Maternal Smoking During Pregnancy and the Risk of Conduct Disorder in Boys

Wakschlag, Lauren S.; Lahey, Benjamin B.; Loeber, Rolf; Green, Stephanie M.; Gordon, Rachel A.; Leventhal, Bennett L.

doi:10.1001/archpsyc.1997.01830190098010

Cited by 289 publications

(210 citation statements)

References 41 publications

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“…These results are consistent with previous work with prenatal nicotine treatment, which showed male-female differences in neurochemical and behavioral outcomes and in the synthesis of sex steroids (Lichtensteiger and Schlumpf, 1985;Pauly et al, 2004;Sarasin et al, 2003;Segarra and Strand, 1989;Tizabi et al, 1997). These have distinct parallels in the effects of maternal smoking during pregnancy on behavior, which is similarly gender-selective (Fergusson et al, 1998;Wakschlag and Hans, 2002;Wakschlag et al, 1997). Adolescent nicotine administration in animal models also shows distinct sex differences, both in the present study and in previous work from our and other laboratories (Faraday et al, 2001;Klein et al, 2004;Slotkin, 2002;Slotkin et al, 2002;Xu et al, 2002Xu et al, , 2003.…”

Section: Effects Of Prenatal Nicotine Exposure On the Response To Nicsupporting

confidence: 92%

Prenatal Nicotine Exposure Alters the Responses to Subsequent Nicotine Administration and Withdrawal in Adolescence: Serotonin Receptors and Cell Signaling

Slotkin

Tate

Cousins

et al. 2005

Neuropsychopharmacol

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Offspring of women who smoke during pregnancy are themselves more likely to take up smoking in adolescence, effects that are associated with a high rate of depression and increased sensitivity to withdrawal symptoms. To evaluate the biological basis for this relationship, we assessed effects on serotonin (5-hydroxytryptamine, 5HT) receptors and 5HT-mediated cellular responses in rats exposed to nicotine throughout prenatal development and then given nicotine in adolescence (postnatal days PN30-47.5), using regimens that reproduce plasma nicotine levels found in smokers. Evaluations were then made during the period of adolescent nicotine treatment and for up to one month after the end of treatment. Prenatal nicotine exposure, which elicits damage to 5HT projections in the cerebral cortex and striatum, produced sex-selective changes in the expression of 5HT 1A and 5HT 2 receptors, along with induction of adenylyl cyclase (AC), leading to sensitization of heterologous inputs operating through this signaling pathway. Superimposed on these effects, the AC response to 5HT was shifted toward inhibition. By itself, adolescent nicotine administration, which damages the same pathways, produced similar effects on receptors and the 5HT-mediated response, but a smaller overall induction of AC. Animals exposed to prenatal nicotine showed a reduced response to nicotine administered in adolescence, results in keeping with earlier findings of persistent desensitization. Our results indicate that prenatal nicotine exposure alters parameters of 5HT synaptic communication lasting into adolescence and changes the response to nicotine administration and withdrawal in adolescence, actions which may contribute to a subpopulation especially vulnerable to nicotine dependence.

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Section: Effects Of Prenatal Nicotine Exposure On the Response To Nicsupporting

confidence: 92%

Prenatal Nicotine Exposure Alters the Responses to Subsequent Nicotine Administration and Withdrawal in Adolescence: Serotonin Receptors and Cell Signaling

Slotkin

Tate

Cousins

et al. 2005

Neuropsychopharmacol

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“…with police obtained by city police records (Gibson, Piquero, & Tibbets, 2000), Oppositional Defiant Disorder (Wakschlag & Keenan, 2001), Conduct Disorder (Fergusson, Woodward, & Horwood, 1998;Wakschlag & Hans, 2002;Wakschlag & Keenan, 2001;Wakschlag et al, 1997;Weissman, Warner, Wickramaratne, & Kandel, 1999) and Attention-Deficit/ Hyperactivity Disorder (Mick, Biederman, Faraone, Sayer, & Kleinman, 2002;Rodriguez & Bohlin, 2005). …”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

