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Thinking positively: The genetics of high intelligence
Abstract
High intelligence (general cognitive ability) is fundamental to the human capital that drives societies in the information age. Understanding the origins of this intellectual capital is important for government policy, for neuroscience, and for genetics. For genetics, a key question is whether the genetic causes of high intelligence are qualitatively or quantitatively different from the normal distribution of intelligence. We report results from a sibling and twin study of high intelligence and its links with the normal distribution. We identified 360,000 sibling pairs and 9000 twin pairs from 3 million 18-year-old males with cognitive assessments administered as part of conscription to military service in Sweden between 1968 and 2010. We found that high intelligence is familial, heritable, and caused by the same genetic and environmental factors responsible for the normal distribution of intelligence. High intelligence is a good candidate for “positive genetics” — going beyond the negative effects of DNA sequence variation on disease and disorders to consider the positive end of the distribution of genetic effects.
... This can result in less accurate polygenic scores in the tails of the trait distribution (12), but can also produce dissimilarity between siblings beyond what is expected under polygenecity. For example, studies on the intellectual ability of sibling pairs have demonstrated similarity for average intellectual ability (13), regression-to-the-mean for siblings at the upper tail of the distribution (13), and complete discordance when one sibling is at the lower extreme tail of the distribution (14). Findings from such studies such as Reichenberg et al. 2016 (14) are are consistent with the presence of de novo alleles of large effect in the trait tails, alongside alternative explanations such as specific environmental exposures. ...
... This can result in less accurate polygenic scores in the tails of the trait distribution (12), but can also produce dissimilarity between siblings beyond what is expected under polygenecity. For example, studies on the intellectual ability of sibling pairs have demonstrated similarity for average intellectual ability (13), regression-to-the-mean for siblings at the upper tail of the distribution (13), and complete discordance when one sibling is at the lower extreme tail of the distribution (14). Findings from such studies such as Reichenberg et al. 2016 (14) are are consistent with the presence of de novo alleles of large effect in the trait tails, alongside alternative explanations such as specific environmental exposures. ...
The use of siblings to infer the factors influencing complex traits has been a cornerstone of quantitative genetics. Here we utilise siblings for a novel application: the identification of genetic architecture, specifically that in individuals with extreme trait values (e.g. in the top 1%). Establishing genetic architecture in these individuals is important because they are at greatest risk of disease and are most likely to harbour rare variants of large effect due to natural selection. We develop a theoretical framework that derives expected trait distributions of siblings based on an index sibling's trait value and trait heritability. This framework is used to develop statistical tests that can infer complex genetic architecture in trait tails, distinguishing between polygenic, de novo and Mendelian tail architecture. We apply our tests to UK Biobank data here, while they can be used to infer genetic architecture in any cohort or health registry that includes siblings, without requiring genetic data. We describe how our approach has the potential to help disentangle the genetic and environmental causes of extreme trait values, to identify individuals likely to carry pathogenic variants for follow-up clinical genetic testing, and to improve the design and power of future sequencing studies to detect rare variants.
... These factors accounted entirely for the heritability of early childhood internalising problems. Shared environmental factors (C2; 27% [95% CI [25][26][27][28][29][30] variance explained) and unique environmental factors (E2; 31% [27][28][29][30][31][32][33][34] variance explained) also accounted for variation in offspring internalising problems (figure 3). ...
... The impact of this limitation depends on the extent to which mechanisms of risk differed in particularly severe cases. Previous studies 33,34 of the causes of the extremes of distributions of psychological traits have found them to be highly similar to those underpinning so-called normal variation, so there is no specific reason to expect this to be the case. Nonetheless, the possibility remains and could be explored further in clinical samples. ...
Background:
Maternal prenatal depression is a known risk factor for early-life psychopathology among offspring; however, potential risk transmission mechanisms need to be distinguished. We aimed to test the relative importance of passive genetic transmission, direct exposure, and indirect exposure in the association between maternal prenatal depressive symptoms and early-life internalising and externalising psychopathology in offspring.
Methods:
We used structural equation modelling of phenotypic data and genetically informative relationships from the families of participants in the Norwegian Mother and Child Birth Cohort Study (MoBa). The analytic subsample of MoBa used in the current study comprises 22 195 mothers and 35 299 children. We used mothers' self-reported depressive symptoms during pregnancy, as captured by the Symptom Checklist, and their reports of symptoms of psychopathology in their offspring during the first few years of life (measured at 18, 36, and 60 months using the Child Behavior Checklist).
Findings:
Maternal prenatal depressive symptoms were found to be associated with early-life psychopathology primarily via intergenerationally shared genetic factors, which explained 41% (95% CI 36-46) of variance in children's internalising problems and 37% (30-44) of variance in children's externalising problems. For internalising problems, phenotypic transmission also contributed significantly, accounting for 14% (95% CI 5-19) of the association, but this contribution was found to be explained by exposure to concurrent maternal depressive symptoms, rather than by direct exposure in utero.
Interpretation:
Associations between maternal prenatal depressive symptoms and offspring behavioural outcomes in early childhood are likely to be at least partially explained by shared genes. This genetic confounding should be considered when attempting to quantify risks posed by in-utero exposure to maternal depressive symptoms.
Funding:
UK Economic and Social Research Council, Norwegian Research Council, Norwegian Ministries of Health and Care Services, and Education & Research, Wellcome Trust, Royal Society, and National Institute for Health Research.
... Twin studies of attention-deficit hyperactivity disorder (ADHD) traits have also revealed substantial group heritability for extreme scores on ADHD traits ( Levy et al. 1997; Larsson ) PRS: PRS derived using a clinical ASD discovery GWAS showed significant association with social-communication problems at age 8 years but not ages 11, 14, and 17 years in the general population ( St Pourcain et al. 2017) and self-reported autistic traits in adults (in particular symptoms related to attention to detail, but also rigidity and childhood behaviors) ( Bralten et al. 2017), although 1 smaller study does not find an association with autistic traits in children ( Krapohl et al. 2016) Other: rare de novo loss-of-function and missense mutations associated with Vineland composite scores in ASD probands and unaffected siblings ( Robinson et al. 2016) ADHD Twin studies: high group heritability from DeFries-Fulker analysis ( Levy et al. 1997;Larsson et al. 2011;Greven et al. 2016) LDSC: ADHD and population traits of ADHD: rg = 0.96 ( Middeldorp et al. 2016); replicated in a larger study: rg = 0.94 ( Demontis et al. 2017). ADHD and traits of extraversion in the population: rg = 0.30 ( Lo et al. 2016) PRS: multiple analyses of independent target samples find associations between clinically-defined ADHD PRS and population traits of ADHD and vice versa, although 1 smaller study does not find an association ( Groen ID Twin studies: Cognitive abilities in the general population seem to share genetic risks with milder forms of ID ( Spinath et al. 2004;Reichenberg et al. 2016) and extremely high IQ ( Shakeshaft et al. 2015). There is some evidence, however, of discontinuity between cognitive abilities and severe forms of ID ( Reichenberg et al. 2016) Other: Rare, likely pathogenic copy number variants (which are associated with developmental delay) are also associated with lower cognitive ability in the population ( Männik et al. 2015;Kendall et al. 2016) Anxiety disorders Twin studies: extreme over-anxiety and specific fears, such as of animals, seem to share genetic risks with milder trait anxiety ( Stevenson et al. 1992;Goldsmith & Lemery, 2000). ...
... ( Middeldorp et al. 2016;Demontis et al. 2017), with a moderate genetic correlation (r g = 0.30) between ADHD diagnosis and extraversion traits in the population ( Lo et al. 2016). Cognitive abilities display a similar pattern of significant group heritability in studies of mild intellectual disability (ID) ( Spinath et al. 2004), different quantiles of reading assessments ( Logan et al. 2012), and high levels of intelligence ( Shakeshaft et al. 2015). However, severe ID appears to be an exception to this pattern ( Reichenberg et al. 2016). ...
