The pooled estimate for maternal prenatal substance use showed an association with total ADHD symptoms, while not for fathers (OR SMOKING = 1.03, 95% CI = 0.95–1.13 OR ALCOHOL = 0.83, 95% CI = 0.47–1.48 OR CAFFEINE = 1.02, 95% CI = 0.97–1.07). MeasurementsĪ measure of offspring ADHD symptoms at age 7–8 years was derived by dichotomizing scores from questionnaires and parental self-reported prenatal substance use was measured at the second pregnancy trimester. Genotype data available for mothers was: N ALSPAC = 7074 N MOBA = 14 583. We used data from three longitudinal pregnancy cohorts: Avon Longitudinal Study of Parents and Children (ALSPAC) in the United Kingdom, Generation R study (GenR) in the Netherlands and Norwegian Mother, Father and Child Cohort study (MoBa) in Norway. We triangulated the results across the two approaches to infer causality. Maternal PRS for smoking, alcohol and coffee consumption were regressed against ADHD symptoms. Secondly, we used polygenic risk scores (PRS) as proxies for exposures. The results were meta-analysed across the cohorts. Three models were used for negative control analyses: unadjusted (without confounders), adjusted (including confounders) and mutually adjusted (including confounders and partner's substance use).

Designįirst, we used a negative control design comparing maternal and paternal substance use. We measured associations between prenatal smoking, alcohol and caffeine consumption with childhood ADHD symptoms accounting for shared familial factors. Studies have indicated that maternal prenatal substance use may be associated with offspring attention deficit hyperactivity disorder (ADHD) via intrauterine effects.

Prenatal alcohol exposure x adhd