Maternal Smoking During Pregnancy and Offspring Conduct Problems

Gaysina, Darya; Fergusson, David M.; Leve, Leslie D.; Horwood, L. John; Reiss, David; Shaw, Daniel S.; Elam, Kit K.; Natsuaki, Misaki N.; Neiderhiser, Jenaè M.; Harold, Gordon Thomas

doi:10.1001/jamapsychiatry.2013.127

Cited by 136 publications

(65 citation statements)

References 61 publications

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“…The continued impact of intrauterine tobacco exposure into adolescence confirms other studies that have shown that such exposure has been associated with conduct disorder and behavioral problems in childhood and adolescence in samples without IUCE (Brook, Zhang, Rosenberg, & Brook, 2006; Desrosiers et al, 2013; Gaysina et al, 2013; Rantakallio, et al, 1992). Furthermore, the findings on intrauterine tobacco expose misconceptions about relative impact of intrauterine exposure to legal compared to illegal substances on long term behavioral outcomes.…”

Section: Discussionsupporting

confidence: 85%

Prenatal substance exposure: What predicts behavioral resilience by early adolescence?

Liebschutz¹,

Crooks²,

Rose-Jacobs³

et al. 2015

Psychology of Addictive Behaviors

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Understanding behavioral resilience among at-risk adolescents may guide public policy decisions and future programs. We examined factors predicting behavioral resilience following intrauterine substance exposure (IUSE) in a prospective longitudinal birth-cohort study of 136 early adolescents (age 12.4–15.9) at-risk for poor behavioral outcomes. We defined behavioral resilience as a composite measure of lack of early substance use initiation (before age 14), lack of risky sexual behavior, or lack of delinquency. IUSEs included in this analysis were cocaine (IUCE), tobacco (IUTE), alcohol (IUAE), and marijuana (IUME). We recruited participants from Boston Medical Center as mother-infant dyads between 1990 and 1993. The majority of the sample was African-American/Caribbean (88%) and 49% female. In bivariate analyses, none and lower IUCE level predicted resilience compared to higher IUCE, but this effect was not found in an adjusted model. Instead, strict caregiver supervision (adjusted odds ratio (AOR)=6.02, 95% confidence interval (CI)=1.90–19.00, p=0.002), lower violence exposure (AOR=4.07, 95% CI=1.77–9.38, p<0.001), and absence of intrauterine tobacco exposure (AOR=3.71, 95% CI= 1.28–10.74, p=0.02) predicted behavioral resilience. In conclusion, caregiver supervision in early adolescence, lower violence exposure in childhood, and lack of intrauterine tobacco exposure predict behavioral resilience among a cohort of early adolescents with significant social and environmental risk. Future interventions should work to enhance parental supervision as a way to mitigate the effects of adversity on high-risk groups of adolescents.

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Section: Discussionsupporting

confidence: 85%

Prenatal substance exposure: What predicts behavioral resilience by early adolescence?

Liebschutz¹,

Crooks²,

Rose-Jacobs³

et al. 2015

Psychology of Addictive Behaviors

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“…IVF (Rice et al, 2009; Thapar et al, 2009) and offspring of siblings/twins studies (D’Onofrio et al, 2010; Kuja-Halkola et al, 2010) suggest that SDP does not cause psychopathology; rather, genetic factors that vary between families account for the association between SDP and offspring psychopathology. These findings are consistent with a recent adoption study that suggests that postnatal genetic factors (e.g., the children’s genetic factors influencing the adoptive parents behaviors) do not account for the association between SDP and offspring conduct problems (Gaysina et al, 2013). Family-based quasi-experimental studies, therefore, strongly suggest that most of the existing research on SDP and offspring psychopathology using traditional comparisons of unrelated individuals have overstated the causal influence (D’Onofrio et al, 2013; Jaffee, Strait, & Odgers, 2012; Knopik, 2009), although there remains considerable debate in the field (Slotkin, 2013).…”

Section: Quasi-experimental Studies Of Pregnancy-related Risk Factorssupporting

confidence: 91%

“…This is because the biological mothers provide genetic and prenatal environmental factors, but not the postnatal environment to the children. Thus, the design cannot remove effects of genetic confounding from prenatal environmental influences on children, such as smoking during pregnancy (SDP) (Gaysina, Fergusson, Leve, & et al, 2013). By using a sample of children adopted-at-birth and their genetically unrelated rearing parents the design is, on the other hand, able to control for genetic confounding when examining the association between postnatal environmental factors (e.g., parenting) and child outcomes (Harold et al, 2013).…”

