The association between prenatal cocaine exposure and physiological regulation at 13 months of age

Prenatal exposure to cocaine (PCE) has been linked to nonoptimal developmental outcomes including an increased risk of dysregulation during infancy and childhood (Coles, Platzman, Smith, James, & Falek, 1992; Karmel & Gardner, 1996; Mayes & Bornstein, 1995). One particularly useful biological measure of regulatory processes is respiratory sinus arrhythmia (RSA), which Porges terms vagal tone (Vna; Porges & Byrne, 1992). RSA is a measure of the variability in heart rate (HR) that occurs at the frequency of respiration and is believed to index the parasympathetic influence of heart rate variability (HRV) via the vagus nerve. Two commonly used indices of physiological regulation (Porges, 1996) include baseline RSA (BRSA) and changes in RSA during environmental demands (RSA regulation; Bornstein & Suess, 2000; Calkins, 1997). BRSA is a measure of the infant’s ability to maintain physiological homeostasis during periods of minimal external stimulation. During challenges to homeostasis as a result of exogenous stimulation, the myelinated vagal system optimally responds by functioning as a brake (Porges, Doussard-Roosevelt, Portales, & Greenspan, 1996) and decreasing RSA (suppression). RSA suppression during periods of environmental challenge is believed to reflect the infant’s ability to appropriately engage or disengage with the environment (Bornstein & Suess, 2000; Porges, 1996). Thus, the measurement of change in RSA from baseline to challenging situations is an important concurrent and predictive index of parasympathetic regulation in infants. The majority of studies examining parasympathetic regulation as a function of PCE have focused on neonates and findings have been somewhat mixed. Some studies suggest increased parasympathetic activity during rest among CE neonates (Regalado, Schechtman, Khoo, & Bean, 2001; Silvestri, Long, Weese-Mayer, & Barkov, 1991), while others have not found any effects of PCE on BRSA (Mehta et al., 1993), per-haps due to lower sample sizes. Beyond the neonatal period, baseline indices of RSA are not as indicative of an infant’s ability to modulate arousal (DiPietro, Porges, & Uhly, 1992). However, few studies have examined changes in physiological regulation in response to environmental challenge among CE infants. One exception is findings from the sample in the present study at 7 months of age indicating that CE infants did not have a significant RSA suppression during a task designed to elicit NA at 7 months although the NE infants did show the expected RSA suppression (Schuetze, Eiden, & Coles, 2007). It is unclear if this difference persists into later infancy. Thus, the first goal of this study was to examine the association between PCE and physiological regulation during environmental stimulation at 13 months of age. We hypothesized that CE infants would have a lower BRSA, reflecting a less optimal capacity to react appropriately to environmental stimulation, and a reduced RSA suppression during environmental challenge, indicating poorer physiological regulation. Viewing developmental trajectories from a developmental psychopathology framework suggests that there may be multiple pathways to risk among biologically vulnerable children (Luthar & Zelazo, 2003). One such pathway for CE infants may be through higher maternal depression/anxiety (MDA). Numerous studies have found that mothers who used cocaine during pregnancy reported higher levels of depression and anxiety (Singer et al., 1995; Woods, Eyler, Behnke, & Conlon, 1993). There is a large literature highlighting the predictive role of MDA for numerous developmental outcomes, including regulation (Davis et al., 2007; McGrath, Records, & Rice, 2008). Infants of depressed mothers have elevated cortisol and lower vagal tone reflecting autonomic dysregulation (Feldman & Eidelman, 2007). Thus, MDA may be one pathway explaining the potential association between PCE and dysregulation among exposed infants. Consequently, another goal of the present study was to examine if MDA mediates or moderates the association between PCE and infant regulation. For moderation, we hypothesized that the association between CE and regulation would be stronger under conditions of increased MDA. Evidence is also accumulating that suggests gender may moderate the association between PCE and developmental outcome. Studies have consistently found that boys are more vulnerable to a range of developmental problems (Gualitieri & Hicks, 1985) including externalizing behavior problems (Campbell, Shaw, & Gilliom, 2000). Gender differences seem particularly pronounced among at-risk infants (e.g., Hay, 1997; Weinberg, Tronick, Cohn, & Olson, 1999) including CE infants (Bendersky et al., 2006; Moe & Slining, 2001). Consequently, another goal of the present study was to determine if gender moderated the association between CE and physiological regulation. We hypothesized that the association between CE and regulation would be stronger for boys. Finally, it is important to note that cocaine is a polydrug issue. The majority of women using cocaine also use alcohol, cigarettes, and marijuana. Alcohol and cigarettes have been known to have similar effects on infant regulation (e.g., Fried & Makin, 1987; Schuetze & Eiden, 2006). Thus, the associations between CE and infant regulation can only be examined in the context of associations with other substance use. Thus, we considered the possible impact of prenatal exposure to other substances in all analyses.