Genetic influences play a significant role in risk for psychiatric disorders, prompting numerous endeavors to further understand their underlying genetic architecture. In this paper, we summarize and review evidence from traditional twin studies and more recent genome-wide molecular genetic analyses regarding two important issues that have proven particularly informative for psychiatric genetic research. First, emerging results are beginning to suggest that genetic risk factors for some (but not all) clinically diagnosed psychiatric disorders or extreme manifestations of psychiatric traits in the population share genetic risks with quantitative variation in milder traits of the same disorder throughout the general population. Second, there is now evidence for substantial sharing of genetic risks across different psychiatric disorders. This extends to the level of characteristic traits throughout the population, with which some clinical disorders also share genetic risks. In this review, we summarize and evaluate the evidence for these two issues, for a range of psychiatric disorders. We then critically appraise putative interpretations regarding the potential meaning of genetic correlation across psychiatric phenotypes. We highlight several new methods and studies which are already using these insights into the genetic architecture of psychiatric disorders to gain additional understanding regarding the underlying biology of these disorders. We conclude by outlining opportunities for future research in this area.
... Intelligence is a highly polygenic trait [92] and a large literature shows that intelligence is highly heritable (see [93] for a survey). Furthermore, studies show that the high end of intelligence is just as heritable [94]. A pairing of Type I should, on average, produce a Type I offspring. ...
A main objective of this paper is to provide the first model of how climate change, working through sexual selection, could have led to dramatic increases in hominin brain size, and presumably intelligence, in the Middle Pleistocene. The model is built using core elements from the field of family economics, including assortative mating and specialization and complementarities between mates. The main assumptions are that family public goods (e.g., conversation, shelter, fire) were particularly cognitively intensive to produce and became increasingly important for child survival during glacial phases. Intermediate climates (e.g., not the depths of severe glacial phases) create the largest gains from specialization, encouraging negative assortative mating. In contrast, severe glacial phases encourage positive assortative mating because of the rising importance of family public goods. One testable hypothesis is that absence of severe glacial phases should have led to stasis in brain size. Two other testable hypotheses are that severe glacial phases should have led to speciation events, as well as increases in brain size. The evidence shows that there was a million-year stasis in cranial size prior to the start of the severe glacial phases. This stasis is broken by a speciation event (Homo heidelbergensis), with the oldest fossil evidence dated near the close of the first severe glacial phase. In the next 300 kyr, there are two additional severe glacial phases, accompanied by considerable increases in cranial capacity. The last speciation event is Homo sapiens, with the earliest fossils dated near the end of the last of these two glacial phases.
... Since then, genetic analysis has enormously refined our understanding of IQ and intellectual disability. There is a roughly smooth normal distribution of intelligence in the population that is polygenically determined in a way that accounts for the upper reaches, although the nature of extreme genius remains disputed 122 . The extreme low end of the distribution, on the other hand, appears to consist of two components. ...
In 1978, G. Klerman published an essay in which he named the then-nascent “neo-Kraepelinian” movement and formulated a “credo” of nine propositions expressing the movement's essential claims and aspirations. Klerman's essay appeared on the eve of the triumph of neo-Kraepelinian ideas in the DSM-III. However, this diagnostic system has subsequently come under attack, opening the way for competing proposals for the future of psychiatric nosology. To better understand what is at stake, in this paper I provide a close reading and consideration of Klerman's credo in light of the past forty years of research and reflection. The credo is placed in the context of two equally seminal publications in the same year, one by S. Guze, the leading neo-Kraepelinian theorist, and the other by R. Spitzer and J. Endicott, defining mental disorder. The divergences between Spitzer and standard neo-Kraepelinianism are highlighted and argued to be much more important than is generally realized. The analysis of Klerman's credo is also argued to have implications for how to satisfactorily resolve the current nosological ferment in psychiatry. In addition to issues such as creating descriptive syndromal diagnostic criteria, overthrowing psychoanalytic dominance of psychiatry, and making psychiatry more scientific, neo-Kraepelinians were deeply concerned with the conceptual issue of the nature of mental disorder and the defense of psychiatry's medical legitimacy in response to antipsychiatric criticisms. These issues cannot be ignored, and I argue that proposals currently on offer to replace the neo-Kraepelinian system, especially popular proposals to replace it with dimensional measures, fail to adequately address them.
... William Stern took the findings of the Binet-Simon test and the Stanford-Binet test and designed what is the most widely known intelligence test is the 'intelligence quotient' or 'IQ' (Derksen, 2013). The theory behind the IQ test is that intelligence is a phenotype which is generally distributed across societies and cultures (Shakeshaft et al., 2015). The problem with the above-named measures is that they reliably predict achievements, however, are extremely poor in predicting 'exceptional' ability (Lubinski, 2009) and that they are susceptible to cultural and social factors (Serpell, 2000). ...
... Group heritability suggests therefore that 2 Relaxing some of the assumptions of the standard variance decomposition reduces the share of income explained by genetic heritability; see Björklund et al. (2005). earnings at the extreme parts of and in the rest of the distribution are, at least in part, related to the same genetic factors (Plomin and Kovas 2005;Shakeshaft et al. 2015). ...
Using twenty years of earnings data on Finnish twins, we find that about 40% of the variance of women’s and little more than half of men’s lifetime labour earnings are linked to genetic factors. The contribution of the shared environment is negligible. We show that the result is robust to using alternative definitions of earnings, to adjusting for the role of education, and to measurement errors in the measure of genetic relatedness.
... Spain et al. (2016) found that while the bottom tail was associated with increased incidence of genetic mutations (rare alleles), the upper tail had, if anything, a reduced frequency of rare alleles. The upper tail appears to be driven by the same genetic influences that operate throughout the rest of the population distribution, with the discontinuity at the lower extreme being the sole exception (Shakeshaft et al., 2015). The wider picture is that genetic contributions to intelligence stem from many common genetic variations each of small effect, known as the 'polygenic' (Plomin & Deary, 2015); rare functional variants are more often detrimental than beneficial to intelligence. ...
From the genetic side, giftedness in cognitive development is the result of contribution of many common genetic variants of small effect size, so called polygenicity (Spain et al., 2016). From the environmental side, educationalists have argued for the importance of the environment for sustaining early potential in children, showing that bright poor children are held back in their subsequent development (Feinstein, 2003a). Such correlational data need to be complemented by mechanistic models showing how gifted development results from the respective genetic and environmental influences. A neurocomputational model of cognitive development is presented, using artificial neural networks to simulate the development of a population of children. Variability was produced by many small differences in neurocomputational parameters each influenced by multiple artificial genes, instantiating a polygenic model, and by variations in the level of stimulation from the environment. The simulations captured several key empirical phenomena, including the non-linearity of developmental trajectories, asymmetries in the characteristics of the upper and lower tails of the population distribution, and the potential of poor environments to hold back bright children. At a computational level, ‘gifted’ networks tended to have higher capacity, higher plasticity, less noisy neural processing, a lower impact of regressive events, and a richer environment. However, individual instances presented heterogeneous contributions of these neurocomputational factors, suggesting giftedness has diverse causes.
... 20 The quantitative genetic model could be construed to suggest that the extreme low end of the distribution of intelligence is the mirror image of the extreme high end; however, new mutations may be drivers of very low IQ, as they can more easily disrupt than improve finely tuned neurocognitive performance. Recent quantitative genetic research supports the hypothesis that extremely high intelligence is caused by the same DNA variants responsible for individual differences in intelligence throughout the normal distribution, 21 whereas extremely low intelligence is caused by DNA variants that are not associated with individual differences in intelligence in the normal distribution. 22 Here we capitalize on the increased power of association at the high extreme of intelligence as a strategy to facilitate the discovery of alleles that contribute to genetic variation in intelligence throughout the distribution. ...
We used a case–control genome-wide association (GWA) design with cases consisting of 1238 individuals from the top 0.0003 (~170 mean IQ) of the population distribution of intelligence and 8172 unselected population-based controls. The single-nucleotide polymorphism heritability for the extreme IQ trait was 0.33 (0.02), which is the highest so far for a cognitive phenotype, and significant genome-wide genetic correlations of 0.78 were observed with educational attainment and 0.86 with population IQ. Three variants in locus ADAM12 achieved genome-wide significance, although they did not replicate with published GWA analyses of normal-range IQ or educational attainment. A genome-wide polygenic score constructed from the GWA results accounted for 1.6% of the variance of intelligence in the normal range in an unselected sample of 3414 individuals, which is comparable to the variance explained by GWA studies of intelligence with substantially larger sample sizes. The gene family plexins, members of which are mutated in several monogenic neurodevelopmental disorders, was significantly enriched for associations with high IQ. This study shows the utility of extreme trait selection for genetic study of intelligence and suggests that extremely high intelligence is continuous genetically with normal-range intelligence in the population.
