Abstract
Objectives: This study examined the association between prenatal cocaine exposure and children’s self-regulation at 3 years of child age. In addition to direct effects of prenatal cocaine exposure on children’s self-regulation, we hypothesized there would be indirect associations between cocaine exposure and self-regulation via higher maternal harshness and poor autonomic regulation in infancy. Methods: The sample consisted of 216 mother–infant dyads recruited at delivery from local area hospitals (116 cocaine-exposed, 100 non-exposed). Infant autonomic regulation was measured at 7 months of age during an anger/frustration task, maternal harshness was coded from observations of mother–toddler interactions at 2 years of age, and children’s self-regulation was measured at 3 years of age using several laboratory paradigms. Results: Contrary to hypotheses, there were no direct associations between maternal cocaine use during pregnancy and children’s self-regulation. However, results from testing our conceptual model including the indirect effects via maternal harshness or infant parasympathetic regulation indicated that this model fit the data well, χ2 (23) = 34.36, p > 0.05, Comparative Fit Index = 0.95, RMSEA = 0.05. Cocaine using mothers displayed higher intensity of harshness toward their toddlers during lab interactions across a variety of tasks at 2 years of age (β = 0.23, p < 0.05), and higher intensity of harshness at 2 years was predictive of lower self-regulation at 3 years (β = −0.36, p < 0.01). Maternal cocaine use was also predictive of a non-adaptive increase in respiratory sinus arrhythmia (RSA) from baseline to the negative affect task, but RSA change in infancy was not predictive of self-regulation at 3 years. Conclusion: Results are supportive of animal models indicating higher aggression among cocaine treated dams, and indicate that higher maternal harshness among cocaine using mothers is predictive of child self-regulatory outcomes in the preschool period.
Highlights
Maternal cocaine use remains a significant problem affecting large numbers of mothers and their children (Savitz et al, 2002)
PARTICIPANTS The sample consisted of 216 mother–infant dyads participating in an ongoing longitudinal study of prenatal cocaine exposure (116 cocaine-exposed or CE, 100 not cocaine-exposed or NCE)
Correlational analyses with these demographic variables and child self-regulation indicated no significant associations
Summary
Maternal cocaine use remains a significant problem affecting large numbers of mothers and their children (Savitz et al, 2002). Studies have indicated that prenatal exposure to cocaine is associated with alterations in infant behavioral and physiological regulation. Because cocaine crosses the fetal blood– brain barrier, it has the potential to directly alter neurotransmitter systems in the developing fetal brain. Cocaine is known to inhibit the re-uptake of monoamines at the presynaptic junction, leading to higher concentrations of norepinephrine, serotonin, and dopamine in the synaptic cleft and higher levels of activation in the catecholaminergic systems (Gawin and Ellinwood, 1988; Nassogne et al, 1998). A number of human studies have consistently reported significant associations between prenatal cocaine exposure and some aspects of the regulatory system including both behavioral (Karmel and Gardner, 1996; Bendersky and Lewis, 1998; Mayes et al, 1998)
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