Offspring Attention-deficit Hyperactivity Disorder Symptoms Research Articles

Maternal postpartum depression symptoms and early childhood hyperactive/aggressive behavior are independently associated with later attention deficit/hyperactivity symptoms

Attention deficit/hyperactivity behaviors in children are often unnoticed until they reach school age; however, evidence suggests that attention deficit hyperactivity disorder (ADHD) tends to develop at an earlier age. Recent studies also indicate that perinatal maternal mental health is associated with ADHD symptoms in offspring. This study examines the association between maternal postpartum depression, early hyperactive/aggressive behavior, and later ADHD symptoms. This longitudinal cohort study used data from health checkups and surveys. Mothers with a postpartum Edinburgh postnatal depression scale score ⩾ 9 were considered as having postpartum depression symptoms. The presence of early hyperactive/aggressive behavior was determined based on 3-year-old children’s health checkup data. The ADHD rating scale (ADHD-RS) answered by the caregivers of 182 sixth-grade children was used for the analysis. ADHD-RS scores were significantly higher in children with early hyperactive and/or aggressive behavior (p = .002) and for children of mothers who had postpartum depression symptoms (p < .001). Early hyperactive/aggressive behavior did not mediate the predictive association of maternal postpartum depression symptoms with ADHD symptoms in sixth grade. ADHD symptoms in the sixth grade were independently associated with childhood hyperactive/aggressive behavior at age 3 and maternal postpartum depression symptoms.

Exposure to chlorpyrifos and pyrethroid insecticides and symptoms of Attention Deficit Hyperactivity Disorder (ADHD) in preschool children from the Odense Child Cohort

BackgroundAttention Deficit Hyperactivity Disorder (ADHD) is a common childhood psychiatric disorder with severe and lifelong impact on mental health and socioeconomic achievements. Environmental factors may play a role in the increasing incidens rates. Previous studies on associations between prenatal and childhood exposure to organophosphate and pyrethroid insecticides and ADHD symptoms have yielded mixed findings. ObjectivesTo investigate associations between prenatal and childhood exposure to chlorpyrifos and pyrethroids and ADHD symptoms in 5-year-old children from the Odense Child Cohort. MethodsSpot urine samples from pregnant women in gestational week 28 (n = 614) and offspring at 5 years of age (n = 814) were collected and analyzed for the specific metabolite of chlorpyrifos, TCPY (3,5,6-trichloro-2-pyridinol), as well as the generic pyrethroid metabolite, 3-PBA (3-phenoxybenzoic acid). Offspring ADHD symptoms were assessed at age 5 years using the parent reported “ADHD scale” from the “Child Behavior Checklist 1½-5” (n = 1114). Associations between insecticide exposure variables and an ADHD score ≥90th percentile were analyzed using logistic regression for all children and stratified by sex. ResultsMost pregnant women had detectable concentrations of 3-PBA (93%) and TCPY (91%) with median concentrations of 0.20 μg/L and 1.62 μg/L, respectively. In children, 3-PBA and TCPY concentrations were detectable in 88% and 82% of the samples, and the median concentrations were 0.17 and 1.16 μg/L. No statistically significant associations were observed between insecticide metabolites and an ADHD score ≥90th percentile at age 5. ConclusionIn this relatively large Danish birth cohort study with mainly low dietary insecticide exposure, we found no statistically significant associations between prenatal or childhood exposure to chlorpyrifos or pyrethroids, and excess ADHD-symptom load, in 5-year-old children. Prospective studies with multiple urine samples across vulnerable windows of neurodevelopment is warranted to improve assessment of safe exposure levels, which is particularly relevant for pyrethroids, since their use is increasing.

Prenatal sleep health and risk of offspring ADHD symptomatology and associated phenotypes: a prospective analysis of timing and sex differences in the ECHO cohort