... Because no comparison samples of extremely high intelligence are available, we tested the generalization of case-control associations to individual differences in two unselected population samples. If a SNP were associated with extremely high intelligence, we test the prediction that the SNP will also be associated with individual differences in intelligence in the expected direction within the normal distribution of intelligence, a prediction supported by quantitative genetic data 23 . The first unselected sample is our control group of 3,253 individuals for whom intelligence scores were available; associations for individual differences within the control sample should be independent of case-control differences, as we are testing the quantitative variation in these Imputation of HLA variants in the exome data. ...
General cognitive ability (intelligence) is one of the most heritable behavioural traits and most predictive of socially important outcomes and health. We hypothesized that some of the missing heritability of IQ might lie hidden in the human leukocyte antigen (HLA) region, which plays a critical role in many diseases and traits but is not well tagged in conventional GWAS. Using a uniquely powered design, we investigated whether fine-mapping of the HLA region could narrow the missing heritability gap. Our case-control design included 1,393 cases with extremely high intelligence scores (top 0.0003 of the population equivalent to IQ > 147) and 3,253 unselected population controls. We imputed variants in 200 genes across the HLA region, one SNP (rs444921) reached our criterion for study-wide significance. SNP-based heritability of the HLA variants was small and not significant (h² = 0.3%, SE = 0.2%). A polygenic score from the case-control genetic association analysis of SNPs in the HLA region did not significantly predict individual differences in intelligence in an independent unselected sample. We conclude that although genetic variation in the HLA region is important to the aetiology of many disorders, it does not appear to be hiding much of the missing heritability of intelligence.
... Liungman, 1970, p. 134). However, in recent years the tide has turned somewhat, following the rapid developments in genetics (e.g., Panizzon et al., 2014;Shakeshaft et al., 2015). Scopus yields 53 hits for intelligence in titles or abstracts from Sweden in 1980-1989, 119 hits in 1990-1999, 401 in 2000-2009, and 559 in 2010-2016. ...
Studies reporting sex differences in intelligence among the Swedish adult population were systematically reviewed. Five studies from 1959 to 2008 fulfilled the inclusion criteria, and were supplemented with three studies from 1988 to 2015 using nonrepresentative but large samples. The analyses comprise 37 subtest effects that yielded a total of 57 effects. Males tend to exhibit higher performance on spatial and non-verbal reasoning tests, corresponding to ∼0.15-0.25 standard deviations, and lower performance on memory tests (only one study). There were mostly non-significant trends for verbal test results.
... Despite our large sample and different family designs, we did not find statistically significant shared environmental covariance between CA and substance misuse events. This was irrespective of shared environmental influences explaining 12-20% of variance in CA in late adolescence, which is in line with previous estimates [6,33]. In contrast, there was no statistically significant shared environmental variance for substance misuse events in any of the three family-based designs. ...
Aims:
To investigate the association in males between cognitive ability in late adolescence and subsequent substance misuse-related events, and to study the underlying genetic and environmental correlations.
Design:
A population-based longitudinal study with three different family-based designs. Cox proportional hazards models were conducted to investigate the association at the individual level. Bivariate quantitative genetic modeling in (1) full brothers and maternal half-brothers, (2) full brothers reared together and apart, and (3) monozygotic and dizygotic twin brothers was used to estimate genetic and environmental correlations.
Setting:
Register-based study in Sweden.
Participants:
The full sample included 1,402,333 Swedish men born 1958-1991 and conscripted at mean age 18.2 (SD = 0.5) years. 1,361,066 men who had no substance misuse events before cognitive assessment at mandatory military conscription were included in the Cox regression models with a follow-up time of up to 35.6 years.
Measures:
Cognitive ability was assessed at conscription with the Swedish Enlistment Battery. Substance misuse events included alcohol and drug related court convictions, medical treatments, and deaths, available from governmental registries.
Findings:
Lower cognitive ability in late adolescence predicted an increased risk for substance misuse events (hazard ratio [HR] for a 1-stanine unit decrease in cognitive ability: 1.29, 95% CI: 1.29-1.30). The association was somewhat attenuated within clusters of full brothers (HR = 1.21, 95% CI: 1.20-1.23). Quantitative genetic analyses indicated that the association was primarily due to genetic influences; the genetic correlations ranged between -.39 (95% CI: -.45, -.34) and -.52 (-.55, -.48) in the three different designs.
Conclusions:
Shared genetic influences appear to underlie the association between low cognitive ability and subsequent risk for substance misuse events among Swedish men.
... A large-scale study of intelligence in Swedish conscripts (Shakeshaft et al., 2015) concluded, that "high intelligence is familial, heritable, and caused by the same genetic and environmental factors responsible for the normal distribution of intelligence". They also found that "very bright" groups have reduced variance. ...
Jensen (1971) found that black girls score 3 IQ points higher than black boys, and white boys 1.5 IQ points higher than white girls. He, nevertheless, concluded that this did not support his Race. × Sex × Ability interaction theory. Jensen (1998) further analyzed data, some from the National Longitudinal Survey of Youth (NLSY79), and suggested that there is no sex difference in general intelligence, g. Other studies have questioned Jensen's null sex difference theory. The present study tested both theories with data from the ensuring NLSY97 survey, which represents the 15. + million 12-17. year old adolescents living in the US in 1997.Total sample analyses confirmed the existence of significant inverse white-black IQ sex differences, and disconfirmed the null sex difference theory.Separate race-age analyses demonstrated, however, that robust IQ sex differences materialize only after age 16, with no white-black interaction. At age 17, female IQ trails male by 3.6-7.03 points in three races, respectively.Classical IQ probability curves foretell that more males than females will enter the highest echelons of society, irrespective of race, and white Male/Female ratios at IQ 145 successfully predicted real-life sex differences in educational and occupational achievement. White males with IQ 55 can be expected to run a very high risk of encountering severe achievement problems, a risk shared to some extent with Hispanic male, but black females with this low IQ can be expected to perform worse than black males.The paper finally proposed models to account for the origin of sex and race differences in IQ and related educational and occupational differences, involving gene copy numbers, brain size, and steroid hormones. It was suggested that the evolutionary background and physiological nature of sex and race differences explain why social engineering fails to eradicate them.
... For instance, there may be potential genetic background factors that contribute to the protective properties of occupational attainment. Studies have suggested that genetic factors modulate intelligence, 39 enabling an individual to achieve a high occupational status. These individuals may have neuronal richness and greater brain connectivity, allowing the brain to sustain greater disease burden before succumbing. ...
To examine the influence of occupational attainment and education on survival in autopsy-confirmed cases of frontotemporal lobar degeneration (FTLD) and Alzheimer disease (AD).
We performed a retrospective chart review of 83 demographically matched, autopsy-confirmed FTLD (n = 34) and AD (n = 49) cases. Each patient's primary occupation was classified and ranked. Level of education was recorded in years. Survival was defined as time from symptom onset until death. Linear regression was used to test for associations among occupational attainment, education, and patient survival.
Median survival was 81 months for FTLD and 95 months for AD. Years of education and occupational attainment were similar for both groups. We found that higher occupational attainment was associated with longer survival in FTLD but not AD.
Our findings suggest that higher occupational attainment is associated with longer survival in autopsy-confirmed FTLD. The identification of protective factors associated with FTLD survival has important implications for estimates of prognosis and longitudinal studies such as treatment trials.
© 2015 American Academy of Neurology.
