Attention-deficit hyperactivity disorder (ADHD) is a common childhood-onset behavioural disorder affecting about 5% of school-age children. It has been shown that ADHD is highly heritable, and polymorphisms in several genes appear to increase susceptibility to the disorder. Most of these genes encode proteins involved in the brains’ dopaminergic neurotransmitter system, regulating processes like attention, movement, and reward. A number of environmental factors have also been linked to increased risk for the disorder. In particular, it is known that in utero exposure to maternal smoking and alcohol can increase the risk of developing ADHD. Neither genes nor the environment, however, are likely to act independently, and interactions between both sets of factors are probably important in mediating disease susceptibility.
In a study to be published in the journal Biological Psychiatry, Rosalind Neuman and colleagues at Washington University School of Medicine have examined the joint effects of genetic and prenatal substance exposure on the prevalence of ADHD. Using logistic regression analysis they assessed the relationship between ADHD, dopaminergic gene polymorphisms, and prenatal substance exposures in a birth-record sample of male and female twin pairs, aged 7–19 years.
They report interactions between prenatal exposure to smoking and polymorphisms in both the dopamine D4 receptor gene (DRD4) and the dopamine transporter gene (DAT1). These results are important as they indicate that smoking during pregnancy is associated severe forms of ADHD, particularly in genetically susceptible children.
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