiac mechanics are sensitive markers of subclinical myocardial dysfunction. Improved understanding of the clinical correlates and heritability of cardiac mechanics could result in novel insight into the acquired and genetic risk factors for myocardial dysfunction. Therefore, we sought to determine the clinical correlates and heritability of indices of cardiac mechanics in whites and African Americans (AAs).
Methods:
We examined 2058 participants stratified by race (1104 whites, 954 AA) in the Hypertension Genetic Epidemiology Network (HyperGEN), a population- and family-based study, and performed digitization of analog echocardiograms with subsequent speckle-tracking analysis. We used linear mixed effects models to determine the clinical correlates of indices of cardiac mechanics (longitudinal, circumferential, radial strain; early diastolic strain rate; and early diastolic tissue velocities). Heritability estimates for cardiac mechanics were calculated using maximum-likelihood variance component analyses in Sequential Oligogenic Linkage Analysis Routine (SOLAR), with adjustment for clinical and echocardiographic covariates.
Results:
Several clinical characteristics and conventional echocardiographic parameters were found to be associated with speckle-tracking traits of cardiac mechanics. Male sex, blood pressure, and fasting glucose were associated with worse longitudinal strain (LS) (P < 0.05 for all) after multivariable adjustment. After adjustment for covariates, LS, e' velocity, and early diastolic strain rate were found to be heritable; LS and e' velocity had higher heritability estimates in AAs compared to whites.
Conclusions:
Indices of cardiac mechanics are heritable traits even after adjustment for clinical and conventional echocardiographic correlates. These findings provide the basis for future studies of genetic determinants of these traits that may elucidate race-based differences in heart failure development.
Heritability is essential for understanding the biological causes of disease but requires laborious patient recruitment and phenotype ascertainment. Electronic health records (EHRs) passively capture a wide range of clinically relevant data and provide a resource for studying the heritability of traits that are not typically accessible. EHRs contain next-of-kin information collected via patient emergency contact forms, but until now, these data have gone unused in research. We mined emergency contact data at three academic medical centers and identified 7.4 million familial relationships while maintaining patient privacy. Identified relationships were consistent with genetically derived relatedness. We used EHR data to compute heritability estimates for 500 disease phenotypes. Overall, estimates were consistent with the literature and between sites. Inconsistencies were indicative of limitations and opportunities unique to EHR research. These analyses provide a validation of the use of EHRs for genetics and disease research.
Background:
Although dichotomous criteria for the metabolic syndrome (MetS) appear heritable, it is not known whether MetS severity as assessed by a continuous MetS score is heritable and whether this varies by race.
Methods and results:
We used SOLAR (Sequential Oligogenic Linkage Analysis Routines) to evaluate heritability of Adult Treatment Panel-III MetS and a sex- and race-specific MetS severity Z score among 3 large familial cohorts: the JHS (Jackson Heart Study, 1404 black participants), TOPS (Take Off Pounds Sensibly, 1947 white participants), and PLRS (Princeton Lipid Research Study, 229 black and 527 white participants). Heritability estimates were larger for Adult Treatment Panel-III MetS among black compared with white cohort members (JHS 0.48; 95% confidence interval [CI], 0.28-0.68 and PLRS blacks 0.93 [95% CI, 0.73-1.13] versus TOPS 0.21 [95% CI, -0.18 to 0.60] and PLRS whites 0.27 [95% CI, -0.04 to 0.58]). The difference by race narrowed when assessing heritability of the MetS severity score (JHS 0.52 [95% CI, 0.38, 0.66] and PLRS blacks 0.64 [95% CI, 0.13-1.15] versus TOPS 0.23 [95% CI, 0.15-0.31] and PLRS whites 0.60 [95% CI, 0.33-0.87]). There was a high degree of genetic and phenotypic correlation between MetS severity and the individual components of MetS among all groups, although the genetic correlations failed to reach statistical significance among PLRS blacks. Meta-analyses revealed a combined heritability estimate for Adult Treatment Panel-III MetS of 0.24 (95% CI, 0.11-0.36) and for the MetS severity score of 0.50 (95% CI, -0.05 to 0.99).
