Ashley K Hagaman1, Victoria Baranov2, Esther Chung3, Katherine LeMasters3, Nafeesa Andrabi4, Lisa M Bates5, Atif Rahman6, Siham Sikander7, Elizabeth Turner8, Joanna Maselko3. 1. Department of Social and Behavioral Science, Yale School of Public Health, Yale University, New Havern, CT, USA; Carolina Population Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. Electronic address: Ashley.Hagaman@yale.edu. 2. Department of Economics, University of Melbourne, Melbourne, Australia. 3. Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; Carolina Population Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. 4. Department of Sociology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; Carolina Population Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. 5. Mailman School of Public Health, Columbia University, New York, NY, USA. 6. Department of Psychological Sciences, University of Liverpool, Liverpool, UK; Human Development Research Foundation, Islamabad, Pakistan. 7. Human Development Research Foundation, Islamabad, Pakistan; Health Services Academy, Islamabad, Pakistan. 8. Department of Biostatistics and Bioinformatics, Duke University, Durham, NC, USA; Duke Global Health Institute, Duke University, Durham, NC, USA.
Abstract
BACKGROUND: Each year, almost 35% of children are exposed to maternal depression and more grow up in persistent poverty, increasing the risk for stress-related disease and other socio-developmental deficits later in life. These impacts are likely related to chronic stress via the hypothalamic-pituitary-adrenal (HPA) axis. However, there is little evidence relating early windows of child HPA axis activity to multiple exposures. METHODS: We investigated chronic measures of hair-derived HPA axis hormones (cortisol and dehydroepiandrosterone (DHEA)) in 104 one-year old infants from rural Pakistan and longitudinal measures of maternal depression, intimate partner violence (IPV), socio-economic status (SES), and the home environment. RESULTS: Estimates from adjusted linear mixed effects models did not reveal consistent significant associations between infant cortisol and maternal depression or home adversities. By contrast, infants exposed to maternal depression during pregnancy had lower DHEA levels (ß= -0.18 95% confidence interval [CI]: -0.34, -0.02) as did those whose mothers experienced multiple types of IPV (ß=-4.14 95% CI: -7.42, -0.79) within one year postpartum. Higher SES had a significant positive association with infant DHEA levels (ß= 0.77 95% CI: 0.08, 1.47). Depression severity and chronicity at one year postpartum had near significant associations with infant DHEA. Measures of home environment had no observable impacts on infant HPA axis activity. LIMITATIONS: Limitations include the modest sample size and aggregation of hair samples for analysis. CONCLUSION: Results point to possible early HPA axis dysregulation driven by changes in DHEA activity, but not cortisol at one year of age. Findings contribute to growing research examining intergenerational transmissions of maternal depression, IPV, and household environment on infant stress-response systems.
BACKGROUND: Each year, almost 35% of children are exposed to maternal depression and more grow up in persistent poverty, increasing the risk for stress-related disease and other socio-developmental deficits later in life. These impacts are likely related to chronic stress via the hypothalamic-pituitary-adrenal (HPA) axis. However, there is little evidence relating early windows of child HPA axis activity to multiple exposures. METHODS: We investigated chronic measures of hair-derived HPA axis hormones (cortisol and dehydroepiandrosterone (DHEA)) in 104 one-year old infants from rural Pakistan and longitudinal measures of maternal depression, intimate partner violence (IPV), socio-economic status (SES), and the home environment. RESULTS: Estimates from adjusted linear mixed effects models did not reveal consistent significant associations between infant cortisol and maternal depression or home adversities. By contrast, infants exposed to maternal depression during pregnancy had lower DHEA levels (ß= -0.18 95% confidence interval [CI]: -0.34, -0.02) as did those whose mothers experienced multiple types of IPV (ß=-4.14 95% CI: -7.42, -0.79) within one year postpartum. Higher SES had a significant positive association with infant DHEA levels (ß= 0.77 95% CI: 0.08, 1.47). Depression severity and chronicity at one year postpartum had near significant associations with infant DHEA. Measures of home environment had no observable impacts on infant HPA axis activity. LIMITATIONS: Limitations include the modest sample size and aggregation of hair samples for analysis. CONCLUSION: Results point to possible early HPA axis dysregulation driven by changes in DHEA activity, but not cortisol at one year of age. Findings contribute to growing research examining intergenerational transmissions of maternal depression, IPV, and household environment on infant stress-response systems.
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