Sleep difficulties are common in pregnancy, yet poor prenatal sleep may be related to negative long-term outcomes for the offspring, including risk for attention-deficit/hyperactivity disorder (ADHD). Existing studies are few and have not examined timing of exposure effects or offspring sex moderation. We thus aimed to test the hypotheses that poor sleep health in pregnancy is associated with increased risk for ADHD symptoms and offspring sleep problems at approximately 4 years of age. Participants were 794 mother-child dyads enrolled in the NIH Environmental Influences on Child Health Outcomes Study (ECHO). Participants self-reported on sleep duration, quality, and disturbances during pregnancy and on children's ADHD symptoms and sleep problems on the Child Behaviour Checklist. Pregnant participants were 32.30±5.50 years and children were 46% female. 44 percent of pregnant participants identified as Hispanic or Latine; 49% identified as White. Second-trimester sleep duration was associated with offspring ADHD symptoms (b=-0.35 [95% CI=-0.57,-0.13], p=0.026), such that shorter duration was associated with greater symptomatology. Poorer sleep quality in the second trimester was also associated with increased ADHD symptomatology (b=0.66 [95% CI=0.18, 1.14], p=0.037). Greater sleep disturbances in the first trimester were associated with offspring ADHD (b=1.03 [95% CI=0.32, 1.03], p=0.037) and in the second trimester with sleep problems (b=1.53 [95% CI=0.42, 2.92], p=0.026). We did not document substantial offspring sex moderation. Poor prenatal sleep health, particularly quality and duration in the second trimester, may be associated with offspring risk of neurodevelopmental disorders and sleep problems in early childhood. Further research is needed to understand mechanisms, yet our study suggests that prenatal maternal sleep may be a modifiable target for interventions aimed at optimizing early neurodevelopment. NIH grants U2COD023375, U24OD023382, U24OD023319, UH3OD023320, UH3OD023305, UH3OD023349, UH3OD023313, UH3OD023272, UH3OD023328, UH3OD023290, K08MH117452 and NARSAD Young Investigator Award28545.

Prenatal smoking, drinking, or caffeine does not affect ADHD symptoms in offspring

A recent study has found that in contrast to some previously published studies, maternal prenatal substance use with legal substances is not associated with offspring attention‐deficit hyperactivity disorder (ADHD). For the study, researchers measured associations between prenatal smoking, alcohol, and caffeine consumption with childhood ADHD symptoms. They took into consideration shared familial factors.

Maternal use of substances while pregnant does not affect ADHD symptoms in offspring

A recent study has found that in contrast to some previously published studies, maternal prenatal substance use with legal substances is not associated with offspring attention‐deficit hyperactivity disorder (ADHD). For the study, researchers measured associations between prenatal smoking, alcohol, and caffeine consumption with childhood ADHD symptoms. They took into consideration shared familial factors.

Prenatal smoking, alcohol and caffeine exposure and maternal-reported attention deficit hyperactivity disorder symptoms in childhood: triangulation of evidence using negative control and polygenic risk score analyses.

Studies have indicated that maternal prenatal substance use may be associated with offspring attention deficit hyperactivity disorder (ADHD) via intrauterine effects. We measured associations between prenatal smoking, alcohol and caffeine consumption with childhood ADHD symptoms accounting for shared familial factors. First, we used a negative control design comparing maternal and paternal substance use. Three models were used for negative control analyses: unadjusted (without confounders), adjusted (including confounders) and mutually adjusted (including confounders and partner's substance use). The results were meta-analysed across the cohorts. Secondly, we used polygenic risk scores (PRS) as proxies for exposures. Maternal PRS for smoking, alcohol and coffee consumption were regressed against ADHD symptoms. We triangulated the results across the two approaches to infer causality. 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. Phenotype data available for children were: NALSPAC = 5455-7751; NGENR = 1537-3119; NMOBA = 28 053-42 206. Genotype data available for mothers was: NALSPAC = 7074; NMOBA = 14 583. A measure of offspring ADHD symptoms at age 7-8years was derived by dichotomizing scores from questionnaires and parental self-reported prenatal substance use was measured at the second pregnancy trimester. The pooled estimate for maternal prenatal substance use showed an association with total ADHD symptoms [odds ratio (OR)SMOKING = 1.11, 95% confidence interval (CI) = 1.00-1.23; ORALCOHOL = 1.27, 95% CI = 1.08-1.49; ORCAFFEINE = 1.05, 95% CI = 1.00-1.11], while not for fathers (ORSMOKING = 1.03, 95% CI = 0.95-1.13; ORALCOHOL = 0.83, 95% CI = 0.47-1.48; ORCAFFEINE = 1.02, 95% CI = 0.97-1.07). However, maternal associations did not persist in sensitivity analyses (substance use before pregnancy, adjustment for maternal ADHD symptoms in MoBa). The PRS analyses were inconclusive for an association in ALSPAC or MoBa. There appears to be no causal intrauterine effect of maternal prenatal substance use on offspring attention deficit hyperactivity disorder symptoms.

