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Pediatrics

Prenatal oxidative stress and rapid infant weight gain

Abstract

Background and objectives

Infant weight patterns predict subsequent weight outcomes. Rapid infant weight gain, defined as a >0.67 increase in weight-for-age z-score (WAZ) between two time points in infancy, increases obesity risk. Higher oxidative stress, an imbalance between antioxidants and reactive oxygen species, has been associated with low birthweight and paradoxically also with later obesity. We hypothesized that prenatal oxidative stress may also be associated with rapid infant weight gain, an early weight pattern associated with future obesity.

Methods

Within the NYU Children’s Health and Environment Study prospective pregnancy cohort, we analyzed associations between prenatal lipid, protein, and DNA urinary oxidative stress biomarkers and infant weight data. Primary outcome was rapid infant weight gain (>0.67 increase in WAZ) between birth and later infancy at the 8 or 12 month visit. Secondary outcomes included: very rapid weight gain (>1.34 increase in WAZ), low (<2500 g) or high (≥4000 g) birthweight, and low (< −1 WAZ) or high (>1 WAZ) 12 month weight.

Results

Pregnant participants consented to the postnatal study (n = 541); 425 participants had weight data both at birth and in later infancy. In an adjusted binary model, prenatal 8-iso-PGF2α, a lipid oxidative stress biomarker, was associated with rapid infant weight gain (aOR 1.44; 95% CI: 1.16, 1.78, p = 0.001). In a multinomial model using ≤0.67 change in WAZ as a reference group, 8-iso-PGF2α was associated with rapid infant weight gain (defined as >0.67 but ≤1.34 WAZ; aOR 1.57, 95% CI: 1.19, 2.05, p = 0.001) and very rapid infant weight gain (defined as >1.34 WAZ; aOR 1.33; 95% CI: 1.02, 1.72, p < 0.05) Secondary analyses detected associations between 8-iso-PGF2α and low birthweight outcomes.

Conclusions

We found an association between 8-iso-PGF2α, a lipid prenatal oxidative stress biomarker, and rapid infant weight gain, expanding our understanding of the developmental origins of obesity and cardiometabolic disease.

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Fig. 1: Multinomial model of 8-iso-PGF2α and rate of infant weight gain.

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Data availability

The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

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Acknowledgements

We thank all of the NYU CHES participants and staff for their important contributions. This work was supported by the institutional funds of NYU Grossman School of Medicine as well as the NIH Office of the Director (UG3/UH3OD023305). CD-L acknowledges support from training grants by the National Center for Advancing Translational Sciences, National Institutes of Health 2KL2TR001446-06 and the Life Course Intervention Research Network (Health Resources and Services Administration) UA6MC32492.

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Contributions

CD-L conceptualized and designed the study, analyzed data, reviewed the analyses, drafted the initial manuscript, and reviewed and revised the manuscript. LT and AG conceptualized and designed the study, supervised acquisition of data, reviewed the analyses, and reviewed and revised the manuscript. KK contributed substantially to the design of the study, supervised acquisition of the data, reviewed the analyses, and reviewed and revised the manuscript. RSG, RO, and AG substantially contributed to interpretation of data, and reviewed and revised the manuscript for important intellectual content. YA, ML, and LS contributed substantially to data collection and reviewed and revised the manuscript. All authors approved the final manuscript as submitted and agree to be accountable for all aspects of the work.

Corresponding author

Correspondence to Carol Duh-Leong.

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Duh-Leong, C., Ghassabian, A., Kannan, K. et al. Prenatal oxidative stress and rapid infant weight gain. Int J Obes 47, 583–589 (2023). https://doi.org/10.1038/s41366-023-01302-8

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