Heritability and genome-wide analyses of problematic peer relationships during childhood and adolescence

St Pourcain, Beate, Haworth, C. M. A., Davis, O. S. P., Wang, Kai, Timpson, Nicholas J., Evans, David M., Kemp, John P., Ronald, Angelica, Price, Tom, Meaburn, Emma, Ring, Susan M., Golding, Jean, Hakonarson, Hakon, Plomin, R. and Smith, George Davey (2014) Heritability and genome-wide analyses of problematic peer relationships during childhood and adolescence. Human Genetics, 134 6: 539-551. doi:10.1007/s00439-014-1514-5


Author St Pourcain, Beate
Haworth, C. M. A.
Davis, O. S. P.
Wang, Kai
Timpson, Nicholas J.
Evans, David M.
Kemp, John P.
Ronald, Angelica
Price, Tom
Meaburn, Emma
Ring, Susan M.
Golding, Jean
Hakonarson, Hakon
Plomin, R.
Smith, George Davey
Title Heritability and genome-wide analyses of problematic peer relationships during childhood and adolescence
Journal name Human Genetics   Check publisher's open access policy
ISSN 0340-6717
1432-1203
Publication date 2014-12-17
Year available 2014
Sub-type Article (original research)
DOI 10.1007/s00439-014-1514-5
Open Access Status
Volume 134
Issue 6
Start page 539
End page 551
Total pages 13
Place of publication Heidelberg, Germany
Publisher Springer
Collection year 2015
Language eng
Formatted 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-h 2(Meta) ≤ 0.11) though these influences become stronger in adolescence (13–17 years, 0.14 < GCTA-h 2(ALSPAC) ≤ 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
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2015 Collection
UQ Diamantina Institute Publications
 
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Created: Wed, 25 Mar 2015, 13:45:49 EST by Kylie Hengst on behalf of UQ Diamantina Institute