Johanna R Jahnke1, Enrique Terán2, Francisca Murgueitio3, Holger Cabrera4, Amanda L Thompson5. 1. Department of Anthropology, 301 Alumni Building CB #3115, University of North Carolina at Chapel Hill, Chapel Hill, 27599, USA; Carolina Population Center, 123 West Franklin Street, Chapel Hill, NC, 27516, USA. Electronic address: hjahnke@live.unc.edu. 2. Colegio de Ciencias de la Salud, Universidad San Francisco de Quito. Hospital de los Valles, Ed. Especialidades Médicas, PB, Av. Interoceánica Km. 12 ½; y Av. Florencia, Casilla Postal 17-1200-841, Quito, Ecuador; Galapagos Science Center. Avenida Alsacio Northia, Puerto Baquerizo Moreno, Ecuador San Cristobal, Galapagos Archipelago, Ecuador. Electronic address: eteran@usfq.edu.ec. 3. Hospital Oskar Jandl, Ministerio de Salud Publica. San Cristóbal, Galápagos Archipiélago, Ecuador. Electronic address: maria.murgueitio@hoj.gob.ec. 4. Hospital Oskar Jandl, Ministerio de Salud Publica. San Cristóbal, Galápagos Archipiélago, Ecuador. Electronic address: holger.cabrera@hoj.gob.ec. 5. Department of Anthropology, 301 Alumni Building CB #3115, University of North Carolina at Chapel Hill, Chapel Hill, 27599, USA; Carolina Population Center, 123 West Franklin Street, Chapel Hill, NC, 27516, USA; Department of Nutrition, Gillings School of Global Public Health, University of North Carolina at Chapel Hill 170 Rosenau Hall, CB #7400, 135 Dauer Drive, Chapel Hill, NC, 27599, USA. Electronic address: althomps@email.unc.edu.
Abstract
INTRODUCTION: Prenatal stress is known to influence fetal hypothalamic-pituitary-adrenal axis (HPA axis) development. Placental 11β-hydroxysteroid dehydrogenase type 2 (HSD11B2) is a central gene in this pathway, but little is known about what influences its functioning. We assess how maternal distress influences HSD11B2 functioning, and how HSD11B2 in turn, is associated with infant HPA axis development. METHODS: Data come from 24 mother-infant dyads on the Galápagos Islands. Using adjusted linear regression models, we assess the effects of maternal psychosocial (stress and depressive symptoms, measured by the Perceived Stress Scale and the Patient Health Questionnaire-8, respectively) and physiological (HPA axis dysregulation) distress during pregnancy on HSD11B2 methylation and expression and then test how these HSD11B2 measures influence infant HPA axis development. RESULTS: Maternal HPA axis dysregulation during pregnancy is associated with lower placental HSD11B2 expression, which is associated with an exaggerated cortisol reactivity in infants. Sex-specific analyses revealed that maternal depressive symptoms may influence the functioning of placental HSD11B2 differently in girls (n = 11, 46%) than in boys (n = 13, 54%), though the sample size was small. DISCUSSION: These results support a disrupted adaptive framework, in which the ability to upregulate HSD11B2 expression in response to acute stress diminishes as maternal stress becomes chronic. In this model, chronic stress may exhaust the protective mechanism of HSD11B2, leaving the infant vulnerable to high levels of maternal cortisol, which could injure the fetal HPA axis and disrupt long-term neurobehavioral and metabolic development. While larger studies will be needed to confirm these findings, this study offers exploratory results on the effects of maternal distress on both HSD11B2 methylation and expression and the effect of HSD11B2 on offspring HPA axis development.
INTRODUCTION: Prenatal stress is known to influence fetal hypothalamic-pituitary-adrenal axis (HPA axis) development. Placental 11β-hydroxysteroid dehydrogenase type 2 (HSD11B2) is a central gene in this pathway, but little is known about what influences its functioning. We assess how maternal distress influences HSD11B2 functioning, and how HSD11B2 in turn, is associated with infant HPA axis development. METHODS: Data come from 24 mother-infant dyads on the Galápagos Islands. Using adjusted linear regression models, we assess the effects of maternal psychosocial (stress and depressive symptoms, measured by the Perceived Stress Scale and the Patient Health Questionnaire-8, respectively) and physiological (HPA axis dysregulation) distress during pregnancy on HSD11B2 methylation and expression and then test how these HSD11B2 measures influence infant HPA axis development. RESULTS: Maternal HPA axis dysregulation during pregnancy is associated with lower placental HSD11B2 expression, which is associated with an exaggerated cortisol reactivity in infants. Sex-specific analyses revealed that maternal depressive symptoms may influence the functioning of placental HSD11B2 differently in girls (n = 11, 46%) than in boys (n = 13, 54%), though the sample size was small. DISCUSSION: These results support a disrupted adaptive framework, in which the ability to upregulate HSD11B2 expression in response to acute stress diminishes as maternal stress becomes chronic. In this model, chronic stress may exhaust the protective mechanism of HSD11B2, leaving the infant vulnerable to high levels of maternal cortisol, which could injure the fetal HPA axis and disrupt long-term neurobehavioral and metabolic development. While larger studies will be needed to confirm these findings, this study offers exploratory results on the effects of maternal distress on both HSD11B2 methylation and expression and the effect of HSD11B2 on offspring HPA axis development.
Authors: Laura R Stroud; George D Papandonatos; Stephanie H Parade; Amy L Salisbury; Maureen G Phipps; Barry M Lester; James F Padbury; Carmen J Marsit Journal: Psychosom Med Date: 2016 Nov/Dec Impact factor: 4.312
Authors: Sam Schoenmakers; E J Joanne Verweij; Roseriet Beijers; Hilmar H Bijma; Jasper V Been; Régine P M Steegers-Theunissen; Marion P G Koopmans; Irwin K M Reiss; Eric A P Steegers Journal: Int J Environ Res Public Health Date: 2022-04-13 Impact factor: 4.614