ABSTRACT
OBJECTIVE: To examine whether the dopamine receptor D4 gene (DRD4) exon III VNTR moderates the risk of infants with regulatory disorders for developing attention-deficit/hyperactivity disorder (ADHD) later in childhood. STUDY DESIGN: In a prospective longitudinal study of children at risk for later psychopathology, 300 participants were assessed for regulatory problems in infancy, DRD4 genotype, and ADHD symptoms and diagnoses from childhood to adolescence. To examine a potential moderating effect on ADHD measures, linear and logistic regressions were computed. Models were fit for the main effects of the DRD4 genotype (presence or absence of the 7r allele) and regulatory problems (presence or absence), with the addition of the interaction term. All models were controlled for sex, family adversity, and obstetric risk status. RESULTS: In children without the DRD4-7r allele, a history of regulatory problems in infancy was unrelated to later ADHD. But in children with regulatory problems in infancy, the additional presence of the DRD4-7r allele increased the risk for ADHD in childhood. CONCLUSIONS: The DRD4 genotype seems to moderate the association between regulatory problems in infancy and later ADHD. A replication study is needed before further conclusions can be drawn, however.
Subject(s)
Attention Deficit Disorder with Hyperactivity/genetics , Infant Behavior , Receptors, Dopamine D4/genetics , Adolescent , Alleles , Child , Child, Preschool , Female , Genotype , Humans , Infant , Male , Polymorphism, Genetic , Receptors, Dopamine D4/physiologyABSTRACT
OBJECTIVE: To demonstrate that children homozygous for the 10-repeat allele of the common dopamine transporter (DAT1) polymorphism who were exposed to maternal prenatal smoke exhibited significantly higher hyperactivity-impulsivity than children without these environmental or genetic risks. STUDY DESIGN: We performed a prospective longitudinal study from birth into early adulthood monitoring the long-term outcome of early risk factors. Maternal prenatal smoking was determined during a standardized interview with the mother when the child was 3 months old. At age 15 years, 305 adolescents participated in genotyping for the DAT1 40 base pair variable number of tandem repeats polymorphism and assessment of inattention, hyperactivity-impulsivity, and oppositional defiant/conduct disorder symptoms with the Kiddie-Sads-Present and Lifetime Version. RESULTS: There was no bivariate association between DAT1 genotype, prenatal smoke exposure and symptoms of attention deficit hyperactivity disorder. However, a significant interaction between DAT1 genotype and prenatal smoke exposure emerged (P = .012), indicating that males with prenatal smoke exposure who were homozygous for the DAT1 10r allele had higher hyperactivity-impulsivity than males from all other groups. In females, no significant main effects of DAT1 genotype or prenatal smoke exposure or interaction effects on any symptoms were evident (all P > .25). CONCLUSIONS: This study provides further evidence for the multifactorial nature of attention deficit hyperactivity disorder and the importance of studying both genetic and environmental factors and their interaction.
Subject(s)
Attention Deficit Disorder with Hyperactivity/etiology , Attention Deficit Disorder with Hyperactivity/genetics , Dopamine Plasma Membrane Transport Proteins/genetics , Genotype , Tobacco Smoke Pollution/adverse effects , Adolescent , Alleles , Child , Child, Preschool , Environment , Female , Homozygote , Humans , Male , Models, Genetic , Polymorphism, Genetic , Pregnancy , Prenatal Exposure Delayed Effects , Regression AnalysisABSTRACT
The aim of the present study was to investigate the P300 amplitude as a possible vulnerability marker in children of alcoholic (COA) fathers with and without paternal delinquency. Event-related potentials (ERPs) of 122 children aged 8 years (63 boys, 59 girls) were compared depending on father's alcoholism subtype: 30 COAs without paternal delinquency, 10 COAs with paternal delinquency, and 82 children of non-alcoholic and non-delinquent fathers. ERPs were recorded from Fz, Cz, and Pz, using an auditory oddball paradigm. Sinus tones of 60 dB HL were presented binaurally at 1,000 Hz (standard stimulus) and 2,000 Hz (target stimulus), at a relative frequency ratio of 80:20. Two trial blocks of 250 stimuli each were collected. Results indicated that only COAs with paternal delinquency displayed significant differences from the control group, characterized by reduced P300 amplitude at frontal site and in the second trial block. Thus, the combination of fathers' alcoholism and delinquency was more likely to relate to attenuated P300 amplitude in the offspring than paternal alcoholism alone. Our results suggest that both alcoholic and delinquent family history appear to play a role in P300 amplitude reduction in the offspring.
Subject(s)
Alcoholism/psychology , Child of Impaired Parents/psychology , Crime/psychology , Event-Related Potentials, P300/physiology , Child , Electroencephalography , Fathers , Female , Humans , Longitudinal Studies , Male , Prospective Studies , Psychomotor Performance/physiology , Risk , Socioeconomic FactorsABSTRACT
O desenvolvimento de criancas expostas a fatores de risco biologicos (complicacoes obstetricas) e psicossociais (ambiente familiar desfavoravel) foi acompanhado por meio de estudo prospectivo longitudinal, desde o nascimento ate a idade escolar.Em uma amostra de 362 criancas...