Akhgar Ghassabian1,2,3, Mady Hornig4, Zhen Chen5, Edwina Yeung6, Stephen L Buka7, Jing Yu8, Gina Ma8, Jill M Goldstein9,10,11,12, Stephen E Gilman8,13. 1. Department of Pediatrics, School of Medicine, New York University, New York, New York, USA. 2. Department of Environmental Medicine, School of Medicine, New York University, New York, New York, USA. 3. Department of Population Health, School of Medicine, New York University, New York, New York, USA. 4. Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York, USA. 5. Biostatistics and Bioinformatics Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA. 6. Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA. 7. Department of Epidemiology, School of Public Health, Brown University, Providence, Rhode Island, USA. 8. Social and Behavioral Sciences Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA. 9. Department of Psychiatry, Harvard Medical School, Harvard University, Boston, Massachusetts, USA. 10. Department of Medicine, Harvard Medical School, Harvard University, Boston, Massachusetts, USA. 11. Department of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts, USA. 12. Department of Obstetrics and Gynecology, Massachusetts General Hospital, Boston, Massachusetts, USA. 13. Department of Mental Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA.
Abstract
OBJECTIVE: This study examined the extent to which maternal immune activity during pregnancy is associated with childhood adiposity, and if so, whether associations at birth differ from those in infancy and childhood. Sex-specific associations were also examined. METHODS: Participants were 1,366 singleton pregnancies from the Collaborative Perinatal Project (1959-1966). Interleukin-1β (IL-1β), IL-6, TNF-α, IL-8, and IL-10 in maternal sera were assayed repeatedly during pregnancy. Children's BMI was calculated repeatedly from birth through age 8 and derived age- and sex-normalized BMI z scores (BMIz). Linear mixed models were used to estimate the cumulative concentration of each cytokine in the second and third trimesters and then related this concentration to child BMIz. RESULTS: Children exposed to higher IL-1β, IL-6, IL-8, and IL-10 concentrations had lower BMIz at birth but higher BMIz during childhood. Higher concentrations of IL-8 and IL-1β were also associated with higher BMIz during infancy (B per log increase in IL-8 = 0.04; 95% CI: 0.02 to 0.07; B per log increase in IL-1β = 0.03; 95% CI: 0.001 to 0.06). The associations between TNF-α and BMIz were in opposing directions in boys (B = -0.13; 95% CI: -0.31 to 0.04) and girls (B = 0.14; 95% CI: 0.02 to 0.26) during childhood. CONCLUSIONS: Maternal prenatal inflammation contributes to the age- and sex-specific programming of obesity risk in childhood.
OBJECTIVE: This study examined the extent to which maternal immune activity during pregnancy is associated with childhood adiposity, and if so, whether associations at birth differ from those in infancy and childhood. Sex-specific associations were also examined. METHODS:Participants were 1,366 singleton pregnancies from the Collaborative Perinatal Project (1959-1966). Interleukin-1β (IL-1β), IL-6, TNF-α, IL-8, and IL-10 in maternal sera were assayed repeatedly during pregnancy. Children's BMI was calculated repeatedly from birth through age 8 and derived age- and sex-normalized BMI z scores (BMIz). Linear mixed models were used to estimate the cumulative concentration of each cytokine in the second and third trimesters and then related this concentration to childBMIz. RESULTS:Children exposed to higher IL-1β, IL-6, IL-8, and IL-10 concentrations had lower BMIz at birth but higher BMIz during childhood. Higher concentrations of IL-8 and IL-1β were also associated with higher BMIz during infancy (B per log increase in IL-8 = 0.04; 95% CI: 0.02 to 0.07; B per log increase in IL-1β = 0.03; 95% CI: 0.001 to 0.06). The associations between TNF-α and BMIz were in opposing directions in boys (B = -0.13; 95% CI: -0.31 to 0.04) and girls (B = 0.14; 95% CI: 0.02 to 0.26) during childhood. CONCLUSIONS: Maternal prenatal inflammation contributes to the age- and sex-specific programming of obesity risk in childhood.
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