Genetics of intelligence

Deary, Ian J.; Spinath, Frank M.; Bates, Timothy C.

doi:10.1038/sj.ejhg.5201588

Cited by 230 publications

(185 citation statements)

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“…Our cognitive ability exceeds that of our closest primate relatives and some of the genetic changes during human speciation have affected our intelligence. At the same time IQ is a highly heritable trait in humans with estimates of broad-sense heritability up to 80% (McGue et al 1993;Deary et al 2006). Genetic linkage and association studies have shown before that segregating variants influence individual differences in cognitive ability (Buyske et al 2006;Luciano et al 2006;Posthuma et al 2005).…”

Section: Discussionmentioning

confidence: 99%

A Functional Polymorphism under Positive Evolutionary Selection in ADRB2 is Associated with Human Intelligence with Opposite Effects in the Young and the Elderly

et al. 2008

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Comparative genomics offers a novel approach to unravel the genetic basis of complex traits. We performed a two stage analysis where genes ascertained for enhanced protein evolution in primates are subsequently searched for the presence of non-synonymous coding SNPs in the current human population at amino acid sites that differ between humans and chimpanzee. Positively selected genes among primates are generally presumed to determine phenotypic differences between humans and chimpanzee, such as the enhanced cognitive ability of our species. Amino acid substitutions segregating in humans at positively selected amino acid sites are expected to affect phenotypic differences among humans. Therefore we conducted an association study in two family based cohorts and one population based cohort between cognitive ability and the most likely candidate gene among the five that harbored more than one such polymorphism. The derived, human-specific allele of the beta-2 adrenergic receptor Arg16Gly polymorphism was found to be the increaser allele for performance IQ in the young, family based cohort but the decreaser allele for two different measures of cognition in the large Scottish cohort of unrelated individuals. The polymorphism is known to affect signaling activity and modulation of beta-2 adrenergic signaling has been shown to adjust memory consolidation, a trait related 123Behav Genet (2009) 39:15-23 DOI 10.1007 to cognition. The opposite effect of the polymorphism on cognition in the two age classes observed in the different cohorts resembles the effect of ADRB2 on hypertension, which also has been reported to be age dependent. This result illustrates the relevance of comparative genomics to detect genes that are involved in human behavior.

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Section: Discussionmentioning

confidence: 99%

A Functional Polymorphism under Positive Evolutionary Selection in ADRB2 is Associated with Human Intelligence with Opposite Effects in the Young and the Elderly

et al. 2008

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“…In this type of analysis, it is not the environmental and genetic contributions to a single phenotype that are measured, but the environmental and genetic contributions to the association between two phenotypes. Because both IQ and mortality are partly heritable (79,80), some fraction of their phenotypic correlation may represent a genetic correlation (common genetic roots). Moreover, there is evidence from a study of adoptees that part of the association between parental socioeconomic position and mortality might be heritable (81).…”

Section: Iq and Later Mortality Riskmentioning

confidence: 99%

Premorbid (early life) IQ and Later Mortality Risk: Systematic Review

Batty

Deary

Gottfredson³

2007

Annals of Epidemiology

418

347

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PURPOSE: Studies of middle-aged and particularly older-aged adults found that those with higher scores on tests of IQ (cognitive function) had lower rates of later mortality. Interpretation of such findings potentially is hampered by the problem of reverse causality: such somatic diseases as diabetes or hypertension, common in older adults, can decrease cognitive function. Studies that provide extended follow-up of the health experience of individuals who had their (premorbid) IQ assessed in childhood and/or early adulthood minimize this concern. The purpose of the present report is to systematically locate, evaluate, and interpret the findings of all such studies. METHODS: We systematically identified individual-level studies linking premorbid IQ with later mortality by using four approaches: search of electronic databases (MEDLINE, EMBASE, and PSYCHINFO); scrutiny of the reference sections of identified reports; search of our own files; and contact with researchers in the field. Study quality was assessed by using predefined criteria. RESULTS: Nine cohort studies met the inclusion criteria. Overall, study quality was moderate. All reports showed an inverse IQ-mortality relation; i.e., higher IQ scores were associated with decreased mortality risk. The nature of this relation (i.e., dose-response or threshold) and whether it differs by sex was unclear. The IQ-mortality association did not appear to be explained by reverse causality or selection bias. Confounding by other early-life factors also did not seem to explain the association, although some studies were not well characterized in this regard. Adult socioeconomic position appeared to mediate the IQ-mortality association in some studies, but this was not a universal finding. CONCLUSIONS: In all studies, higher IQ in the first two decades of life was related to lower rates of total mortality in middle to late adulthood. Some plausible mechanistic pathways exist, but further examination is required. The precise nature of the IQ-mortality relation (particularly in ethnic minorities and women) and the link between IQ and disease-specific outcomes also warrants further research. Ann Epidemiol -;-:-. Ó

