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Dopamine transporter gene polymorphism moderates the effects of severe deprivation on ADHD symptoms: Developmental continuities in gene–environment interplay
Author(s) -
Stevens Suzanne E.,
Kumsta Robert,
Kreppner Jana M.,
Brookes Keeley J.,
Rutter Michael,
SonugaBarke Edmund J. S.
Publication year - 2009
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.31010
Subject(s) - dopamine transporter , haplotype , dopamine , polymorphism (computer science) , psychology , attention deficit hyperactivity disorder , exon , genotype , genetics , gene , psychiatry , dopaminergic , biology , neuroscience
Early institutional deprivation is a risk factor for Attention‐Deficit/Hyperactivity Disorder (ADHD) symptoms. However not all individuals are affected. We tested the hypothesis that this heterogeneity is influenced by gene x environment (GxE) interaction and that genetic polymorphisms involved in dopamine neurotransmission moderate the effects of severe early institutional deprivation on symptoms of ADHD (sADHD). Using a prospective‐longitudinal design sADHD were measured at ages 6, 11, and 15 years in a sample of individuals who experienced severe institutional deprivation (up to 42 months of age) in Romanian orphanages and a non‐institutionalized comparison group. Individuals were genotyped for polymorphisms in the dopamine D4 receptor ( DRD4 48‐bp VNTR in exon 3) and dopamine transporter gene ( DAT1 haplotypes combining a 40‐bp VNTR in 3'UTR and a 30‐bp VNTR in intron 8). The risk for sADHD associated with early institutional deprivation was moderated by the DAT1 but not the DRD4 genotypes; an effect that was first apparent in early‐, and persisted to mid‐adolescence. The results (i) provide evidence for developmental continuities in G x E interaction, (ii) explain some of the heterogeneity in ADHD outcomes following institutional deprivation and, (iii) add to our understanding of environmental determinants of sADHD. © 2009 Wiley‐Liss, Inc.