Maternal and offspring genetic risk score analyses of fetal alcohol exposure and attention-deficit hyperactivity disorder risk in offspring.

BackgroundStudies investigating the effects of prenatal alcohol exposure on childhood attention‐deficit hyperactivity disorder (ADHD) symptoms using conventional observational designs have reported inconsistent findings, which may be affected by unmeasured confounding and maternal and fetal ability to metabolize alcohol. We used genetic variants from the alcohol metabolizing genes, alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), as proxies for fetal alcohol exposure to investigate their association with risk of offspring ADHD symptoms around age 7–8 years.MethodsWe used data from 3 longitudinal pregnancy cohorts: Avon Longitudinal Study of Parents and Children (ALSPAC), Generation R study (GenR), and the Norwegian Mother, Father and Child Cohort study (MoBa). Genetic risk scores (GRS) for alcohol use and metabolism using 36 single nucleotide polymorphisms (SNPs) from ADH and ALDH genes were calculated for mothers (N ALSPAC = 8196; NMOBA = 13,614), fathers (N MOBA = 13,935), and offspring (N ALSPAC=8,237; N MOBA=14,112; N GENR=2,661). Associations between maternal GRS and offspring risk of ADHD symptoms were tested in the full sample to avoid collider bias. Offspring GRS analyses were stratified by maternal drinking status.ResultsThe pooled estimate in maternal GRS analyses adjusted for offspring GRS in ALSPAC and MoBa was OR = 0.99, 95%CI 0.97–1.02. The pooled estimate in offspring GRS analyses stratified by maternal drinking status across all the cohorts was as follows: ORDRINKING = 0.98, 95% CI 0.94–1.02; ORNO DRINKING = 0.99, 95% CI 0.97–1.02. These findings remained similar after accounting for maternal genotype data in ALSPAC and maternal and paternal genotype data in MoBa.ConclusionsWe did not find evidence for a causal effect of fetal alcohol exposure on risk of ADHD symptoms in offspring. The results may be affected by limited power to detect small effects and outcome assessment.

The link between attention deficit hyperactivity disorder (ADHD) symptoms and obesity-related traits: genetic and prenatal explanations

Attention-deficit/hyperactivity disorder (ADHD) often co-occurs with obesity, however, the potential causality between the traits remains unclear. We examined both genetic and prenatal evidence for causality using Mendelian Randomisation (MR) and polygenic risk scores (PRS). We conducted bi-directional MR on ADHD liability and six obesity-related traits using summary statistics from the largest available meta-analyses of genome-wide association studies. We also examined the shared genetic aetiology between ADHD symptoms (inattention and hyperactivity) and body mass index (BMI) by PRS association analysis using longitudinal data from Northern Finland Birth Cohort 1986 (NFBC1986, n = 2984). Lastly, we examined the impact of the prenatal environment by association analysis of maternal pre-pregnancy BMI and offspring ADHD symptoms, adjusted for PRS of both traits, in NFBC1986 dataset. Through MR analyses, we found evidence for bidirectional causality between ADHD liability and obesity-related traits. PRS association analyses showed evidence for genetic overlap between ADHD symptoms and BMI. We found no evidence for a difference between inattention and hyperactivity symptoms, suggesting that neither symptom subtype is driving the association. We found evidence for association between maternal pre-pregnancy BMI and offspring ADHD symptoms after adjusting for both BMI and ADHD PRS (association p-value = 0.027 for inattention, p = 0.008 for hyperactivity). These results are consistent with the hypothesis that the co-occurrence between ADHD and obesity has both genetic and prenatal environmental origins.

