title: Heritability and genome-wide analyses of problematic peer relationships during childhood and adolescence.
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.
authors.affiliation: MRC Integrative Epidemiology Unit (MRC IEU), University of Bristol, Oakfield House, Oakfield Grove, Bristol, BS8 2BN, UK, beate.stpourcain@bristol.ac.uk.
authors.forename: Beate
authors.initials: B
authors.lastname: St Pourcain
authors.forename: C M A
authors.initials: CM
authors.lastname: Haworth
authors.forename: O S P
authors.initials: OS
authors.lastname: Davis
authors.forename: Kai
authors.initials: K
authors.lastname: Wang
authors.forename: Nicholas J
authors.initials: NJ
authors.lastname: Timpson
authors.forename: David M
authors.initials: DM
authors.lastname: Evans
authors.forename: John P
authors.initials: JP
authors.lastname: Kemp
authors.forename: Angelica
authors.initials: A
authors.lastname: Ronald
authors.forename: Tom
authors.initials: T
authors.lastname: Price
authors.forename: Emma
authors.initials: E
authors.lastname: Meaburn
authors.forename: Susan M
authors.initials: SM
authors.lastname: Ring
authors.forename: Jean
authors.initials: J
authors.lastname: Golding
authors.forename: Hakon
authors.initials: H
authors.lastname: Hakonarson
authors.forename: R
authors.initials: R
authors.lastname: Plomin
authors.forename: George
authors.initials: G
authors.lastname: Davey Smith
mesh_terms: D000293:Adolescent; D001321:Autistic Disorder / Q000235:genetics*; D002648:Child; D002675:Child, Preschool; D005260:Female; D005790:General Adaptation Syndrome / Q000235:genetics*; D055106:Genome-Wide Association Study; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D040641:Quantitative Trait Loci; D006113:United Kingdom