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Prenatal risk including substance exposure has been increasingly linked to differences in autonomic functioning during childhood. To date, these studies have primarily utilized a variable-centered approach in which group differences in individual autonomic nervous system (ANS) variables are examined. Often this approach fails to capture that sympathetic (SNS) and parasympathetic (PNS) components of ANS are not independent traits but rather function as part of an integrated system with an individual. Several theoretical frameworks, including the recent Adaptive Calibration Model (Del Giudice et al., 2011) propose a priori patterns of multisystem functioning. Thus, using a person-centered latent profile analysis (LPA) approach, this investigation sought to identify potential theoretically-based ANS regulatory profiles in samples of polysubstance-exposed children and to explore whether these profiles might be associated with a range of demographic and environmental factors.
One sample consisted of 216 mother-child dyads (110 girls) and the second sample consisted of 298 mother-child dyads (146 girls) recruited into two individual, ongoing prospective longitudinal studies of maternal pregnancy substance use and child development. Postnatal assessments occurred at several time points during infancy, early childhood and kindergarten. Demographics and measures of caregiving environmental risk were collected at each assessment. At the kindergarten assessment, both studies collected PNS (respiratory sinus arrhythmia; RSA) and SNS (pre-ejection period [PEP] or skin conductance levels [SCL] measures during a 3-minute baseline period and during two different frustration paradigms taken from the Laboratory Temperament Assessment Battery (LABTAB; Goldsmith et al., 2001).
For each of the two samples, latent profile analysis (LPA) revealed four distinct patterns of responses to the PNS and SNS measures (See Figures 1&2). Some class differences in demographics/environmental risk emerged. In the sample of cocaine/polysubstance-exposed children, children who experienced cumulative caregiving instability from 7- to 60-months of age were more likely to fall into the non-reactive class (r = .29, p < .001) and less likely to be in the moderate SNS-activation class (r = -.23, p = .004) at 60 months. In the sample of cigarette-exposed children, Black (vs. non-Black) children were more likely to be in the non-reactive class (r = .24, p = .001) and less likely to be in the moderate SNS-activation class (r = -.30, p < .001).
These results support the presence of distinctive autonomic profiles among substance-exposed children. Specifically, both samples included profiles of non-reactors, children who show very little PNS or SNS activation during environmental challenge. Both samples also include children with predominantly moderate SNS-activation and a group with low to moderate PNS-activation. However, the sample of cocaine-exposed children also included a group of children with high SNS-activation while the cigarette-exposed sample had a group with high PNS-activation. These findings also highlight the fact that variations in prenatal, demographic and environmental risk have unique effects on the development of regulatory processes. Results will be discussed in terms of their theoretical and practical implications.