Everyday life's hygiene and professional realities, especially in economically developed countries, indicate the need to modify the standards of pro-health programs as well as modern hygiene and work ergonomics programs. These observations are based on the problem of premature death caused by civilization diseases. The biological mechanisms associated with financial risk susceptibility are well described, but there is little data explaining the biological basis of neuroaccounting. Therefore, the aim of the study was to present relationships between personality traits, cognitive competences and biological factors shaping behavioral conditions in a multidisciplinary aspect. This critical review paper is an attempt to compile biological and psychological factors influencing the development of professional competences, especially decent in the area of accounting and finance. We analyzed existing literature from wide range of scientific disciplines (including economics, psychology, behavioral genetics) to create background to pursuit multidisciplinary research models in the field of neuroaccounting. This would help in pointing the best genetically based behavioral profile of future successful financial and accounting specialists.
Production systems have to meet quality requirements despite increasing product individuality, varying batch sizes and a scarcity of resources. The transfer of experience-based knowledge in a flexible and self-optimizing production and process planning offers the potential to meet these challenges. Biological systems solve conceptually similar challenges pertaining to the transfer of knowledge, flexibility of individual reactions and adaptation over time. Thus, in the context of digital transformation, mechanisms derived from biology are interpreted and applied to the knowledge domain of production technology. To be able to exploit the potential of bio-inspired production systems, genetic and intelligent properties of technical components and machines were identified and brought together under the concept of “Gentelligence”. Expanding upon this concept with the new idea of process-DNA and biologically inspired optimization algorithms facilitates a more flexible, learning and self-optimizing production, which is shown in three different applications. By using the new concept of gentelligent process planning it is possible to determine machine-specific process parameters in turning processes in order to ensure appropriate roughness within the requirements. Furthermore, the combination of the concept with a material removal simulation allows the determination of the resulting process force in tool grinding for subsequent unknown workpiece geometries. As a result of using the process-DNA, a workpiece-independent knowledge transfer and thus process adaptation for shape error compensation becomes possible. Gentelligent production scheduling enables a process-parallel, holistically optimized machine allocation, and as a result, a significantly reduced lead time.
Tanulmányunkban a tehetség két aspektusát elemezzük. Az egyik szinten arra a kérdésre keresünk választ, hogy milyen örökletes tényezők tehetők felelőssé a lángész kialakulásáért. Megállapítjuk, hogy a jelenlegi kutatások szerint a tehetség mögött nem fedezhetők fel specifikus gének, de lehetségesek olyan genetikai hatások, amelyek egyfajta emergens szerveződése teremti meg az alapját a lángész kialakulásának – természetesen a különböző környezeti hatásokkal kölcsönhatásban. A másik szintű elemzésben a tehetség evolúciós eredetére kérdezünk rá, és négy olyan humánspecifikus kognitív képesség kialakulását elemezzük, amelyek fontos szerepet játszhatnak a szellemi kiválóság megjelenésében. Nevezetesen arra teszünk kísérletet, hogy megértsük az elmeolvasás, rugalmas gondolkodás, nyelv és kreativitás evolúciós létrejöttét. Ehhez olyan magyarázó model-leket veszünk igénybe, mint a Szociális Intelligencia, Machiavelli Intelligencia, Szexuális Szelekció és Fluid Intelligencia hipotézisek. E magyarázatok megerősítése további kutatásokat igényel.
A bstract
The sequencing of the human genome and advances in gene therapy and genomic editing, coupled with embryo selection techniques and a potential gerontological intervention, are some examples of the rapid technological advances of the “genetic revolution.” This article addresses the methodological issue of how we should theorize about justice in the genomic era. Invoking the methodology of non-ideal theory , I argue that theorizing about justice in the genomic era entails theorizing about (1) the new inequalities that the genetic revolution could exacerbate (e.g., genetic discrimination, disability-related injustices, and gender inequality), and (2) those inequalities that the genetic revolution could help us mitigate (e.g., the risks of disease in early and late life). By doing so, normative theorists can ensure that we develop an account of justice that takes seriously not only individual rights, equality of opportunity, the cultural and sociopolitical aspects of disability, and equality between the sexes, but also the potential health benefits (to both individuals and populations) of attending to the evolutionary causes of morbidity and disability.
When you hear the word Super-Recognizer, you may think of comic-book-hero-esque agents searching the underground to find people who went missing decades ago. Compared to this fantasy, the reality seems somewhat less exciting. Super-Recognizers (SRs) were initially reported a decade ago as a collateral while developing tests for developmental prosopagnosia. Today, the topic of SRs sparks interest from groups seeking to enhance scientific knowledge, public safety, or their monetary gain. With no immediate consequences of erroneous SR-identification, there has been no pressure to establish a clear SR-definition. This promotes heterogenous empirical evidence and the proliferation of unsupported claims in the media. Not only is this status quo unfortunate, it stands in opposition to the potential of special populations – both for science and application. SRs are a special population with imminent real-world value that can advance our understanding of brain functioning. To exploit their potential, I propose a needed formal framework for SR-diagnosis, and introduce 70 cases identified based hereupon. These cases represent the core of a growing SR cohort, studied in my lab in the course of a long-term, multi-methodological research agenda involving academic and government collaborators. Finally, I provide recommendations for those interested in SR work, and highlight current caveats and future challenges.
Production systems have to meet quality requirements despite increasing product individuality, varying batch sizes and a scarcity of resources. The transfer of experience-based knowledge in a flexible and self-optimizing production and process planning offers the potential to meet these challenges. Biological systems solve conceptually similar challenges pertaining to the transfer of knowledge, flexibility of individual reactions and adaptation over time. Thus, in the context of digital transformation, mechanisms derived from biology are interpreted and applied to the knowledge domain of production technology. To be able to exploit the potential of bio-inspired production systems, genetic and intelligent properties of technical components and machines were identified and brought together under the concept of “Gentelligence”. Expanding upon this concept with the new idea of process-DNA and biologically inspired optimization algorithms facilitates a more flexible, learning and self-optimizing production, which is shown in three different applications. By using the new concept of gentelligent process planning it is possible to determine machine-specific process parameters in turning processes in order to ensure appropriate roughness within the requirements. Furthermore, the combination of the concept with a material removal simulation allows the determination of the resulting process force in tool grinding for subsequent unknown workpiece geometries. As a result of using the process-DNA, a workpiece-independent knowledge transfer and thus process adaptation for shape error compensation becomes possible. Gentelligent production scheduling enables a process-parallel, holistically optimized machine allocation, and as a result, a significantly reduced lead time.
Az IQ az egyik legjobb pszichometriai tulajdonságokkal rendelkező és legnagyobb prediktív erővel bíró pszichológiai mutató. Viselkedésgenetikai eredmények régóta arra utaltak, hogy az IQ erősen örökletes, azaz egyéni különbségeit nagyrészt genetikai különbségek okozzák, és az egy családban felnövő testvérek által közösen tapasztalt környezet, például a lakóhely vagy a szocioökonómiai státusz hatása a felnőttkori IQ-ra minimális. A közelmúltban ezt a korábbinál jóval nagyobb kvantitatív genetikai vizsgálatok, a kvantitatív és molekuláris genetikai megközelítéseket ötvöző SNP-örökletességi vizsgálatok, valamint az IQ hátterében álló konkrét genetikai variánsokat felfedő teljesgenom-asszociációs vizsgálatok egészítették ki. A teljesgenom-asszociációs vizsgálatok eredményei alapján poligénes pontszámok alkothatóak, amelyek korrelációja a valós kognitív teljesítménnyel 0.3 körüli. Az IQ genetikai
hátterének pontosabb megismerése, különösképpen a poligénes pontszámok alkalmazása igazolja a korábbi kvantitatív genetikai paradigmákat és számos alkalmazott pszichológiai felhasználásnak nyit utat, ugyanakkor bioetikai problémákat is felvet.
Sensory Processing Sensitivity (SPS) is a common, heritable and evolutionarily conserved trait describing inter-individual differences in sensitivity to both negative and positive environments. Despite societal interest in SPS, scientific knowledge is lagging behind. Here, we critically discuss how SPS relates to other theories, how to measure SPS, whether SPS is a continuous vs categorical trait, its relation to other temperament and personality traits, the underlying aetiology and neurobiological mechanisms, and relations to both typical and atypical development, including mental and sensory disorders. Drawing on the diverse expertise of the authors, we set an agenda for future research to stimulate the field. We conclude that SPS increases risk for stress-related problems in response to negative environments, but also provides greater benefit from positive and supportive experiences. The field requires more reliable and objective assessment of SPS, and deeper understanding of its mechanisms to differentiate it from other traits. Future research needs to target prevention of adverse effects associated with SPS, and exploitation of its positive potential to improve well-being and mental health.
