Prenatal Cocaine Exposure and Infant Cortisol Reactivity

Authors


  • The authors thank parents and infants who participated in this study and the research staff who were responsible for conducting numerous assessments with these families. Special thanks to Drs. Pamela Schuetze, Claire Coles, and Phillip S. Zeskind for their collaboration on the larger study; to Drs. Amol Lele and Luther Robinson for collaboration on data collection at Women of Children’s Hospital of Buffalo; and to Dr. Michael Ray for his collaboration on data collection at Sisters of Charity Hospital of Buffalo. This study was made possible by a grant from National Institute on Drug Abuse (1R01DA013190). In the interest of full disclosure, Dr. Granger is president and founder of Salimetrics, LLC (State College, PA).

concerning this article should be addressed to Rina D. Eiden, 1021 Main Street, Buffalo, NY 14203. Electronic mail may be sent to eiden@ria.buffalo.edu.

Abstract

This study examined the effects of prenatal cocaine exposure on infant hypothalamic–pituitary–adrenal axis activity and reactivity at 7 months of infant age. Participants were 168 caregiver–infant dyads (87 cocaine exposed, 81 not cocaine exposed; 47% boys). Maternal behavior, caregiving instability, and infant growth and behavior were assessed, and children’s saliva was sampled before, during, and after standardized procedures designed to elicit emotional arousal. Results revealed cocaine-exposed infants had a high amplitude trajectory of cortisol reactivity compared to non-cocaine-exposed infants. Infant gender and caregiving instability moderated this association. The findings support a dual hazard vulnerability model and have implications for evolutionary-developmental theories of individual differences in biological sensitivity to context.

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