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“…The findings emerging from twin and family studies have univocally indicated: (1) a role of genetic factors in the etiology of intelligence (e.g., Bouchard & McGue, 1981;Deary et al, 2006;Plomin & Spinath, 2004;Plomin et al, 2008), and (2) an age-dependent pattern of heritability, with individual differences in late adolescence and adulthood being more strongly influenced by genetic factors than those in childhood (the heritability estimates typically ranging from ß20% in infancy to ß40-50% in middle childhood and ß60-80% in adulthood; e.g., Bartels et al, 2002;Bishop et al, 2003;Boomsma & van Baal, 1998;Deary et al, 2006;Haworth et al, 2009;Hoekstra et al, 2007;McGue et al, 1993;Petrill et al, 2004;Plomin, 1986;Polderman et al, 2006). Environmental factors that contribute to similarity between family members (e.g., shared family environment) typically decline in etiological relevance throughout childhood and adolescence, while environmental factors that Sanja Franić, Conor V. Dolan, Catherina E.M. van Beijsterveldt, Hilleke E. Hulshoff Pol, Meike Bartels & Dorret I. Boomsma facilitate differentiation between family members appear to play a persistently modest to moderate role (e.g., Bartels et al, 2002;Boomsma & van Baal, 1998;Haworth et al, 2009).…”

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confidence: 99%

Genetic and Environmental Stability of Intelligence in Childhood and Adolescence

et al. 2014

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The present study examined the genetic and environmental contributions to the temporal stability of verbal, non-verbal and general intelligence across a developmental period spanning childhood and adolescence (5-18 years). Longitudinal twin data collected in four different studies on a total of 1,748 twins, comprising 4,641 measurement points in total, were analyzed using genetic adaptations of the simplex model. The heterogeneity in the type of instrument used to assess psychometric intelligence across the different subsamples and ages allowed us to address the auxiliary question of how to optimally utilize the existing longitudinal data in the context of gene-finding studies. The results were consistent across domains (verbal, non-verbal and general intelligence), and indicated that phenotypic stability was driven primarily by the high stability of additive genetic factors, that the stability of common environment was moderate, and that the unique environment contributed primarily to change. The cross-subscale stability was consistently low, indicating a small overlap between different domains of intelligence over time. The high stability of additive genetic factors justifies the use of a linear combination of scores across the different ages in the context of gene-finding studies.Keywords: intelligence, longitudinal measures, genetic stability, environmental stability, simplex model, heritability, structural equation modelingIntelligence is one of the most frequently studied human behavioral traits. Over the past century it has motivated research across a diverse range of fields, including not only the behavioral sciences, but also genetics, neuroscience, molecular biology, and economics. It is one of the strongest known determinants of major life outcomes, such as educational attainment, occupational success, health and longevity (Deary et al

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Genetics of intelligence

Cited by 230 publications

References 80 publications

A Functional Polymorphism under Positive Evolutionary Selection in ADRB2 is Associated with Human Intelligence with Opposite Effects in the Young and the Elderly

A Functional Polymorphism under Positive Evolutionary Selection in ADRB2 is Associated with Human Intelligence with Opposite Effects in the Young and the Elderly

Premorbid (early life) IQ and Later Mortality Risk: Systematic Review

Genetic and Environmental Stability of Intelligence in Childhood and Adolescence

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