Conclusions:
MetS severity seems highly heritable among whites and blacks. This continuous MetS severity Z score may provide a more useful means of characterizing phenotypic MetS in genetic studies by minimizing racial differences.
The mainstream status achievement model of sociology and economics views individual careers as sequences of causally linked status-related traits and outcomes such as ability, educational attainment, and occupational status. The variance decomposition models of quantitative genetics interpret variation in these traits and status outcomes as produced by latent factors summarizing genetic, shared environmental and nonshared environmental sources of influence. This article proposes that the two approaches can be combined and together provide valuable insights into core issues of social stratification research. The argument is illustrated with respect to three issue areas: (1) Nature of family environmental influences in educational attainment; (2) Sources of associations among successive status-related outcomes; (3) Implications of the combined status achievement / quantitative genetic model for the relative strengths of opportunities for mobility versus social forces of reproduction facing individuals in different social positions and in different societies.
Introduction:
Although epidemiologic studies suggest low levels of cigarette use among African American adolescents relative to White U.S. adolescents, it is not known whether this may be due to racial differences in the relative contribution of genes and environment to cigarette use initiation and progression to regular use.
Methods:
Using data from White (n=2665) and African American (n=809) twins and full siblings sampled in the National Longitudinal Study of Adolescents, we fitted age-, sex- and race-specific variance decomposition models to estimate the magnitude of genetic and environmental effects on cigarette use initiation and cigarette use quantity in Whites and African Americans across adolescence and adulthood. We employ a causal-contingent-common pathway model to estimate the amount of variance explained in quantity of cigarettes smoked contingent on cigarette use initiation.
Results:
African Americans had lower cigarette use prevalence from adolescence through adulthood, and used cigarettes less heavily than Whites. Race-specific causal-contingent-common pathway models indicate that racial differences in genetic and environmental contributions to cigarette use initiation and cigarette use quantities are not present in adolescence but appear in young adulthood. Additive genetic factors were an important risk factor for cigarette use initiation for White but not African American young adults and adults.
Conclusions:
Genetic and environmental contributions for cigarette use are similar by race in adolescence. In adulthood, genes have a stronger influence for cigarette use among White adolescents while the influence of the environment is minimal. For African Americans, both genetic and environmental influences are important in young adulthood and adulthood.
The poor performance of black children on IQ tests and in school has been hypothesized to arise from (a) genetic racial differences or (6) cultural/ environmental disadvantages. To separate genetic fac- tors from rearing conditions, 130 black/interracial chil- dren adopted by advantaged white families were studied. The socially classified black adoptees, whose natural parents were educationally average, scored above the IQ and the school achievement mean of the white popu- lation. Biological children of the adoptive parents scored even higher. Genetic and environmental de- terminants of differences among the black/interracial adoptees were largely confounded. The high IQ scores of the socially classified black adoptees indicate malle- ability for IQ under rearing conditions that are relevant to the tests and the schools. It is well known that black children reared by their own families achieve IQ scores that average about a standard deviation (IS points) below whites (Jensen, 1973; Loehlin, Lindzey, & Spuhler, 197S). This finding is at the heart of a continuing contro- versy in the educational arena. Recent studies (Cleary, Humphreys, Kendrick, & Wesman, 1975) confirm the hypothesis that low IQ scores predict poor school performance, regardless of race. Thus, more black children than white children fail to achieve academically and to earn the credentials required by higher occupational status, with its
Researchers who are interested in breathing new life into the long dormant Louisville Twin Study (LTS) presented several papers at the 2015 meeting of the behavior genetics association. This brief introduction provides a short history of the Kentucky LTS as well as synopses of expanded analyses from the presentations on genetic change and continuity in cognitive and behavioral development and those exploring aspects of the influence of gene-environment interaction on cognition.
