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Heritability and genome-wide analyses of problematic peer relationships during childhood and adolescence
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St Pourcain, Beate, Haworth, Claire M. A., Davis, Oliver S. P., Wang, Kai, Timpson, Nicholas J., Evans, David M., Kemp, John P., Ronald, Angelica, Price, Tom S., Meaburn, Emma, Ring, Susan M., Golding, Jean, Hakonarson, Hakon, Plomin, Robert and Smith, George Davey (2014) Heritability and genome-wide analyses of problematic peer relationships during childhood and adolescence. Human Genetics . doi:10.1007/s00439-014-1514-5 ISSN 1432-1203.
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Official URL: http://dx.doi.org/10.1007/s00439-014-1514-5
Abstract
Peer behaviour plays an important role in the development of social adjustment, though little is known about its genetic architecture. We conducted a twin study combined with a genome-wide complex trait analysis (GCTA) and a genome-wide screen to characterise genetic influences on problematic peer behaviour during childhood and adolescence. This included a series of longitudinal measures (parent-reported Strengths-and-Difficulties Questionnaire) from a UK population-based birth-cohort (ALSPAC, 4–17 years), and a UK twin sample (TEDS, 4–11 years). Longitudinal twin analysis (TEDS; N ≤ 7,366 twin pairs) showed that peer problems in childhood are heritable (4–11 years, 0.60 < twin-h 2 ≤ 0.71) but genetically heterogeneous from age to age (4–11 years, twin-r g = 0.30). GCTA (ALSPAC: N ≤ 5,608, TEDS: N ≤ 2,691) provided furthermore little support for the contribution of measured common genetic variants during childhood (4–12 years, 0.02<GCTA−h2Meta ≤ 0.11) though these influences become stronger in adolescence (13–17 years, 0.14<GCTA−h2ALSPAC ≤ 0.27). A subsequent cross-sectional genome-wide screen in ALSPAC (N ≤ 6,000) focussed on peer problems with the highest GCTA-heritability (10, 13 and 17 years, 0.0002 < GCTA-P ≤ 0.03). Single variant signals (P ≤ 10−5) were followed up in TEDS (N ≤ 2835, 9 and 11 years) and, in search for autism quantitative trait loci, explored within two autism samples (AGRE: N Pedigrees = 793; ACC: N Cases = 1,453/N Controls = 7,070). There was, however, no evidence for association in TEDS and little evidence for an overlap with the autistic continuum. In summary, our findings suggest that problematic peer relationships are heritable but genetically complex and heterogeneous from age to age, with an increase in common measurable genetic variation during adolescence.
Item Type: | Journal Article | ||||||||
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Subjects: | R Medicine > RJ Pediatrics | ||||||||
Divisions: | Faculty of Science, Engineering and Medicine > Science > Psychology | ||||||||
Library of Congress Subject Headings (LCSH): | Behavior disorders in children, Behavior genetics | ||||||||
Journal or Publication Title: | Human Genetics | ||||||||
Publisher: | Springer | ||||||||
ISSN: | 1432-1203 | ||||||||
Official Date: | 17 December 2014 | ||||||||
Dates: |
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Number of Pages: | 13 | ||||||||
DOI: | 10.1007/s00439-014-1514-5 | ||||||||
Status: | Peer Reviewed | ||||||||
Publication Status: | Published | ||||||||
Access rights to Published version: | Open Access (Creative Commons) | ||||||||
Date of first compliant deposit: | 28 December 2015 | ||||||||
Date of first compliant Open Access: | 28 December 2015 | ||||||||
Funder: | Medical Research Council (Great Britain) (MRC), University of Bristol, Autism Speaks (Organisation), Wellcome Trust (London, England), National Institutes of Health (U.S.) (NIH), British Academy (BA), European Research Council (ERC) | ||||||||
Grant number: | WT092731/Z/10/Z (WT), 7132 (AS), MC_UU_12013/1-9 (MRC), G0800582 (MRC), WT083431MA (WT), G0901245 (MRC), HD044454 (NIH), HD059215 (NIH), 085475/B/08/Z (WT), 085475/Z/08/Z (WT), WT088984 (WT), G19/2 (MRC), 295366 (ERC), 1U24MH081810 (NIH) |
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