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Prenatal Drug Exposure and Drug-Abusing Environments
Research Findings from September, 2001 Director's Report
This section lists selected summaries from NIDA funded research projects that investigate the consequences of prenatal drug exposure. The summaries provided were selected from recent issues of the Director's Report to the National Advisory Council on Drug Abuse. For a more comprehensive listing of NIDA funded projects see the Director's Report.
Prenatal Exposure to Methamphetamine Increases the Male Offspring's Vulnerability, When Adults, to Methamphetamine's Neurotoxicity, in Mice
The use of club drugs, such as methamphetamine, by women of childbearing age has become a public health concern. Dr. Alfred Heller and his colleagues at the University of Chicago and Illinois Institute of Technology, modeled this situation in mice. They administered a neurotoxic dose of methamphetamine to pregnant mice during gestational days 7 to 18. Fetal exposure alone did not produce neurotoxicity. The researchers also gave methamphetamine to the offspring after they had become young adults (11 weeks of age), at minimally neurotoxic doses. They observed an enhanced neurotoxicity in the male offspring when they were injected with methamphetamine as adults. The neurotoxicity was evidenced by greater methamphetamine-induced lasting reductions of dopamine and its metabolites in the striatum and of dopamine in the ventral brainstem. Some effects of prenatal methamphetamine exposure were observed in female offspring, but these were much less than those seen in males. The ability of methamphetamine to induce neurotoxicity is associated, in part, with its ability to raise body temperature (hyperthermia). These doses of methamphetamine did not raise the body temperature of the adult female offspring, while the methamphetamine injections did raise the body temperature of the adult males. However, the hyperthermic response to methamphetamine was the same in the adult males whether or not they had been exposed to methamphetamine in utero. These findings raise the concern that male methamphetamine abusers may have an enhanced risk for the neurotoxic effects of the drug if they were previously exposed to it in utero. Furthermore, the mother's methamphetamine abuse may predispose her male offspring to other neuropathological disorders, such as Parkinson's disease. Heller, A., Bubula, N., Lew, R., Heller, B., and Won, L. Gender-Dependent Enhanced Adult Neurotoxic Response to Methamphetamine Following Fetal Exposure to the Drug. J. Pharmacol. Exp. Ther., 298 (2), pp. 1-11,
Developing Language Skills of Cocaine-Exposed Infants
In a prospective, longitudinal, quasi-experimental, matched cohort design, Singer et al. assessed the association between level of fetal cocaine exposure and auditory comprehension skills underlying speech-language skills at 1 year corrected age. Maternal self-report and meconium assay were used to define 3 cocaine exposure groups, including nonexposure (n = 131), heavy exposure (n = 66), and light exposure (n = 68). After controlling for drug, medical, and environmental factors, several differences among the exposure groups emerged indicating an association between amount of cocaine exposure and poor infant outcomes. Infants in the heavy exposure group received lower total language scores than infants in the light exposure and nonexposure groups. And, in comparison to infants in the nonexposure group, infants in the heavy exposure group received lower auditory comprehension scores and were more likely to be classified as mildly delayed by total language scores. These findings document significant behavioral teratogenic effects of heavy prenatal exposure to cocaine on developmental precursors of speech-language development. Singer, L.T., Arendt, R., Minnes, S, Salvator, A., Siegel, A.C., and Lewis, B.A. Developing Language Skills of Cocaine-Exposed Infants. Pediatrics, 107, pp. 1057-1064, 2001.
The Search for Congenital Malformations in Newborns With Fetal Cocaine Exposure
Using a prospective longitudinal design, Behnke et al. assessed the association between prenatal cocaine exposure and congenital anomalies in a sample of 272 infants of 154 prenatally identified crack/cocaine users and 154 nonusing matched controls (perinatal deaths and infants not examined within 7 days of birth were not included). Mothers' cocaine use during pregnancy was measured using repeated in-depth histories and urine screens. Measured infant outcomes included 16 anthropometric measurements and a checklist of 180 physical features. In comparison to nonexposed infants, exposed infants were more likely to be born prematurely and to have lower mean birthweights, lengths, and head circumferences. Exposed and nonexposed infants did not differ on remaining anthropometric measurements. Timing and amount of cocaine exposure were not associated with infant outcomes, nor was a consistent pattern of abnormalities associated with prenatal exposure identified. Behnke, M., Eyler, F.D., Garvan, C.W., and Wobie, K. The Search for Congenital Malformations in Newborns with Fetal Cocaine Exposure. Pediatrics, 107, e74, 2001.
Genetic and Environmental Influences on Antisocial Personality Disorder in Adoptees
This investigation used data from the Iowa Adoption studies to examine the biological and environmental influences and clinical correlates of adult antisocial behavior, a well-established risk factor for drug abuse. We defined three subgroups: antisocials with conduct disorder (n = 30), antisocials without conduct disorder (n = 25), and controls (n = 142). Results demonstrate that having an antisocial biological parent was a specific risk factor for ASPD. In contrast, fetal alcohol exposure, male gender, and adverse environmental factors were associated with the adult antisocial syndrome, regardless of a history of conduct disorder in childhood. The two antisocial groups were similar with respect to clinical characteristics including sociopathy scores, comoribid disorders, and most individual symptoms. Because the phenotypic expression of the potential genetic-risk for ASPD appears to be manifest before adulthood, findings suggest that a history of conduct disorder may be more relevant to the etiological than clinical understanding of adult antisocial behavior. Langbehn, D.R. and Cadoret, R.J. The Adult Antisocial Syndrome with and without Antecedent Conduct Disorder: Comparisons from an Adoption Study. Comprehensive Psychiatry, 42(4), pp. 272-282, 2001.
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