Objective: Prenatal exposure to excess cortisol can affect postnatal metabolic health by epigenetic mechanisms. We aimed to investigate if prenatal exposure to pharmacological glucocorticoids increases the risk of overweight/obesity in childhood.
Design: A nationwide population registry-based cohort study.
Methods: We identified 383 877 children born in Denmark (2007-2012), who underwent routine anthropometric evaluation at 5-8 years of age. Prenatal exposure to glucocorticoids was divided into systemic and topical glucocorticoids, cumulative systemic dose, and use by trimester. The comparison cohort included children without exposure, born to maternal never-users. Negative control exposures were used to investigate confounding from an underlying disease or unmeasured characteristics. Such exposures included children without glucocorticoid exposure born to maternal users of non-steroidal anti-inflammatory drugs or immunotherapy during pregnancy, maternal former users of glucocorticoids, or paternal users of glucocorticoids during the pregnancy of their partner. We estimated sex-stratified adjusted prevalence ratios (aPR) of overweight/obesity at 5-8 years of age, as epigenetic modifications have shown to be sex-specific.
Results: In the study, 21 246 (11%) boys and 27 851 (15%) girls were overweight/obese at 5-8 years of age. Overall, neither systemic nor topical glucocorticoids were associated with overweight/obesity. In boys, high-dose systemic glucocorticoids was associated with higher prevalence of overweight/obesity vs the comparison cohort (aPR: 1.41 (95% CI: 1.07-1.86), prevalence: 16% vs 11%). Negative control exposures indicated robustness to confounding.
Conclusion: Overweight/obesity might be an adverse effect of prenatal exposure to high-dose systemic glucocorticoids in boys. We found no association for neither prenatal exposure to lower doses of systemic nor topical glucocorticoids. These results merit clinical attention.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8942335 | PMC |
| http://dx.doi.org/10.1530/EJE-21-0846 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Preventing Infant Mortality Through Medicaid-Administered Prenatal Care Coordination: Evidence From Wisconsin.
Health Serv Res
January 2025
School of Nursing, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Objective: To estimate associations between Wisconsin Medicaid's Prenatal Care Coordination (PNCC) program and infant mortality.
Data Sources And Study Setting: We analyzed birth records, Medicaid claims, and infant death records for all resident and in-state Medicaid-paid live deliveries during 2010-2018.
Study Design: We measured PNCC exposure during pregnancy dichotomously (none; any) and categorically (none; assessment/care plan only; service receipt).
Longitudinal DNA methylation profiles in saliva of offspring from mothers with gestational diabetes: associations with early childhood growth patterns.
Cardiovasc Diabetol
January 2025
Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, 29010, Málaga, Spain.
Background: The prevalence of obesity and type 2 diabetes mellitus (T2DM) is rising globally, particularly among children exposed to adverse intrauterine environments, such as those associated with gestational diabetes mellitus (GDM). Epigenetic modifications, specifically DNA methylation, have emerged as mechanisms by which early environmental exposures can predispose offspring to metabolic diseases. This study aimed to investigate DNA methylation differences in children born to mothers with GDM compared to non-GDM mothers, using saliva samples, and to assess the association of these epigenetic patterns with early growth measurements.
View Article and Find Full Text PDFMaternal asthma imprints fetal lung ILC2s via glucocorticoid signaling leading to worsened allergic airway inflammation in murine adult offspring.
Nat Commun
January 2025
Division of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
The root of asthma can be linked to early life, with prenatal environments influencing risk. We investigate the effects of maternal asthma on the offspring's lungs during fetal and adult life. Adult offspring of asthmatic mothers show an increase in lung group 2 innate lymphoid cell (ILC2) number and function with allergen-induced lung inflammation.
View Article and Find Full Text PDFAssociation of early life co-exposure to ambient PM and O with the offspring's growth within two years of age: A birth cohort study.
Int J Hyg Environ Health
January 2025
Department of Maternal and Child Health, School of Public Health, Sun Yat-sen University, Guangzhou, Guangdong, China; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, School of Public Health, Sun Yat-Sen University, Guangzhou, Guangdong, China. Electronic address:
Background: Previous studies indicated that early life exposure to particulate matter of 2.5 μm or less (PM) could impair children's growth. However, the adverse effects of maternal ozone (O) and its interplay with PM on offspring's growth are unclear.
View Article and Find Full Text PDFUrban air pollution and child neurodevelopmental conditions: a systematic bibliometric review.
Curr Opin Psychiatry
December 2024
Department of Neuroscience, Carleton University.
Purpose Of Review: Using advanced bibliometric analysis, we systematically mapped the most current literature on urban air pollution and neurodevelopmental conditions to identify key patterns and associations. Here, we review the findings from the broader literature by discussing a distilled, validated subset of 44 representative studies.
Recent Findings: Literature highlights a complex relationship between environmental toxins, neurodevelopmental disorders in children, and neurobehavioral pathways involving oxidative stress, neuroinflammation, and protein aggregation.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!