Sensory Processing Sensitivity (SPS) is a trait describing inter-individual differences in sensitivity to environments, both positive and negative ones. SPS has attracted growing societal interest. However, (neuro)scientific evidence is lagging behind. We critically discuss how to measure SPS, how it relates to other theories of Environmental Sensitivity and other temperament and personality traits, how SPS interacts with environments to influence (a)typical development, what the underlying aetiologies and mechanisms are, and its relation to mental disorders involving sensory sensitivities. Drawing on the diverse expertise of the authors, we set an agenda for future research to stimulate the field. We conclude that SPS is a heritable, evolutionarily conserved trait, linked to increased risk for psychopathology and stress-related problems in response to negative environments, as well as to greater benefits (e.g., intervention responsivity, positive mood) in positive environments. We need advances in objective assessment of SPS, understanding mechanisms, differentiating it from (seemingly) related mental disorders, to exploit the potential of SPS to improve mental health, preserve human capital, and prevent adverse effects.
Three studies analyzed the effect of education and social variables on intelligence (represented by one cognitive measure and at the g level) using samples from the SLATINT Project. The results indicated that intelligence, as measured by one measure (e.g., the SPM or IR test), was slightly influenced by education or the SES of schools. However, when intelligence was represented at the latent level (or g factor), the influence of social variables decreased. On the other hand, school performance was primarily influenced by cognitive differences, and secondly by the SES of schools.
Although individual differences in intelligence (general cognitive ability) are highly heritable, molecular genetic analyses to date have had limited success in identifying specific loci responsible for its heritability. This study is the first to investigate exome variation in individuals of extremely high intelligence. Under the quantitative genetic model, sampling from the high extreme of the distribution should provide increased power to detect associations. We therefore performed a case-control association analysis with 1409 individuals drawn from the top 0.0003 (IQ >170) of the population distribution of intelligence and 3253 unselected population-based controls. Our analysis focused on putative functional exonic variants assayed on the Illumina HumanExome BeadChip. We did not observe any individual protein-altering variants that are reproducibly associated with extremely high intelligence and within the entire distribution of intelligence. Moreover, no significant associations were found for multiple rare alleles within individual genes. However, analyses using genome-wide similarity between unrelated individuals (genome-wide complex trait analysis) indicate that the genotyped functional protein-altering variation yields a heritability estimate of 17.4% (s.e. 1.7%) based on a liability model. In addition, investigation of nominally significant associations revealed fewer rare alleles associated with extremely high intelligence than would be expected under the null hypothesis. This observation is consistent with the hypothesis that rare functional alleles are more frequently detrimental than beneficial to intelligence.Molecular Psychiatry advance online publication, 4 August 2015; doi:10.1038/mp.2015.108.
Intelligence is a core construct in differential psychology and behavioural genetics, and should be so in cognitive neuroscience. It is one of the best predictors of important life outcomes such as education, occupation, mental and physical health and illness, and mortality. Intelligence is one of the most heritable behavioural traits. Here, we highlight five genetic findings that are special to intelligence differences and that have important implications for its genetic architecture and for gene-hunting expeditions. (i) The heritability of intelligence increases from about 20% in infancy to perhaps 80% in later adulthood. (ii) Intelligence captures genetic effects on diverse cognitive and learning abilities, which correlate phenotypically about 0.30 on average but correlate genetically about 0.60 or higher. (iii) Assortative mating is greater for intelligence (spouse correlations ~0.40) than for other behavioural traits such as personality and psychopathology (~0.10) or physical traits such as height and weight (~0.20). Assortative mating pumps additive genetic variance into the population every generation, contributing to the high narrow heritability (additive genetic variance) of intelligence. (iv) Unlike psychiatric disorders, intelligence is normally distributed with a positive end of exceptional performance that is a model for 'positive genetics'. (v) Intelligence is associated with education and social class and broadens the causal perspectives on how these three inter-correlated variables contribute to social mobility, and health, illness and mortality differences. These five findings arose primarily from twin studies. They are being confirmed by the first new quantitative genetic technique in a century-Genome-wide Complex Trait Analysis (GCTA)-which estimates genetic influence using genome-wide genotypes in large samples of unrelated individuals. Comparing GCTA results to the results of twin studies reveals important insights into the genetic architecture of intelligence that are relevant to attempts to narrow the 'missing heritability' gap.Molecular Psychiatry advance online publication, 16 September 2014; doi:10.1038/mp.2014.105.
Rather than investigating the extent to which training can improve performance under experimental conditions (‘what could be’), we ask about the origins of expertise as it exists in the world (‘what is’). We used the twin method to investigate the genetic and environmental origins of exceptional performance in reading, a skill that is a major focus of educational training in the early school years. Selecting reading experts as the top 5% from a sample of 10,000 12-year-old twins assessed on a battery of reading tests, three findings stand out. First, we found that genetic factors account for more than half of the difference in performance between expert and normal readers. Second, our results suggest that reading expertise is the quantitative extreme of the same genetic and environmental factors that affect reading performance for normal readers. Third, growing up in the same family and attending the same schools account for less than a fifth of the difference between expert and normal readers. We discuss implications and interpretations (‘what is inherited is DNA sequence variation’; ‘the abnormal is normal’). Finally, although there is no necessary relationship between ‘what is’ and ‘what could be’, the most far-reaching issues about the acquisition of expertise lie at the interface between them (‘the nature of nurture: from a passive model of imposed environments to an active model of shaped experience’).
Youth identified before age 13 (N = 320) as having profound mathematical or verbal reasoning abilities (top 1 in 10,000) were tracked for nearly three decades. Their awards and creative accomplishments by age 38, in combination with specific details about their occupational responsibilities, illuminate the magnitude of their contribution and professional stature. Many have been entrusted with obligations and resources for making critical decisions about individual and organizational well-being. Their leadership positions in business, health care, law, the professoriate, and STEM (science, technology, engineering, and mathematics) suggest that many are outstanding creators of modern culture, constituting a precious human-capital resource. Identifying truly profound human potential, and forecasting differential development within such populations, requires assessing multiple cognitive abilities and using atypical measurement procedures. This study illustrates how ultimate criteria may be aggregated and longitudinally sequenced to validate such measures.
Accession Number: 2002-08562-001. First Author & Affiliation: Ronald, Angelica; Inst of Psychiatry, Social Genetic & Developmental Psychiatry Research Ctr, London, United Kingdom. Other Journal Titles: European Journal for High Ability. Release Date: 20030115. Publication Type: Journal, (0100); Peer Reviewed Journal, (0110); . Media Covered: Print. Document Type: Journal Article. Language: English. Major Descriptor: Cognitive Ability; Cognitive Development; Etiology; Twins. Classification: Cognitive & Perceptual Development (2820) . Population: Human (10); Male (30); Female (40); . Location: England; Wales. Age Group: Childhood (birth-12 yrs) (100) Preschool Age (2-5 yrs) (160) . Methodology: Empirical Study. References Available: Y.. Page Count: 12.. Issue Publication Date: Dec, 2002
OpenMx is free, full-featured, open source, structural equation modeling (SEM) software. OpenMx runs within the R statistical programming environment on Windows, Mac OS–X, and Linux computers. The rationale for developing OpenMx is discussed
along with the philosophy behind the user interface. The OpenMx data structures are introduced—these novel structures define
the user interface framework and provide new opportunities for model specification. Two short example scripts for the specification
and fitting of a confirmatory factor model are next presented. We end with an abbreviated list of modeling applications available
in OpenMx 1.0 and a discussion of directions for future development.