An expansive literature has revealed that human intelligence is under genetic influence. In an effort to further elucidate the role of genetic influences on intelligence, studies have examined the potential role that family-level socioeconomic status (SES) plays in the moderation of genetic factors. Results have been mixed, but the majority of studies have found that genetic factors have greater influence on IQ in the presence of higher levels of SES. The current study aims to contribute to this line of research by examining the role of school-level SES in moderating genetic and environmental influences on verbal intelligence at the individual level. A sample of sib-ling pairs from the National Longitudinal Study of Adolescent to Adult Health (Add Health) was used to estimate a series of genetically informed multilevel statistical models. The results indicate that genetic factors have a greater influence on verbal IQ for students who attend schools with higher levels of SES, and shared environmental factors have a greater influence on verbal IQ for students who attend schools with lower levels of SES, but only at extremely high and low levels of SES (scoring within the top or bottom 10th percentiles).
Asian Americans are often stereotyped as the “model minority.” Their sizeable presence at elite universities and high household incomes have helped construct the narrative of Asian American “exceptionalism.” While many scholars and activists characterize this as a myth, pundits claim that Asian Americans’ educational attainment is the result of unique cultural values. In The Asian American Achievement Paradox, sociologists Jennifer Lee and Min Zhou offer a compelling account of the academic achievement of the children of Asian immigrants. Drawing on in-depth interviews with the adult children of Chinese immigrants and Vietnamese refugees and survey data, Lee and Zhou bridge sociology and social psychology to explain how immigration laws, institutions, and culture interact to foster high achievement among certain Asian American groups.
For the Chinese and Vietnamese in Los Angeles, Lee and Zhou find that the educational attainment of the second generation is strikingly similar, despite the vastly different socioeconomic profiles of their immigrant parents. Because immigration policies after 1965 favor individuals with higher levels of education and professional skills, many Asian immigrants are highly educated when they arrive in the United States. They bring a specific “success frame,” which is strictly defined as earning a degree from an elite university and working in a high-status field. This success frame is reinforced in many local Asian communities, which make resources such as college preparation courses and tutoring available to group members, including their low-income members.
While the success frame accounts for part of Asian Americans’ high rates of achievement, Lee and Zhou also find that institutions, such as public schools, are crucial in supporting the cycle of Asian American achievement. Teachers and guidance counselors, for example, who presume that Asian American students are smart, disciplined, and studious, provide them with extra help and steer them toward competitive academic programs. These institutional advantages, in turn, lead to better academic performance and outcomes among Asian American students. Yet the expectations of high achievement come with a cost: the notion of Asian American success creates an “achievement paradox” in which Asian Americans who do not fit the success frame feel like failures or racial outliers.
While pundits ascribe Asian American success to the assumed superior traits intrinsic to Asian culture, Lee and Zhou show how historical, cultural, and institutional elements work together to confer advantages to specific populations. An insightful counter to notions of culture based on stereotypes, The Asian American Achievement Paradox offers a deft and nuanced understanding of how and why certain immigrant groups succeed.
Objective
Although prior studies have demonstrated that depression is associated with an overeating–binge eating dimension (OE-BE) phenotypically, little research has investigated whether familial factors contribute to the co-occurrence of these phenotypes, especially in community samples with multiple racial/ethnic groups. We examined the extent to which familial (i.e., genetic and shared environmental) influences overlapped between Major Depressive Disorder (MDD) and OE-BE in a population-based sample and whether these influences were similar across racial/ethnic groups.Method
Participants included 3,226 European American (EA) and 550 African American (AA) young adult women from the Missouri Adolescent Female Twin Study. An adaptation of the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA) was administered to assess lifetime DSM-IV MDD and OE-BE. Quantitative genetic modeling was used to estimate familial influences between both phenotypes; all models controlled for age.ResultsThe best-fitting model, which combined racial/ethnic groups, found that additive genetic influences accounted for 44% (95% CI: 34%, 53%) of the MDD variance and 40% (25%, 54%) for OE-BE, with the remaining variances due to non-shared environmental influences. Genetic overlap was substantial (rg = .61 [.39, .85]); non-shared environmental influences on MDD and OE-BE overlapped weakly (re = .26 [.09, .42]).DiscussionResults suggest that common familial influences underlie MDD and OE-BE, and the magnitude of familial influences contributing to the comorbidity between MDD and OE-BE is similar between EA and AA women. If racial/ethnic differences truly exist, then larger sample sizes may be needed to fully elucidate familial risk for comorbid MDD and OE-BE across these groups. © 2014 Wiley Periodicals, Inc. (Int J Eat Disord 2014)
