Maternal prenatal cortisol programs the infant hypothalamic-pituitary-adrenal axis.
Jessica L Irwin, Amy L Meyering, Gage Peterson, Laura M Glynn, Curt A Sandman, Laurel M Hicks, Elysia Poggi Davis
Author Information
Jessica L Irwin: Department of Psychology, University of La Verne, La Verne, CA 91750, United States; Department of Psychology, Chapman University, Orange, CA 92866, United States. Electronic address: jirwin2@laverne.edu.
Amy L Meyering: Department of Psychology, University of Denver, Denver, CO 80208, United States.
Gage Peterson: Department of Psychology, Chapman University, Orange, CA 92866, United States.
Laura M Glynn: Department of Psychology, Chapman University, Orange, CA 92866, United States; Department of Psychiatry and Human Behavior, University of California, Irvine, CA 92697, United States.
Curt A Sandman: Department of Psychiatry and Human Behavior, University of California, Irvine, CA 92697, United States.
Laurel M Hicks: Renée Crown Wellness Institute, University of Colorado, Boulder, CO 80302, United States.
Elysia Poggi Davis: Department of Psychology, University of Denver, Denver, CO 80208, United States; Department of Psychiatry and Human Behavior, University of California, Irvine, CA 92697, United States.
One of the key proposed agents of fetal programming is exposure to maternal glucocorticoids. Experimental animal studies provide evidence that prenatal exposure to elevated maternal glucocorticoids has consequences for hypothalamic-pituitary-adrenal (HPA) axis functioning in the offspring. There are very few direct tests of maternal glucocorticoids, such as cortisol, during human pregnancy and associations with infant cortisol reactivity. The current study examined the link between maternal prenatal cortisol trajectories and infant cortisol reactivity to the pain of inoculation in a sample of 152 mother-infant (47.4% girls) pairs. The results from the current study provide insight into fetal programming of the infant HPA axis, demonstrating that elevated prenatal maternal cortisol is associated with a larger infant cortisol response to challenge at both 6 and 12 months of age.
