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      Genetics and educational attainment

      research-article
      1 , 2 , 3 ,
      NPJ Science of Learning
      Nature Publishing Group UK

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          Abstract

          We explore how advances in our understanding of the genetics of complex traits such as educational attainment could constructively be leveraged to advance research on education and learning. We discuss concepts and misconceptions about genetic findings with regard to causes, consequences, and policy. Our main thesis is that educational attainment as a measure that varies between individuals in a population can be subject to exactly the same experimental biological designs as other outcomes, for example, those studied in epidemiology and medical sciences, and the same caveats about interpretation and implication apply.

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          Most cited references16

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          GWAS of 126,559 individuals identifies genetic variants associated with educational attainment.

          A genome-wide association study (GWAS) of educational attainment was conducted in a discovery sample of 101,069 individuals and a replication sample of 25,490. Three independent single-nucleotide polymorphisms (SNPs) are genome-wide significant (rs9320913, rs11584700, rs4851266), and all three replicate. Estimated effects sizes are small (coefficient of determination R(2) ≈ 0.02%), approximately 1 month of schooling per allele. A linear polygenic score from all measured SNPs accounts for ≈2% of the variance in both educational attainment and cognitive function. Genes in the region of the loci have previously been associated with health, cognitive, and central nervous system phenotypes, and bioinformatics analyses suggest the involvement of the anterior caudate nucleus. These findings provide promising candidate SNPs for follow-up work, and our effect size estimates can anchor power analyses in social-science genetics.
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            Many sequence variants affecting diversity of adult human height.

            Adult human height is one of the classical complex human traits. We searched for sequence variants that affect height by scanning the genomes of 25,174 Icelanders, 2,876 Dutch, 1,770 European Americans and 1,148 African Americans. We then combined these results with previously published results from the Diabetes Genetics Initiative on 3,024 Scandinavians and tested a selected subset of SNPs in 5,517 Danes. We identified 27 regions of the genome with one or more sequence variants showing significant association with height. The estimated effects per allele of these variants ranged between 0.3 and 0.6 cm and, taken together, they explain around 3.7% of the population variation in height. The genes neighboring the identified loci cluster in biological processes related to skeletal development and mitosis. Association to three previously reported loci are replicated in our analyses, and the strongest association was with SNPs in the ZBTB38 gene.
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              Genetics and intelligence differences: five special findings

              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.
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                Author and article information

                Contributors
                peter.visscher@uq.edu.au
                Journal
                NPJ Sci Learn
                NPJ Sci Learn
                NPJ Science of Learning
                Nature Publishing Group UK (London )
                2056-7936
                1 February 2017
                1 February 2017
                2017
                : 2
                : 4
                Affiliations
                [1 ]ISNI 0000 0004 1936 8753, GRID grid.137628.9, Department of Economics, , New York University, ; New York, NY 10012 United States
                [2 ]ISNI 0000 0000 9320 7537, GRID grid.1003.2, Institute for Molecular Bioscience, University of Queensland, ; Brisbane, QLD 4072 Australia
                [3 ]ISNI 0000 0000 9320 7537, GRID grid.1003.2, Queensland Brain Institute, The University of Queensland, ; Brisbane, QLD 4072 Australia
                Article
                5
                10.1038/s41539-017-0005-6
                6220209
                30631451
                523084dd-9d0f-4f75-83c1-71bc1bf2ae65
                © The Author(s) 2017

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                : 8 October 2016
                : 20 December 2016
                : 22 December 2016
                Categories
                Review Article
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                © The Author(s) 2017

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