Smoking during pregnancy and offspring externalizing problems: An exploration of genetic and environmental confounds

et al. 2008

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Previous studies have documented that smoking during pregnancy (SDP) is associated with offspring externalizing problems, even when measured covariates were used to control for possible confounds. However, the association may be due to non-measured environmental and genetic factors that increase risk for offspring externalizing problems. The current project used the National Longitudinal Survey of Youth and their children, ages 4-10 years, to explore the relations between SDP and offspring conduct problems (CP), oppositional-defiant problems (ODP), and attention deficit hyperactivity problems (ADHP) using methodological and statistical controls for confounds. When offspring were compared to their own siblings who differed in their exposure to prenatal nicotine, there was no effect of SDP on offspring CP and ODP. This suggests that SDP does not have a causal effect on offspring CP and ODP. There was a small association between SDP and ADHP, consistent with a causal effect of SDP, but the magnitude of the association was greatly reduced by methodological and statistical controls. Genetically informed analyses suggest that unmeasured environmental variables influencing both SDP and offspring externalizing behaviors account for the previously observed associations. That is, the current analyses imply that important unidentified environmental factors account for the association between SDP and offspring externalizing problems, not teratogenic effects of SDP. Keywordssmoking during pregnancy; conduct problems; externalizing problems; ADHD; children of twins; causation Smoking during pregnancy (SDP) has been consistently linked with externalizing problems in offspring, particularly in males (reviews in Cnattingius, 2004;Huizink & Mulder, 2005;Wakschlag & Hans, 2002;Wakschlag, Pickett, Cook, Benowitz, & Leventhal, 2002). SDP has been associated with parent-reported conduct problems (Ernst, 2001), arrest history from national crime registries (Brennan, Grekin, & Mednick, 1999;Rasanen et al., 1999), contact 2 All correspondence should be sent to: Brian D'Onofrio, PhD, Department of Psychological and Brain Sciences, Indiana University, 1101 E. 10th St., Bloomington, IN 47405, bmdonofr@indiana.edu. NIH Public Access Author ManuscriptDev Psychopathol. Author manuscript; available in PMC 2013 August 08. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscriptwith police obtained by city police records (Gibson, Piquero, & Tibbets, 2000), Oppositional Defiant Disorder (Wakschlag & Keenan, 2001), Conduct Disorder (Fergusson, Woodward, & Horwood, 1998;Wakschlag & Hans, 2002;Wakschlag & Keenan, 2001;Wakschlag et al., 1997;Weissman, Warner, Wickramaratne, & Kandel, 1999) and Attention-Deficit/ Hyperactivity Disorder (Mick, Biederman, Faraone, Sayer, & Kleinman, 2002;Rodriguez & Bohlin, 2005).Reviews of the literature note that the association is consistent with a causal connection because the association is specific to externalizing problems, has been found across diverse samples and measures, demonstr...

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“…Furthermore, a recent study in adolescent smokers described deficits in visuospatial memory that was greater in individuals exposed to maternal cigarette smoking prenatally, as compared with nonexposed adolescents (Jacobsen et al, 2006). Several studies also revealed an increased incidence of externalizing disorders in general (Breslau and Chilcoat, 2000), and attention-deficit hyperactivity (Milberger et al, 1998) and conduct (Wakschlag et al, 1997;Weissman et al, 1999) disorders in particular. Some studies also observed an association between PEMCS and criminal behavior in adulthood (Brennan et al, 1999;Räsänen et al, 1999), and higher rates of aggression in children and adults (Orlebeke et al, 1999;Räsänen et al, 1999).…”

Section: Introductionmentioning

confidence: 98%

Prenatal Exposure to Maternal Cigarette Smoking and the Adolescent Cerebral Cortex

Toro

Leonard

Lerner

et al. 2007

Neuropsychopharmacol

131

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Smoking during pregnancy is associated with long-term consequences on offspring behavior. We measured thickness of the cerebral cortex using magnetic resonance images obtained in 155 adolescents exposed in utero to maternal smoking and compared them with 159 non-exposed subjects matched by maternal education. Orbitofrontal, middle frontal, and parahippocampal cortices were thinner in exposed, as compared with non-exposed, individuals; these differences were more pronounced in female adolescents. In exposed females, the thickness of the orbitofrontal cortex correlated negatively with a self-rated assessment of caring, one of the components of a model of positive youth development. These findings provide evidence of the long-term impact of prenatal environment on a neural substrate of cognition and social behavior.

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Maternal Smoking During Pregnancy and the Risk of Conduct Disorder in Boys

Cited by 289 publications

References 41 publications

Prenatal Nicotine Exposure Alters the Responses to Subsequent Nicotine Administration and Withdrawal in Adolescence: Serotonin Receptors and Cell Signaling

Prenatal Nicotine Exposure Alters the Responses to Subsequent Nicotine Administration and Withdrawal in Adolescence: Serotonin Receptors and Cell Signaling

Smoking during pregnancy and offspring externalizing problems: An exploration of genetic and environmental confounds

Prenatal Exposure to Maternal Cigarette Smoking and the Adolescent Cerebral Cortex

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