Cited by 142Attention Deficit Hyperactivity DisorderNeurotransmitter Receptor Influence on BehaviorPrenatal Substance Exposure Effects

Interaction of dopamine transporter genotype with prenatal smoke exposure on ADHD symptoms

Becker, Katja, El-Faddagh, Mahha, Schmidt, Martin H., Esser, Günter, Laucht, Manfred·2008·The Journal of Pediatrics

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.

Integrity signals

Registry

Crossref · 10.1016/j.jpeds.2007.07.004

Cites

39 of 39 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • 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

Cites

Flagged first, then by citations

Cited by

Sorted by citations

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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review