Maternal depressive and anxiety symptoms and the risk of attention deficit hyperactivity disorder symptoms in offspring aged 17: Findings from the Raine Study

BackgroundWhile previous studies have suggested that maternal anxiety and depressive symptoms are associated with increased risk of attention-deficit/hyperactivity disorder (ADHD) in their offspring in early and late childhood, studies exploring the risk in late adolescence are however lacking. This study aims to examine the association between maternal anxiety and depressive symptoms and the risk of ADHD symptoms in late adolescence (at age 17). MethodsWe used data from the Raine Study. Maternal depressive and anxiety symptoms were measured when the child was 10 years of age using the Depression, Anxiety, and Stress Scale (DASS). Offspring ADHD symptoms at age 17 were assessed using the DSM-oriented scales of the child behavior checklist (CBCL). Log-binomial regression was used to explore the associations. ResultsWe found an increased risk of ADHD symptoms in offspring of mothers with comorbid anxiety and depressive symptoms when compared with offspring of mothers with no symptoms [RR 5.60 (95%CI 3.02-10.37)]. There was a nearly three-fold increase in the risk of ADHD symptoms in offspring of mothers with increased anxiety symptoms compared with offspring of mothers who were in the normal range [RR 2.84 (95%CI 1.18-6.83)]. No association was observed with maternal depressive symptoms. ConclusionThis study found an increased risk of ADHD symptoms in the offspring of mothers with anxiety as well as comorbid anxiety and depressive symptoms but not among the offspring of mothers with depressive symptoms. Early screening and intervention for ADHD symptoms in offspring with maternal anxiety and comorbid anxiety and depressive symptoms are warranted.

Evaluation of maternal inflammation as a marker of future offspring ADHD symptoms: A prospective investigation

Early life predictors of attention-deficit/hyperactivity disorder (ADHD) are critically needed; they could inform etiological theory and may help identify new prevention targets. The current study examined prospectively whether maternal cytokine levels during pregnancy predict offspring ADHD symptoms at age 4–6 years. Secondarily, we evaluated maternal cytokine levels as a possible common pathway through which prenatal risks exert influence on child ADHD. Data came from a sample of women recruited during the 2nd trimester of pregnancy (N = 62) and followed postnatally until children were 4–6 years old. Maternal inflammation was assessed using 3rd trimester plasma concentrations of three indicators of nuclear factor kappa B signaling: interleukin-6, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 which were combined into a latent variable. Mothers and teachers reported on child ADHD symptoms, negative affect, and externalizing behaviors at 48–72 months of age. Maternal inflammation in the 3rd trimester predicted ADHD symptoms when children were 4–6 years old (β = 0.53, 95% CI = 0.154, 0.905, p = 0.006). Further, maternal inflammation mediated the effect of prenatal distress on child ADHD (β = 0.21, 95% CI = 0.007, 0.419, p = 0.04). The inflammation effect on ADHD was not explained by concurrent child negative affect, externalizing behavior, or familial ADHD status. This is the first human study to prospectively link maternal pregnancy cytokine levels and offspring ADHD symptoms, suggesting that cytokine levels are a possible marker of ADHD risk. Results also provide new evidence that maternal prenatal inflammation may be one common pathway by which prenatal risk factors influence offspring mental health outcomes.

Low-moderate prenatal alcohol exposure and offspring attention-deficit hyperactivity disorder (ADHD): systematic review and meta-analysis.

To evaluate the available evidence on the association between low-to-moderate prenatal alcohol exposure (PAE) and the development of attention-deficit hyperactivity disorder (ADHD) symptoms in the offspring. We systematically reviewed and meta-analysed studies reporting an association between low and/or moderate PAE and offspring ADHD symptoms (attention and/or hyperactivity). Systematic searches were performed in EMBASE, Pubmed, Medline, and PsycINFO and reviewed from selected references. Random effects modelling was conducted to pool adjusted odds ratios (OR) in different alcohol consumption levels (≤ 20g/week, ≤ 50g/week, and ≤ 70g/week). Stratified analysis by sex per alcohol level was conducted to investigate the difference on OR and the magnitude between-study heterogeneity. Ten studies were included in the systematic review and six in the meta-analysis. Eight studies found no association and two studies suggested an apparent protective effect of low PAE in hyperactivity/inattention symptoms in boys. These results were confirmed by the meta-analysis showing no association between ≤ 20g/week [OR 1.01 (0.68-1.49)], ≤ 50g/week [OR 0.94 (0.85-1.03)] and ≤ 70g/week [OR 0.94 (0.86-1.02)] and ADHD symptoms, with no evidence of publication bias. Stratified analysis by sex for a PAE ≤ 50g/week exposed less risk of ADHD symptoms in boys compared to girls [OR 0.89 (0.83-0.96)]. We found no increased risk of ADHD symptoms in offspring born to mothers who drank alcohol up to 70g/week.