Presents discussions by 4 scholars of an article by S. Scarr-Salatapek (see record
1972-30883-001) which described data from a study of twins which tended to support the environmental disadvantage hypothesis of IQ differences. Criticisms are based on the statistical methods used by Scarr-Salatapek, and it is concluded that the data offered are insufficient to provide adequate support for the environmental model. In a reply, Scarr-Salatapek answers the technical criticisms and defends the methods used, while acknowledging that they are not perfect. The extreme difficulties of testing models in human populations, which make it almost impossible to meet the rigorous criteria set up for the "ideal study," are discussed. It is maintained, however, that even studies which are not perfect can contribute to knowledge of the roles of genetic and environmental differences. (30 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
In response to A. Anastasi's (1958) long-standing challenge, the authors propose an empirically testable theoretical model that (1) goes beyond and qualifies the established behavioral genetics paradigm by allowing for nonadditive synergistic effects, direct measures of the environment, and mechanisms of organism–environment interaction, called proximal processes, through which genotypes are transformed into phenotypes; (2) hypothesizes that estimates of heritability (e.g., h–2) increase markedly with the magnitude of proximal processes; (3) demonstrates that heritability measures the proportion of variation in individual differences attributable only to actualized genetic potential, with the degree of nonactualized potential remaining unknown; and (4) proposes that, by enhancing proximal processes and environments, it is possible to increase the extent of actualized genetic potentials for developmental competence. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Background:
Differences in age at initiation of alcohol use and rates of problem drinking between African Americans and European Americans are well documented, but the association between early and problem use-and distinctions by ethnic group in this association-have yet to be examined in a genetically informative framework.
Methods:
Data were derived from a longitudinal study of female twins in Missouri. The sample was composed of 3,532 twins (13.6% African-American [AA], 86.4% European-American [EA]), who participated in the fourth wave of data collection and reported consumption of at least 1 alcoholic drink over the lifetime. Mean age at Wave 4 was 21.7 (range = 18 to 29) years. Twin modeling was conducted to estimate the relative contributions of additive genetic (A), shared environmental (C), and unique environmental (E) factors to variation in age at first drink and problem alcohol use and the cross-phenotype overlap in these influences.
Results:
Early initiation of alcohol use predicted problem use in EA but not AA women. Separate AA and EA twin models produced substantially different estimates (but not statistically different models) of the relative contributions of A and C to problem alcohol use but similar genetic correlations between the phenotypes. Whereas 33% of the variance in the EA model of problem use was attributed to C, no evidence for C was found in the AA model. Heritability estimates for problem alcohol use were 41% in the AA model, 21% in the EA model. Evidence for A and C were found in both AA and EA models of age at first drink, but the A estimate was higher in the EA than AA model (44% vs. 26%).
Conclusions:
Findings are suggestive of distinctions between AA versus EA women in the relative contribution of genetic and environmental influences on the development of problem drinking.
Background
Influential work has explored the role of family socioeconomic status (SES) as an environmental moderator of genetic and environmental influences on cognitive outcomes. This work has provided evidence that socioeconomic circumstances differentially impact the heritability of cognitive abilities, generally supporting the bioecological model in that genetic influences are greater at higher levels of family SES. The present work expanded consideration of the environment, using school-level SES as a moderator of reading comprehension. Methods
The sample included 577 pairs of twins from the Florida Twin Project on Reading, Behavior and Environment. Reading comprehension was measured by the Florida Comprehensive Achievement Test (FCAT) Reading in third or fourth grade. School-level SES was measured by the mean Free and Reduced Lunch Status (FRLS) of the schoolmates of the twins. ResultsThe best-fitting univariate G x E moderation model indicated greater genetic influences on reading comprehension when fewer schoolmates qualified for FRLS (i.e., higher' school-level SES). There was also an indication of moderation of the shared environment; there were greater shared environmental influences on reading comprehension at higher school-level SES. Conclusions
The results supported the bioecological model; greater genetic variance was found in school environments in which student populations experienced less poverty. In general, higher' school-level SES allowed genetic and probably shared environmental variance to contribute as sources of individual differences in reading comprehension outcomes. Poverty suppresses these influences.