Heritability estimates of general intelligence in adulthood generally range from 75 to 85%, with all heritability due to additive genetic influences, while genetic dominance and shared environmental factors are absent, or too small to be detected. These estimates are derived from studies based on the classical twin design and are based on the assumption of random mating. Yet, considerable positive assortative mating has been reported for general intelligence. Unmodeled assortative mating may lead to biased estimates of the relative magnitude of genetic and environmental factors. To investigate the effects of assortative mating on the estimates of the variance components of intelligence, we employed an extended twin-family design. Psychometric IQ data were available for adult monozygotic and dizygotic twins, their siblings, the partners of the twins and siblings, and either the parents or the adult offspring of the twins and siblings (N = 1314). Two underlying processes of assortment were considered: phenotypic assortment and social homogamy. The phenotypic assortment model was slightly preferred over the social homogamy model, suggesting that assortment for intelligence is mostly due to a selection of mates on similarity in intelligence. Under the preferred phenotypic assortment model, the variance of intelligence in adulthood was not only due to non-shared environmental (18%) and additive genetic factors (44%) but also to non-additive genetic factors (27%) and phenotypic assortment (11%).This non-additive nature of genetic influences on intelligence needs to be accommodated in future GWAS studies for intelligence.
Electronic supplementary material
The online version of this article (doi:10.1007/s10519-011-9507-9) contains supplementary material, which is available to authorized users.
We introduce a new method for analyzing twin data called quantile regression. Through the application presented here, quantile regression is able to assess the genetic and environmental etiology of any skill or ability, at multiple points in the distribution of that skill or ability. This method is compared to the Cherny et al. (Behav Genet 22:153-162, 1992) method in an application to four different reading-related outcomes in 304 pairs of first-grade same sex twins enrolled in the Western Reserve Reading Project. Findings across the two methods were similar; both indicated some variation across the distribution of the genetic and shared environmental influences on non-word reading. However, quantile regression provides more details about the location and size of the measured effect. Applications of the technique are discussed.
Traditional economic theories stress the relevance of political, institutional, geographic, and historical factors for economic growth. In contrast, human-capital theories suggest that peoples' competences, mediated by technological progress, are the deciding factor in a nation's wealth. Using three large-scale assessments, we calculated cognitive-competence sums for the mean and for upper- and lower-level groups for 90 countries and compared the influence of each group's intellectual ability on gross domestic product. In our cross-national analyses, we applied different statistical methods (path analyses, bootstrapping) and measures developed by different research groups to various country samples and historical periods. Our results underscore the decisive relevance of cognitive ability--particularly of an intellectual class with high cognitive ability and accomplishments in science, technology, engineering, and math--for national wealth. Furthermore, this group's cognitive ability predicts the quality of economic and political institutions, which further determines the economic affluence of the nation. Cognitive resources enable the evolution of capitalism and the rise of wealth.
Obesity is globally prevalent and highly heritable, but its underlying genetic factors remain largely elusive. To identify genetic loci for obesity susceptibility, we examined associations between body mass index and ∼ 2.8 million SNPs in up to 123,865 individuals with targeted follow up of 42 SNPs in up to 125,931 additional individuals. We confirmed 14 known obesity susceptibility loci and identified 18 new loci associated with body mass index (P < 5 × 10⁻⁸), one of which includes a copy number variant near GPRC5B. Some loci (at MC4R, POMC, SH2B1 and BDNF) map near key hypothalamic regulators of energy balance, and one of these loci is near GIPR, an incretin receptor. Furthermore, genes in other newly associated loci may provide new insights into human body weight regulation.
Although common sense suggests that environmental influences increasingly account for individual differences in behavior as experiences accumulate during the course of life, this hypothesis has not previously been tested, in part because of the large sample sizes needed for an adequately powered analysis. Here we show for general cognitive ability that, to the contrary, genetic influence increases with age. The heritability of general cognitive ability increases significantly and linearly from 41% in childhood (9 years) to 55% in adolescence (12 years) and to 66% in young adulthood (17 years) in a sample of 11 000 pairs of twins from four countries, a larger sample than all previous studies combined. In addition to its far-reaching implications for neuroscience and molecular genetics, this finding suggests new ways of thinking about the interface between nature and nurture during the school years. Why, despite life's 'slings and arrows of outrageous fortune', do genetically driven differences increasingly account for differences in general cognitive ability? We suggest that the answer lies with genotype-environment correlation: as children grow up, they increasingly select, modify and even create their own experiences in part based on their genetic propensities.
Although much genetic research has addressed normal variation in intelligence, little is known about the etiology of high cognitive abilities. Using data from 11,000 twin pairs (age range = 6-71 years) from the genetics of high cognitive abilities consortium, we investigated the genetic and environmental etiologies of high general cognitive ability (g). Age-appropriate psychometric cognitive tests were administered to the twins and used to create g scores standardized within each study. Liability-threshold model fitting was used to estimate genetic and environmental parameters for the top 15% of the distribution of g. Genetic influence for high g was substantial (0.50, with a 95% confidence interval of 0.41-0.60). Shared environmental influences were moderate (0.28, 0.19-0.37). We conclude that genetic variation contributes substantially to high g in Australia, the Netherlands, the United Kingdom and the United States.
The concept of generalist genes operating across diverse domains of cognitive abilities is now widely accepted. Much less is known about the etiology of the high extreme of performance. Is there more specialization at the high extreme? Using a representative sample of 4,000 12-year-old twin pairs from the UK Twins Early Development Study, we investigated the genetic and environmental overlap between web-based tests of general cognitive ability, reading, mathematics and language performance for the top 15% of the distribution using DF extremes analysis. Generalist genes are just as evident at the high extremes of performance as they are for the entire distribution of abilities and for cognitive disabilities. However, a smaller proportion of the phenotypic intercorrelations appears to be explained by genetic influences for high abilities.
Individual differences in intelligence (cognitive abilities) are a prominent aspect of human psychology, and play a substantial role in influencing important life outcomes. Their phenotypic structure-as described by the science of psychometrics-is well understood and well replicated. Approximately half of the variance in a broad range of cognitive abilities is accounted by a general cognitive factor (g), small proportions of cognitive variance are caused by separable broad domains of mental function, and the substantial remainder is caused by variance that is unique to highly specific cognitive skills. The heritability of g is substantial. It increases from a low value in early childhood of about 30%, to well over 50% in adulthood, which continues into old age. Despite this, there is still almost no replicated evidence concerning the individual genes, which have variants that contribute to intelligence differences. Here, we describe the human intelligence phenotype, summarise the evidence for its heritability, provide an overview of and comment on molecular genetic studies, and comment on future progress in the field.
Talents that selectively facilitate the acquisition of high levels of skill are said to be present in some children but not others. The evidence for this includes biological correlates of specific abilities, certain rare abilities in autistic savants, and the seemingly spontaneous emergence of exceptional abilities in young children, but there is also contrary evidence indicating an absence of early precursors of high skill levels. An analysis of positive and negative evidence and arguments suggests that differences in early experiences, preferences, opportunities, habits, training, and practice are the real determinants of excellence.
The classical twin study is the most popular design in behavioural genetics. It has strong roots in biometrical genetic theory,
which allows predictions to be made about the correlations between observed traits of identical and fraternal twins in terms
of underlying genetic and environmental components. One can infer the relative importance of these ‘latent’ factors (model
parameters) by structural equation modelling (SEM) of observed covariances of both twin types. SEM programs estimate model
parameters by minimising a goodness-of-fit function between observed and predicted covariance matrices, usually by the maximum-likelihood criterion. Likelihood ratio statistics also allow the comparison of fit of different competing models. The program Mx, specifically
developed to model genetically sensitive data, is now widely used in twin analyses. The flexibility of Mx allows the modelling
of multivariate data to examine the genetic and environmental relations between two or more phenotypes and the modelling to
categorical traits under liability-threshold models.
Many misunderstandings about the expert-performance approach can be attributed to its unique methodology and theoretical concepts. This approach was established with case studies of the acquisition of expert memory with detailed experimental analysis of the mediating mechanisms. In contrast the traditional individual difference approach starts with the assumption of underlying general latent factors of cognitive ability and personality that correlate with performance across levels of acquired skill. My review rejects the assumption that data on large samples of beginners can be extrapolated to samples of elite and expert performers. Once we can agree on the criteria for reproducible objective expert performance and acceptable methodologies for collecting valid data. I believe that scientists will recognize the need for expert-performance approach to the study of expert performance, especially at the very highest levels of achievement.