Maternal alcohol use during pregnancy and offspring attention-deficit hyperactivity disorder (ADHD): a prospective sibling control study.

Maternal alcohol use during pregnancy has repeatedly been associated with development of attention-deficit hyperactivity disorder (ADHD) in the offspring. It is, however not known whether this reflects a direct casual intra-uterine effect or a non-causal relationship due to confounding. We used three different approaches to control for measured and unmeasured confounding: statistical adjustment for covariates, negative control comparison against maternal pre-pregnancy alcohol use, and comparison among differentially exposed siblings. The sample comprised 114 247 children (34 283 siblings) from 94 907 mothers, recruited to the Norwegian Mother and Child Birth Cohort Study between 1999 and 2008. Self-reported measurements of alcohol use were obtained in week 30 during the pregnancy. Mothers rated offspring ADHD symptoms at 5 years on two measures. Clinical ADHD diagnoses were obtained from the Norwegian Patient Registry. We found an overall positive association between maternal alcohol use during pregnancy and offspring ADHD symptoms, which was only marginally attenuated after inclusion of measured covariates. Both the negative control and the sibling comparison analysis further attenuated the estimated association, but it remained greater than zero [β = 0.017, 95% confidence interval (CI) = 0.005-0.030). No association was found between maternal alcohol use during pregnancy and offspring ADHD diagnosis. For offspring ADHD symptoms we found a weak, but possibly causal association with maternal alcohol use during pregnancy, but no such effect was observed for clinical ADHD diagnosis.

Gestational weight gain, prepregnancy body mass index and offspring attention-deficit hyperactivity disorder symptoms and behaviour at age 10.

To assess offspring attention-deficit hyperactivity disorder (ADHD) symptoms and emotional/behavioural impairments at age 10 years in relation to maternal gestational weight gain (GWG) and prepregnancy body mass index (BMI). Longitudinal birth cohort from Magee-Womens Hospital, Pittsburgh, Pennsylvania (enrolled 1983-86). Mother-infant dyads (n = 511) were followed through pregnancy to 10 years. Self-reported total GWG was converted to gestational-age-standardised z-scores. Multivariable linear and negative binomial regressions were used to estimate effects of GWG and BMI on outcomes. Child ADHD symptoms were assessed with the Conners' Continuous Performance Test. Child behaviour was assessed by parent and teacher ratings on the Child Behaviour Checklist (CBCL) and Teacher Report Form, respectively. The mean (SD) total GWG (kg) was 14.5 (5.9), and 10% of women had a pregravid BMI ≥30 kg/m2 . Prepregnancy obesity (BMI of 30 kg/m2 ) was associated with increased offspring problem behaviours including internalising behaviours (adjusted β 3.3 points, 95% CI 1.7-4.9), externalising behaviours (adjusted β 2.9 points, 95% CI 1.4-4.6), and attention problems (adjusted β 2.3 points, 95% CI 1.1-3.4) on the CBCL, compared with normal weight mothers (BMI of 22 kg/m2 ). There were nonsignificant trends towards increased offspring impulsivity with low GWG among lean mothers (adjusted incidence rate ratio 1.2, 95% CI 0.9-1.5) and high GWG among overweight mothers (adjusted incidence rate ratio 1.7, 95% CI 0.9-2.8), but additional outcomes did not differ by GWG z-score. Results were not meaningfully different after excluding high-substance users. In a low-income and high-risk sample, we observed a small increase in child behaviour problems among children of obese mothers, which could have an impact on child behaviour in the population. Maternal obesity is associated with a small increase in child behaviour problems.

Introduction.

Article AbstractBecause this piece does not have an abstract, we have provided for your benefit the first 3 sentences of the full text.The Focus on Child and Adolescent Mental Health section in this issue of JCP features 2 articles on bipolar disorder: one addresses course of attention-deficit/hyperactivity disorder (ADHD) in youth who have parents with bipolar disorder, and the other evaluates possible precursors of bipolar disorder. This month's section also includes a study examining the skeletal effects of selective serotonin reuptake inhibitors (SSRIs) and second-generation antipsychotics.Offspring of parents with bipolar disorder are at high risk of ADHD in addition to bipolar disorder. Kim and colleagues examined the psychopathology and course of ADHD symptoms in offspring of parents with bipolar disorder compared to offspring of healthy parents or parents with nonbipolar psychopathology (control parents).

