Interaction of dopamine transporter genotype with prenatal smoke exposure on ADHD symptoms
Abstract
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.
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Several early environmental risk factors for ADHD are associated with increased inflammation, including maternal infection, smoking, obesity, poor diet, and pollutant exposure.
“early environmental factors are also implicated in the etiology of ADHD including many factors associated with increased inflammation such as maternal infection (Werenberg Dreier et al., 2016), maternal smoking (Becker et al., 2008; Biederman, 2005; Mick et al., 2002; Neuman et al., 2007; Silva et al., 2014; Thapar et al., 2013), maternal obesity and poor diet (Andersen et al., 2018; Buss et al.,”
From Neuroinflammation as a risk factor for attention deficit hyperactivity disorder (2019) · cites this paper as Becker et al., 2008
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- Authors
- Becker, K., El-Faddagh, M., Schmidt, M. H., Esser, G., & Laucht, M.
- Affiliations
- Central Institute of Mental Health (DE)
- University of Potsdam (DE)
- Corresponding author
- Becker, Katja
- Venue
- The Journal of Pediatrics
- Publisher
- Elsevier BV
- Published
- 2008-02
- Volume
- 152
- Issue
- 2
- Pages
- 263-269.e1
- ISSN
- 0022-3476 (ISSN-L)
- OpenAlex
- W2052135198
- Cited by
- 142
- References
- 39
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 9 · 2022: 2 · 2021: 1 · 2020: 5 · 2019: 7 · 2018: 3 · 2017: 9 · 2016: 5 · 2015: 8 · 2014: 9 · 2013: 15 · 2012: 9
- FWCI
- 8.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Pediatrics (publishedVersion)
- PubMed (publishedVersion)
- publish.UP (University of Potsdam) (submittedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- dopamine transporter gene, DAT1 polymorphism, maternal smoking, maternal smoking exposure, attention deficit hyperactivity disorder, hyperactivity/impulsivity, gene-environment interaction, genetic susceptibility, sex differences
- MeSH terms
- Adolescent, Alleles, Attention Deficit Disorder with Hyperactivity, Child, Child, Preschool, Environment, Female, Genotype, Homozygote, Humans, Male, Models, Genetic, Polymorphism, Genetic, Pregnancy, Prenatal Exposure Delayed Effects, Regression Analysis, Tobacco Smoke Pollution, Dopamine Plasma Membrane Transport Proteins
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