The momentum of genomic science will carry it far into the future and into the heart of research on typical and atypical behavioral development. The purpose of this paper is to focus on a few implications and applications of these advances for understanding behavioral development. Quantitative genetics is genomic and will chart the course for molecular genomic research now that these two worlds of genetics are merging in the search for many genes of small effect. Although current attempts to identify specific genes have had limited success, known as the missing heritability problem, whole-genome sequencing will improve this situation by identifying all DNA sequence variations, including rare variants. Because the heritability of complex traits is caused by many DNA variants of small effect in the population, polygenic scores that are composites of hundreds or thousands of DNA variants will be used by developmentalists to predict children's genetic risk and resilience. The most far-reaching advance will be the widespread availability of whole-genome sequence for children, which means that developmentalists would no longer need to obtain DNA or to genotype children in order to use genomic information in research or in the clinic.
The genetic and environmental etiology of high math performance (at or above the 85%tile) was examined in a population-based
sample of 10-year-old twins (nMZ = 1,279, nDZ = 2,305). Math skills were assessed using a web-based battery of math performance tapping skills related to the UK National
Math Curriculum. Probandwise concordance rates and liability threshold models indicated that genetic and shared environmental
influences were significant, and that these estimates were generally similar to those obtained across the normal range of
ability and did not vary significantly by gender. These results suggest that the genetic and environmental influences at the
high end of ability are likely to be continuous with those that affect the entire range of math performance across all children
irrespective of gender.
In this study no attempt will be made to do original work on the strictly physical aspect of the problem. We shall be satisfied with stating fairly the generally accepted biological views, and pointing out some of the implications of these views. Three possible sources of data presented themselves for consideration. First, it was necessary to secure data on the intellectual behavior of each twin when he worked alone. It was immediately evident that the Stanford-Binet was the most desirable instrument for this purpose. It is necessary to make clear the meaning that is to be given to certain terms that will frequently occur in this part of the study. The results of the study are presented in the form of answers to the three questions asked at the outset. Twins suffer no intellectual handicap. The data show quite conclusively that there are two distinct types of twins.
Study of untangling the influence of home environment and heredity as determiners of mental ability was conducted. Correspondences between the mental status of foster parents and foster children were compared with those between true parents and true children. Since heredity was ruled out in the foster group (and since resemblance due to selective adoption was also largely ruled out by the criteria for inclusion of cases), it was possible to determine how much of ordinary family resemblance resulted from the influence of environment. Stanford-Binet intelligence test records of foster parents, foster children, true parents and true children, together with environmental data upon the cultural, educational, and material aspects of the homes, were used. The foster children were placed in their foster homes during the first year of life (the average age of placement being only three months). Only children placed with white, English-speaking foster parents were included. In selecting the control group, foster parents were matched by controls for intelligence and occupational status, and foster children were matched for age and sex. Correlations are presented between the intelligence quotients of the children and certain hereditary and environmental factors, including that of parental or foster parent intelligence. The contribution of home environment to variance of intelligence is close to 17%; measurable environment one standard deviation above or below the mean of the general population does not shift the IQ by more than 6 to 9 points above or below the value it would have had under normal environmental conditions; and the maximum potency of home environment in ordinary communities enhancing or depressing the IQ is of the order of about 20 IQ points. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
In the past decade, we have witnessed a flood of reports about mutations that cause or contribute to intellectual disability (ID). This rapid progress has been driven in large part by the implementation of chromosomal microarray analysis and next-generation sequencing methods. The findings have revealed extensive genetic heterogeneity for ID, as well as examples of a common genetic etiology for ID and other neurobehavioral/psychiatric phenotypes. Clinical diagnostic application of these new findings is already well under way, despite incomplete understanding of non-Mendelian transmission patterns that are sometimes observed. Expected final online publication date for the Annual Review of Medicine Volume 64 is January 07, 2013. Please see http://www.annualreviews.org/catalog/pubdates.aspx for revised estimates.
The construct validity of the Swedish Enlistment Battery (SEB) used for classification of conscripts according to intellectual capacity was examined. The covariance matrices of three samples of conscripts (N= 501, 1058 and 1057) were analysed in Study 1, testing the hypothesis of one general factor influencing all the four subtests and one residual factor General visualization (Gv′) influencing two of the subsets. The fit of such a model was good. In Study 2 seven reference tests were added to accomplish better definitions of the factors and also to be able to identify a crystallized intelligence (Gc′) factor. Subjects were 113 national servicemen. A general factor was identified, accounting for the dominating part of the total variance. Two factors orthogonal to the general factor were identified; one crystallized-verbal (Gc′) and one general visualization (Gv′) factor, both accounting for a significant but low part of the total variance. More tests must be developed and brought into use in the Enlistment Battery in order to add to the variances in the Gv′ and Gc′ factors. This is a prerequisite for high determinacy and high differential predictive validities of the factors.
Modern computer technology permits efficient evaluation of test scores in terms of basic orthogonal factors of ability. A three-level hierarchical model of cognitive abilities was used as the theoretical basis of the computerized Swedish Enlistment Battery (CAT-SEB). Structural analysis of ten ability tests on a sample of 1,436 conscripts by confirmatory factor analysis (tested by the LISREL system) revealed a general, a verbal and a spatial factor -- although the determinacy of the latter was weak. A nested factor model was used, with direct influences of the latent variables on the tests. This result is a construct validity evaluation of the testing system. Unrelated factor scores of the three latent variables comprise the output of the testing system. Future research should evaluate the efficiency of the prediction from the latent variables.
Berman and Noble (1995) reported significantly reduced visuospatial performance in children with the TAQI A1 allele of the D2 dopamine receptor (DRD2) gene. Given that visuospatial performance loads highly on an unrotated principal component indexing general cognitive ability, we tested the association between DRJD2 and WISC-R IQ comparing 51 high-IQ, 51 average-IQ, and 35 low-IQ children in the IQ Quantitative Trait Loci (QTL) Project. No statistically significant association between the TAQI A DRD2 alleles and IQ was found. Given that a statistically significant portion of genetic variance for specific cognitive abilities is independent of general cognitive ability, it is possible that the TAQI DRD2 association is specific to visuospatial performance and independent of general cognitive ability.
Although there is much evidence of genetic influence on individual differences in cognitive ability, little is known about genetic and environmental contributions to the high and low extremes of intelligence. The etiology of high and low cognitive ability in adulthood was explored by applying the DeFries and Fulker (1985, 1988) multiple regression analysis to data from subjects selected from a sample of 302 twin pairs (M age = 65.6) for scores ± 1 standard deviation on a measure of general cognitive ability in the Swedish Adoption/Twin Study of Aging (SATSA). Estimates of group heritability, the extent to which a mean difference on a quantitative measure between a selected group and the unselected population is heritable, were significant for both high and low ability (h2g=.73 High; h2g=.77 Low); and were similar in magnitude to the heritability of individual differences in the full sample. However, the estimate of group heritability for low ability was constrained using a nonadditive genetic model. These results replicated in an analysis of follow-up test scores obtained 3 years later. Thus, the etiology of high and low ability may be the same as the etiology in the normal range for this Swedish sample of adult twins.
The past five years have seen many scientific and biological discoveries made through the experimental design of genome-wide association studies (GWASs). These studies were aimed at detecting variants at genomic loci that are associated with complex traits in the population and, in particular, at detecting associations between common single-nucleotide polymorphisms (SNPs) and common diseases such as heart disease, diabetes, auto-immune diseases, and psychiatric disorders. We start by giving a number of quotes from scientists and journalists about perceived problems with GWASs. We will then briefly give the history of GWASs and focus on the discoveries made through this experimental design, what those discoveries tell us and do not tell us about the genetics and biology of complex traits, and what immediate utility has come out of these studies. Rather than giving an exhaustive review of all reported findings for all diseases and other complex traits, we focus on the results for auto-immune diseases and metabolic diseases. We return to the perceived failure or disappointment about GWASs in the concluding section.
