Twins Early Development Study

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The Twins Early Development Study (TEDS) is an ongoing longitudinal twin study headed by principal investigator psychologist Robert Plomin and based at King's College London. The main goal of TEDS is to use behavioural genetic methods to find out how nature (genes) and nurture (environments) can explain why people differ with respect to their cognitive abilities, learning abilities and behaviours. Over 15,000 pairs of twins originally signed up for the study and more than 13,000 pairs remain involved to the present day. This demonstrates the continued support of all twins and their families for more than a decade.

The TEDS sample[edit]

Participants were identified from birth records of all twins born in England and Wales between 1994 and 1996. When the twins were around 12 months old, a parent or guardian of the twins was asked to complete a first contact booklet, which listed a comprehensive range of background variables (e.g. information about ethnic origin, job status and educational qualifications). This background information has been updated through the course of the study and has enabled comparisons of the TEDS sample against UK population data and against participants lost to attrition. These comparisons have led to the conclusion that, despite attrition, TEDS continues to be representative of the UK population, e.g. in terms of ethnicity, maternal education, and parental employment status.[1][2][3] Zygosity of twins was determined either using parental questionnaires or, in instances where questionnaire results were unclear, by DNA typing.[4] Data has been collected longitudinally at ages 2, 3, 4, 7, 8, 9, 10, 12, 14 and 16

Main research topics[edit]

TEDS was originally set up with funding from the Medical Research Council in order to investigate the genetic and environmental origins of common cognitive disabilities and abilities, learning disabilities and abilities (e.g. language, reading, mathematical abilities and disabilities) and behaviour problems (e.g. hyperactivity). Although the main focus remains on these topics, TEDS has also looked at other topics such as gender role development, prosocial behaviour, food choices, asthma, and sources of heterogeneity and comorbidity in psychopathology. TEDS’ research also addresses the relationship between ability and disability, i.e. can disability be understood in terms of the extreme end of a continuum of normal variation in ability. The incorporation of environmental measures (e.g. measures of home and school environment) in genetically sensitive designs allows TEDS to study the interplay between nature and nurture; such as exposure to certain environments for genetic reasons (gene-environment correlation) and differential sensitivity to the environment based on people’s genetic make-up (gene-environment interaction).

Aims[edit]

TEDS follows three major aims.[3]

  • Firstly, to use univariate quantitative genetic methods to explore the genetic and environmental origins of common learning and cognitive abilities and disabilities, i.e. to estimate the extent to which nature and nurture influence these abilities and disabilities.
  • Secondly, to use multivariate and longitudinal quantitative genetic methods to go beyond the rudimentary nature-nurture question, i.e. to address how nature and nurture contribute to stability and change in these abilities and disabilities, and how they influence the relations between different abilities and disabilities. The latter includes within-domain comparisons, e.g. to what extent do different learning disabilities (such as reading and mathematics disability) share a common genetic or environmental origin? It also includes cross-domain comparisons, e.g. to what extent to do learning disabilities (e.g. reading disability) and behaviour problems (e.g. Attention-Deficit Hyperactivity Disorder) share a common origin?

Major findings and contributions[edit]

Oliver & Plomin (2007) [3] provide an overview of TEDS findings. TEDS has made major contributions to the Genetics and Education literature, such as the formulation of the Generalist Genes Hypothesis of learning abilities and disabilities,[5] and important contributions to the literature on the heritability of IQ and school achievement.[6][7] Novel findings from TEDS also include the discovery that social and non-social behaviours exhibited by children with autistic spectrum disorder (ASD) are largely influenced by different genes.[8] With respect to molecular genetics, TEDS has pioneered a novel strategy called SNP Microarrays and Pooling (SNP-MaP), which is a cost-effective and powerful way of genotyping DNA as it allows researchers to use one microarray instead of hundreds to genotype a group’s pooled DNA.[9][10][11] It is hoped that it will eventually be possible to use the insights obtained from studies such as TEDS to help prevent or alleviate common learning disabilities such as dyslexia.[12]

References[edit]

