To examine stress reactivity in a sample of adolescents with prenatal drug exposure (PDE) by examining the consequences of PDE on stress-related adrenocortical reactivity, behavioral problems, and drug experimentation during adolescence.
Participants (76 PDE, 61 non-drug exposed [NE]; 99% African-American; 50% male; mean age = 14.17 yr, SD = 1.17) provided a urine sample, completed a drug use questionnaire, and provided saliva samples (later assayed for cortisol) before and after a mild laboratory stress task. Caregivers completed the Behavior Assessment System for Children, Second Edition (BASC II) and reported their relationship to the adolescent.
The NE group was more likely to exhibit task-related cortisol reactivity compared to the PDE group. Overall behavior problems and drug experimentation were comparable across groups with no differences between PDE and NE groups. In unadjusted mediation analyses, cortisol reactivity mediated the association between PDE and BASC II aggression scores (95% bootstrap confidence interval [CI], 0.04–4.28), externalizing problems scores (95% bootstrap CI, 0.03–4.50), and drug experimentation (95% bootstrap CI, 0.001–0.54). The associations remain with the inclusion of gender as a covariate but not when age is included.
Findings support and expand current research in cortisol reactivity and PDE by demonstrating that cortisol reactivity attenuates the association between PDE and behavioral problems (aggression) and drug experimentation. If replicated, PDE may have long-lasting effects on stress-sensitive physiological mechanisms associated with behavioral problems (aggression) and drug experimentation in adolescence.
*Department of Pediatrics, University of Maryland School of Medicine, Baltimore, MD;
†Institute for Interdisciplinary Salivary Bioscience Research, University of California at Irvine, Irvine, CA;
‡Department of Acute and Chronic Care, Johns Hopkins University School of Nursing, Baltimore, MD;
§Department of Population, Family and Reproductive Health, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD;
‖Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD;
¶Salivary Bioscience Laboratory and Department of Psychology, University of Nebraska, Lincoln, NE.
Address for reprints: Maureen M. Black, PhD, Department of Pediatrics, University of Maryland School of Medicine, 737 W. Lombard St., Suite 161, Baltimore, MD 21201; e-mail: email@example.com.
This study was supported by the National Institute on Drug Abuse (R01-DA07432, R01-DA021059, and F32DA036274) and the National Institute of Diabetes and Digestive and Kidney Diseases' Summer Program in Obesity, Diabetes, and Nutrition Research Training (SPORT) program (T35DK095737).
Disclosure: D.A. Granger is founder and Chief Scientific and Strategy Advisor at Salimetrics LLC and SalivaBio LLC (Carlsbad, CA), and these relationships are managed by the policies of the committees on conflict of interest at the Johns Hopkins University School of Medicine and the University of California at Irvine. The remaining authors declare no conflict of interest.
Received June 30, 2015
Accepted June 11, 2016