Sex-specific and time-dependent effects of prenatal stress on the early behavioral symptoms of ADHD: a longitudinal study in China.

There is increasing evidence that prenatal stressful life events (SLEs) may be a potential risk factor for attention-deficit hyperactivity disorder (ADHD), but the sex-specific and time-dependent effects of prenatal stress on ADHD are less clear. In this prospective longitudinal study, data on prenatal SLEs during different stages of gestation and indicators of buffers against stress, including maternal social support and avoidance coping, were obtained from 1765 pregnant women at 32 weeks of gestation. The behavioral symptoms of ADHD in children aged 48-54 months were evaluated by reports from the parents. There were 226 children (12.8%) above the clinically significant cutoff for ADHD. After adjusting for potential confounders, boys whose mother experienced severe SLEs in the second trimester had a significantly increased risk (OR = 2.41, 95% CI: 1.03-5.66) of developing ADHD symptoms compared with boys whose mothers did not experience severe SLEs at this time. However, no significantly increased risk of ADHD symptoms was observed in girls born to mothers experienced prenatal severe SLEs. Additionally, significant interaction effects of prenatal SLEs, social support and coping style on ADHD symptoms were found in males. Boys whose mothers experienced severe SLEs during the second trimester accompanied by a higher score for avoidance coping (OR = 3.31, 95% CI: 1.13-9.70) or a lower score for social support (OR = 4.39, 95% CI: 1.05-18.31) were likely to be at a higher risk for ADHD symptoms. The epidemiological evidence in this prospective follow-up study suggests that the effect of prenatal SLEs on ADHD symptoms in offspring may depend on the timing of prenatal stress and may vary according to the sex of the offspring.

Parenting Behavior Mediates the Intergenerational Association of Parent and Child Offspring ADHD Symptoms

Although there are likely to be multiple mechanisms underlying parent attention-deficit/hyperactivity disorder (ADHD) symptoms as a key risk factor for offspring ADHD, potential explanatory factors have yet to be reliably identified. Given that parent ADHD symptoms independently predict parenting behavior and child ADHD symptoms, we tested whether individual differences in multiple dimensions of positive and negative parenting behavior (i.e., corporal punishment, inconsistent discipline, positive parenting behavior, observed negative talk, and observed praise) mediated the association between parental and offspring ADHD. We used a prospective design that featured predictors (i.e., parent ADHD symptoms) and mediators (i.e., parenting behavior) that temporally preceded the outcome (i.e., offspring ADHD symptoms). Using a well-characterized sample of 120 children with and without ADHD (ages 5–10 at Wave 1, 7–12 at Wave 2) and their biological parents, we examined multimethod (i.e., observed, self-report) measures of positive and negative parenting behavior as simultaneous mediators of the association of Wave 1 parent and Wave 2 offspring ADHD symptoms. Using a multiple mediation framework, consisting of rigorous bootstrapping procedures and controlling for parent depression, child's baseline ADHD and oppositional defiant disorder, and child's age, corporal punishment significantly and uniquely mediated the association of Wave 1 parent ADHD symptoms and Wave 2 offspring ADHD. We consider the role of parenting behavior in the intergenerational transmission of ADHD as well as implications of these findings for the intervention and prevention of childhood ADHD.

Maternal and Paternal Smoking During Pregnancy and Risk of ADHD Symptoms in Offspring: Testing for Intrauterine Effects

Maternal smoking during pregnancy is associated with attention deficit hyperactivity disorder (ADHD) in offspring. It is assumed by many that this association is causal. Others suggest that observed associations are due to unmeasured genetic factors or other confounding factors. The authors compared risks of maternal smoking during pregnancy with those of paternal smoking during pregnancy. With a causal intrauterine effect, no independent association should be observed between paternal smoking and offspring ADHD. If the association is due to confounding factors, risks of offspring ADHD should be of similar magnitudes regardless of which parent smokes. This hypothesis was tested in 8,324 children from a well-characterized United Kingdom prospective cohort study, the Avon Longitudinal Study of Parents and Children (data from 1991–2000). Associations between offspring ADHD and maternal and paternal smoking during pregnancy were compared using regression analyses. Offspring ADHD symptoms were associated with exposure to both maternal and paternal smoking during pregnancy (mothers: β = 0.25, 95% confidence interval: 0.18, 0.32; fathers: β = 0.21, 95% confidence interval: 0.15, 0.27). When paternal smoking was examined in the absence of maternal smoking, associations remained and did not appear to be due to passive smoking exposure in utero. These findings suggest that associations between maternal smoking during pregnancy and child ADHD may be due to genetic or household-level confounding rather than to causal intrauterine effects.