  1. ^ Trouton, A., Spinath, F. M. & Plomin, R. (2002). "Twins Early Development Study (TEDS): A multivariate, longitudinal genetic investigation of language, cognition and behaviour problems in childhood". Twin Research 5 (5): 444–448. doi:10.1375/136905202320906255. PMID 12537874. 
  2. ^ Harlaar, N., Spinath, F. M., Dale, P. S. & Plomin, R. (2005). "Genetic influences on early word recognition abilities and disabilities: a study of 7-year-old twins". Journal of Child Psychology & Psychiatry 46 (4): 373–384. doi:10.1111/j.1469-7610.2004.00358.x. PMID 15819646. 
  3. ^ a b c Oliver, B. & Plomin, R (2007). "Twins Early Development Study (TEDS): A multivariate, longitudinal genetic investigation of language, cognition and behaviour problems from childhood through adolescence". Twin Research and Human Genetics 10 (1): 96–105. doi:10.1375/twin.10.1.96. PMID 17539369. 
  4. ^ Price, Thomas S; Freeman, Bernard; Craig, Ian; Petrill, Stephen A; Ebersole, Lorna; Plomin, Robert (2000). "Infant zygosity can be assigned by parental report questionnaire data". Twin Research 3 (3): 129–133. doi:10.1375/136905200320565391. PMID 11035484. 
  5. ^ Plomin, R. & Kovas, Y. (2005). "Generalist genes and learning disabilities". Psychological Bulletin 131 (4): 592–617. doi:10.1037/0033-2909.131.4.592. PMID 16060804. 
  6. ^ Kovas, Y., Haworth, C. M. A., Dale, P. S. & Plomin, R. (2007). "The genetic and environmental origins of learning abilities and disabilities in the early school years". Monogr Soc Res Child Dev 72 (3): 1–144. doi:10.1111/j.1540-5834.2007.00453.x. PMID 17995572. 
  7. ^ Plomin, R.; DeFries, J. C., McClearn, G. E. & McGuffin, P. (2008). Behavioral genetics. New York: Worth Publishers. ISBN 1-4292-0577-6. 
  8. ^ Ronald, A., Happé, F. & Plomin, R. (2005). "The genetic relationship between individual differences in social and nonsocial behaviours characteristic of autism". Developmental Science 8 (5): 444–458. doi:10.1111/j.1467-7687.2005.00433.x. PMID 16048517. 
  9. ^ Butcher, L. M., Liu, Lin, Fernandes, Cathy, Hill, Linzy, Al-Chalabi, Ammar, Plomin, Robert, Schalkwyk, Leo, Craig, Ian W. (2004). "Genotyping pooled DNA on microarrays: A systematic genome screen of thousands of SNPs in large samples to detect QTLs for complex traits". Behavior Genetics 34 (5): 549–55. doi:10.1023/B:BEGE.0000038493.26202.d3. PMID 15319578. 
  10. ^ Meaburn, Emma; Butcher, Lee M; Liu, Lin; Fernandes, Cathy; Hansen, Valerie; Al-Chalabi, Ammar; Plomin, Robert; Craig, Ian; Schalkwyk, Leonard C (2005). "Genotyping DNA pools on microarrays: Tackling the QTL problem of large samples and large numbers of SNPs". BMC Genomics 6: 52–60. doi:10.1186/1471-2164-6-52. PMC 1079828. PMID 15811185. 
  11. ^ Meaburn, E., Butcher, L. M., Schalkwyk, L. C. & Plomin, R. (2006). "Genotyping pooled DNA using 100K SNP microarrays: a step towards genomewide association scans". Nucleic Acids Research 34 (4): e27. doi:10.1093/nar/gnj027. PMC 1368655. PMID 16478714. 
  12. ^ Plomin, R. (2008). "State-of-Science Review: SR-D7 - Genetics and the Future Diagnosis of Learning Disabilities" (PDF). Review commissioned as part of UK Government’s Foresight Project, Mental Capital and Wellbeing. Retrieved 2008-11-18. 

External links[edit]