Section: Review Of Family-based Quasi-experimental Designsmentioning

confidence: 99%

Testing the Developmental Origins of Health and Disease Hypothesis for Psychopathology Using Family‐Based, Quasi‐Experimental Designs

D’Onofrio

Class

Lahey

et al. 2014

Child Dev Perspectives

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The Developmental Origin of Health and Disease (DOHaD) hypothesis is a broad theoretical framework that emphasizes how early risk factors have a causal influence on psychopathology. Researchers have raised concerns about the causal interpretation of statistical associations between early risk factors and later psychopathology because most existing studies have been unable to rule out the possibility of environmental and genetic confounding. In this paper we illustrate how family-based quasi-experimental designs can test the DOHaD hypothesis by ruling out alternative hypotheses. We review the logic underlying sibling-comparison, co-twin control, offspring of siblings/twins, adoption, and in vitro fertilization designs. We then present results from studies using these designs focused on broad indices of fetal development (low birth weight and gestational age) and a particular teratogen, smoking during pregnancy. The results provide mixed support for the DOHaD hypothesis for psychopathology, illustrating the critical need to use design features that rule out unmeasured confounding.

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“…Recently, Fergusson et al (2012) reported that the MAOA genotype might act as a general moderator for all kinds of adverse environmental experiences during development, including pre-and perinatal risk factors, early life stress and abnormal educational conditions. In this context, maternal smoking during pregnancy (SDP) is of particular interest as one prenatal risk factor that has often been related to adverse outcomes in the offspring later in life, including conduct problems (Button et al 2005;Gaysina et al 2013;Brion et al 2010;Wakschlag et al 2002) and ADHD (Langley et al 2005;Motlagh et al 2010;Banerjee et al 2007). Concerning the biological mechanisms underlying the association of SDP with externalizing behavior problems in the offspring, several possible explanations have been suggested, including effects of maternal smoking on neurotransmission as well as differentiation and migration of neurons in the fetal brain (Dwyer et al 2009;Slotkin et al 2007;Bublitz and Stroud 2012).…”

Section: Introductionmentioning

confidence: 99%

Interacting effect of MAOA genotype and maternal prenatal smoking on aggressive behavior in young adulthood

et al. 2016

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Findings on the etiology of aggressive behavior have provided evidence for an effect both of genetic factors, such as variation in the monoamine oxidase A (MAOA) gene, and adverse environmental factors. Recent studies have supported the existence of gene × environment interactions, with early experiences playing a key role. In the present study, the effects of prenatal nicotine exposure, MAOA genotype and their interaction on aggressive behavior during young adulthood were examined. In a sample of 272 young adults (129 males, 143 females) from an epidemiological cohort study, smoking during pregnancy was measured with a standardized parent interview at the offspring's age of 3 months. Aggressive behavior was assessed between the ages of 19 and 25 years using the Young Adult Self-Report. DNA was genotyped for the MAOA 5' untranslated region variable number of tandem repeats polymorphism (VNTR). Results revealed a significant interaction between MAOA and smoking during pregnancy, indicating higher levels of aggressive behavior in young adults carrying the MAOA low-expressing genotype who had experienced prenatal nicotine exposure (n = 8, p = .025). In contrast, in carriers of the MAOA high-expressing genotype, maternal smoking during pregnancy had no effect on aggressive behavior during young adulthood (n = 20, p = .145). This study extends earlier findings demonstrating an interaction between MAOA genotype and prenatal nicotine exposure on aggressive behavior into young adulthood. The results point to the long-term adverse effects of smoking during pregnancy on the offspring's mental health, possibly underlining the importance of smoking cessation during pregnancy. According to the nature of the study (particularly sample size and power), analyses are exploratory and results need to be interpreted cautiously.

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Maternal Smoking During Pregnancy and Offspring Conduct Problems

Cited by 136 publications

References 61 publications

Prenatal substance exposure: What predicts behavioral resilience by early adolescence?

Prenatal substance exposure: What predicts behavioral resilience by early adolescence?

Testing the Developmental Origins of Health and Disease Hypothesis for Psychopathology Using Family‐Based, Quasi‐Experimental Designs

Interacting effect of MAOA genotype and maternal prenatal smoking on aggressive behavior in young adulthood

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