After drifting apart for 100 years, the two worlds of genetics - quantitative genetics and molecular genetics - are finally coming together in genome-wide association (GWA) research, which shows that the heritability of complex traits and common disorders is due to multiple genes of small effect size. We highlight a polygenic framework, supported by recent GWA research, in which qualitative disorders can be interpreted simply as being the extremes of quantitative dimensions. Research that focuses on quantitative traits - including the low and high ends of normal distributions - could have far-reaching implications for the diagnosis, treatment and prevention of the problematic extremes of these traits.
Thesis (Ph. D.)--Department of Psychology, Stanford University. "References": p. 309-310.
Preliminaty findings from an on-going study of monozygotic twins reared apart (MZA) and data from a larger sample of twins reared together (MZT and DZT), indicate a surprisingly strong influence of genetic variation on aptitudes, psychophysiological characteristics, personality traits and even dimensions of attitude and interest. For some of these variables, MZT and MZA twins show high intra-class correlations while DZT twins are no more similar than pairs of unrelated persons. It is suggested that such traits are emergenic, i.e., that they are determined by the interaction--rather than the sum--of genetic influences. Emergenic traits, although perhaps strongly genetic, will not tend to run in families and for this reason have been neglected by students of behavior genetics. For this and several other listed reasons, wider use of twins in psychological research is strongly recommended.
A pesar de la relativamente corta historia de la Psicología como ciencia, existen pocos constructos psicológicos que perduren 90 años después de su formulación y que, aún más, continúen plenamente vigentes en la actualidad. El factor «g» es sin duda alguna uno de esos escasos ejemplos y para contrastar su vigencia actual tan sólo hace falta comprobar su lugar de preeminencia en los modelos factoriales de la inteligencia más aceptados en la actualidad, bien como un factor de tercer orden en los modelos jerárquicos o bien identificado con un factor de segundo orden en el modelo del recientemente desaparecido R.B.Cattell.
Differences in heritability and shared environmentality across levels of cognitive ability were assessed in a sample of 264 twin pairs tested at 1 year of age and in subsets tested at 2 and 3 years. Using an extension of the DF multiple regression methodology for analyzing twin data, no evidence was found for a linear or quadratic effect of level of cognitive ability on estimates of heritability or shared environmentality.
Differences in heritability and environmentality were assessed for 54 DZ and 86 MZ same-sex twin pairs between 6 and 12 years of age from the Western Reserve Twin Project. A principal-component score composed of the subtests of the WISC-R, PPVT, WRAT, and MAT represented each twin's cognitive ability. Using a modification of a regression technique developed by DeFries and Fulker (1985), it was possible to assess differential heritability and environmentality across ability level. A number of variants of this procedure were used and all yielded the same result: lower ability subjects show higher heritabilities and lower shared environmentality. This result is attributable to larger differences between DZ twins at low ability levels and to differences between MZ twins, which are either the same across ability level or are smaller at low ability levels. A possible explanation for this effect is a genotype-environment correlation in which higher-ability persons seek out better environments. The results from this study should be regarded as tentative but the methods used can be applied to other twins studies. Investigators should be aware of the importance of representing the low end of the distribution in their samples.
The multiple regression analysis of twin data in which a cotwin's score is predicted from a proband's score and the coefficient of relationship (the basic model) provides a statistically powerful test of genetic etiology. When an augmented model that also contains an interaction term is fitted to the same data set, direct estimates of heritability (h
2) and the proportion of variance due to shared environmental influences (c
2) are obtained. A simple transformation of selected twin data prior to regression analysis facilitates direct estimates of h
2
g
(an index of the extent to which the difference between the mean of probands and that of the unselected population is heritable) and a test of the hypothesis that the etiology of deviant scores differs from that of variation within the normal range.
Reading disability (dyslexia) is a major social, educational, and mental health problem. Although estimates of prevalence vary, up to 10-15% of school-age children have severe reading deficits in spite of average intelligence and adequate educational opportunity. That reading disability may have a constitutional basis has long been recognized, and results of twin and family studies suggest that one or more of its forms may be heritable; however, definitive evidence for a genetic aetiology has not been reported. Establishing a heritable basis for reading disability could suggest possible causes, give improved risk estimates, facilitate early diagnosis, and provide validity tests for ostensible subtypes. In this report, we apply a recently developed multiple regression analysis to data collected from a sample of 64 pairs of identical twins and 55 pairs of fraternal twins, in which at least one member of the pairs is reading disabled, and present evidence for a significant genetic aetiology.
A multiple regression model for the analysis of twin data is described in which a cotwin's score is predicted from a proband's score and the coefficient of relationship (R=1.0 and 0.5 for identical and fraternal twin pairs, respectively). This model is especially appropriate for the analysis of data on twins in which one member of each pair has been selected because of a deviant score, e.g., low reading performance. When the model is fitted to such data, the partial regression of the cotwin's score on the coefficient of relationship provides a powerful test of the extent to which the difference between the mean for probands and that for the unselected population is heritable, i.e., a test for genetic etiology. By fitting an augmented model containing an interaction term to either selected or unselected data sets, direct estimates of heritability and the proportion of variance due to shared environmental influences can also be obtained (subject, of course, to the usual assumptions underlying twin analyses, e.g., a linear polygenic model, little or no assortative mating, and equal shared environmental influences for identical and fraternal twins).
Proband concordance rates in twins provide estimates of correlation among twins in liability to a trait or condition. The correlations in turn can be interpreted genetically by the expression 2(r(MZ)-r(DZ)) which eliminates nongenetic familial effects on twins and estimates the coefficient of genetic determination for the trait. The rates of diagnosis and of ascertainment of individuals and their cotwins must also be taken into account, along with other factors such as differences in frequency between sexes, variable age of onset, and variable expressivity or severity. A set of rules for the minimal set of data required and for a standard form of analysis is presented. The genetic interpretation of other measures of concordance is difficult and their value is questionable. The indices of 'heritability' proposed by Holzinger, widely used by human geneticists, are shown to be unsatisfactory and their use should be discontinued.
Familial patterns of mental retardation were examined among white and black children in the NINCDS Collaborative Perinatal Project population. Among whites, the mildly retarded children had more affected relatives than did the severely retarded, consistent with the traditional two-group theory of mental retardation. In blacks, where differences in family patterns between the mildly and the severely retarded were less clear, most retardation appeared to be of the cultural-familial type.
More is known about the genetics of general cognitive ability (g) than any other trait in psychology. Recent findings on the genetics of g include the following three examples: (1) heritability increases throughout the lifespan; (2) heritabilities of performance in cognitive tests are strongly correlated with the tests' loadings on a g factor; and (3) genetic effects on scholastic achievement largely overlap with genetic effects on cognitive ability. This body of genetic research addresses the aetiology of individual differences in the normal range. Much less is known about the genetics of the high end of the distribution. Finding heritability in the normal range of cognitive ability does not imply that high ability is also genetic in origin. However, the first twin study of high IQ children, which uses a new technique that analyses the average difference between extreme groups and the rest of the population, suggests that high IQ is as heritable as individual differences in the normal range. We are currently engaged in a molecular genetic study that attempts to identify specific genes that contribute to high ability.
Three recent studies have used twin data to explore the possibility of differential contributions of heritability and environmentality to individual differences in cognitive ability as a function of ability level (Detterman, D. K.,et al., Behav. Genet.
20:369–384; 1990; Bailey, M. J. amd Revelle, W.,Behav. Genet.
21:397–404, 1991; Cherny, S. S.,et al., Behav. Genet.
22:153–162, 1992). All arrived at different conclusions: higher heritability at the low end, higher heritability at the high end, and no differential influence, respectively. The current report involves a sample of 148 identical and 135 fraternal twin pairs from the Western Twin Project who were tested on a battery of intelligence and achievement tests to further explore the issue. The results suggest no significant differences in heritability at either the high or the low end, although a trend toward higher heritability for children of higher ability is evident. Individual differences for a composite ability/achievement score showed significantly greater influence of shared family environment at the low end than the rest of the distribution. In general, results for cognitive ability and academic achievement were highly similar.
This essay describes how intelligence can be viewed as developing expertise. The general conception of intelligence as developing expertise is described. Then research examples are given that, in conjunction, seem odd under traditional interpretations of abilities but that make sense as a whole in the context of the developing-expertise model. It is concluded that this new model offers potential for better understanding intelligence-related phenomena. Copyright 1999 Academic Press.