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

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TitleHeritability and genome-wide analyses of problematic peer relationships during childhood and adolescence.
Publication TypeJournal Article
Year of Publication2015
AuthorsSt Pourcain, B, Haworth, CMA, Davis, OSP, Wang, K, Timpson, NJ, Evans, DM, Kemp, JP, Ronald, A, Price, T, Meaburn, E, Ring, SM, Golding, J, Hakonarson, H, Plomin, R, Smith, GDavey
JournalHum Genet
Volume134
Issue6
Pagination539-51
Date Published2015 Jun
ISSN1432-1203
KeywordsAdolescent, Autistic Disorder, Child, Child, Preschool, Female, General Adaptation Syndrome, Genome-Wide Association Study, Humans, Longitudinal Studies, Male, Quantitative Trait Loci, United Kingdom
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.

DOI10.1007/s00439-014-1514-5
Alternate JournalHum. Genet.
PubMed ID25515860
PubMed Central IDPMC4424375
Grant ListMC_UU_12013/1-9 / / Medical Research Council / United Kingdom
WT092731/Z/10/Z / / Wellcome Trust / United Kingdom
G0800582 / / Medical Research Council / United Kingdom
MC_UU_12013/3 / / Medical Research Council / United Kingdom
G0500079 / / Medical Research Council / United Kingdom
WT088984 / / Wellcome Trust / United Kingdom
102215 / / Wellcome Trust / United Kingdom
G19/2 / / Medical Research Council / United Kingdom
HD044454 / HD / NICHD NIH HHS / United States
WT083431MA / / Wellcome Trust / United Kingdom
MC_PC_15018 / / Medical Research Council / United Kingdom
MC_UU_12013/1 / / Medical Research Council / United Kingdom
MRCG0800582 / / Medical Research Council / United Kingdom
085475/B/08/Z / / Wellcome Trust / United Kingdom
G1100226 / / Medical Research Council / United Kingdom
HD059215 / HD / NICHD NIH HHS / United States
G0901245 / / Medical Research Council / United Kingdom
085475/Z/08/Z / / Wellcome Trust / United Kingdom
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