Maternal adiposity prior to pregnancy is associated with ADHD symptoms in offspring: evidence from three prospective pregnancy cohorts

We examine whether pregnancy weight (pre-pregnancy body mass index (BMI) and/or weight gain) is related to core symptoms of attention deficit hyperactivity disorder (ADHD) in school-age offspring. Follow-up of prospective pregnancy cohorts from Sweden, Denmark and Finland within the Nordic Network on ADHD. Maternal pregnancy and delivery data were collected prospectively. Teachers rated inattention and hyperactivity symptoms in offspring. High scores were defined as at least one core symptom rated as 'severe' and two as 'present' (approximately 10% of children scored in this range). Logistic regression and latent class analyses were used to examine maternal pregnancy weight in relation to children's ADHD core symptoms. Teacher rated 12 556 school-aged children. Gestational weight gain outside of the Institute of Medicine guidelines was not related to ADHD symptoms (below recommendations: odds ratio (OR): 0.96; 95% confidence interval (CI): 0.81, 1.14; above recommendations: OR: 0.98; 95% CI: 0.82, 1.16). To examine various patterns of pre-pregnancy BMI and weight gain, we used latent class analysis and found significant associations between classes that included pre-pregnancy overweight or obesity and a high ADHD symptom score in offspring, ORs ranged between 1.37 (95% CI: 1.07, 1.75) and 1.89 (95% CI: 1.13, 3.15) adjusted for gestational age, birth weight, weight gain, pregnancy smoking, maternal age, maternal education, child gender, family structure and cohort country of origin. Children of women who were both overweight and gained a large amount of weight during gestation had a 2-fold risk of ADHD symptoms (OR: 2.10, 95% CI: 1.19, 3.72) compared to normal-weight women. We show for the first time that pre-pregnancy BMI is associated with ADHD symptoms in children. Our results are of public health significance if the associations are causal and will then add ADHD symptoms in offspring to the list of deleterious outcomes related to overweight and obesity in the prenatal period.

Relationship between antisocial behaviour, attention-deficit hyperactivity disorder and maternal prenatal smoking

There is substantial evidence that maternal smoking during pregnancy is associated with both antisocial behaviour and symptoms of attention-deficit hyperactivity disorder (ADHD) in offspring. However, it is not clear whether maternal smoking during pregnancy is independently associated with antisocial behaviour or whether the association arises because antisocial behaviour and ADHD covary. To examine the relationship between maternal smoking during pregnancy, antisocial behaviour and ADHD in offspring. Questionnaires concerning behaviour and environmental factors were sent to twins from the CaStANET study and data analysed using a number of bivariate structural equation models. Maternal prenatal smoking contributed small but significant amounts to the variance of ADHD and of antisocial behaviour. The best fitting bivariate model was one in which maternal prenatal smoking had a specific influence on each phenotype, independent of the effect on the other phenotype. Both antisocial behaviour and ADHD symptoms in offspring are independently influenced by maternal prenatal smoking during pregnancy.

Maternal smoking during pregnancy and attention deficit hyperactivity disorder symptoms in offspring.

The aim of this study was to examine whether smoking during pregnancy is associated with symptoms of attention deficit hyperactivity disorder (ADHD) in offspring and whether these effects are additional to genetic influences. Children's ADHD symptoms (parent- and teacher-rated), maternal smoking during pregnancy, conduct disorder symptoms, and family adversity were assessed with questionnaires for a population-based sample of twins (1,452 twin pairs 5-16 years of age). Although genetic influences accounted for most of the variance in offspring ADHD, maternal smoking during pregnancy was still found to show a significant environmentally mediated association. Maternal smoking remained a significant influence when other potential confounds were taken into account. Maternal smoking during pregnancy appears to show an association with offspring ADHD symptoms that is additional to the effects of genes and not attributable to shared rater effects, clinical referral biases, or covariation with antisocial behavior.