Association between maternal hyperglycemia in pregnancy and offspring anthropometry in early childhood: The pandora wave 1 study

Angela Titmuss, Federica Barzi, Elizabeth L.M. Barr, Vanya Webster, Anna Wood, Joanna Kelaart, Marie Kirkwood, Christine Connors, Jacqueline A. Boyle, Elizabeth Moore, Jeremy Oats, H. David McIntyre, Paul Zimmet, Alex D.H. Brown, Jonathan E. Shaw, Maria E. Craig, Louise J. Maple-Brown

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Background: In-utero hyperglycemia exposure influences later cardiometabolic risk, although few studies include women with pre-existing type 2 diabetes (T2D) or assess maternal body mass index (BMI) as a potential confounder. 

Objective: To explore the association of maternal T2D and gestational diabetes mellitus (GDM) with childhood anthropometry, and the influence of maternal BMI on these associations. 

Methods: The PANDORA cohort comprises women (n = 1138) and children (n = 1163). Women with GDM and T2D were recruited from a hyperglycemia in pregnancy register, and women with normoglycemia from the community. Wave 1 follow-up included 423 children, aged 1.5–5 years (median follow-up age 2.5 years). Multivariable linear regression assessed associations between maternal antenatal variables, including BMI and glycemic status, with offspring anthropometry (weight, height, BMI, skinfold thicknesses, waist, arm and head circumferences). 

Results: Greater maternal antenatal BMI was associated with increased anthropometric measures in offspring independent of maternal glycemic status. After adjustment, including for maternal BMI, children exposed to maternal GDM had lower mean weight (−0.54 kg, 95% CI: −0.99, −0.11), BMI (−0.55 kg/m2, 95% CI: −0.91, −0.20), head (−0.52 cm, 95% CI: −0.88, −0.16) and mid-upper arm (−0.32 cm, 95% CI: −0.63, −0.01) circumferences, and greater mean suprailiac skinfold (0.78 mm, 95% CI: 0.13, 1.43), compared to children exposed to normoglycemia. Adjustment for maternal BMI strengthened the negative association between GDM and child weight, BMI and circumferences. Children exposed to maternal T2D had smaller mean head circumference (−0.82 cm, 95% CI: −1.33, −0.31) than children exposed to normoglycemia. Maternal T2D was no longer associated with greater child mean skinfolds (p = 0.14) or waist circumference (p = 0.18) after adjustment for maternal BMI. 

Conclusions: Children exposed to GDM had greater suprailiac skinfold thickness than unexposed children, despite having lower mean weight, BMI and mid-upper arm circumference, and both GDM and T2D were associated with smaller mean head circumference. Future research should assess whether childhood anthropometric differences influence lifetime cardiometabolic and neurodevelopmental risk.

Original languageEnglish
Pages (from-to)1120-1131
Number of pages12
JournalInternational Journal of Obesity
Issue number11
Early online date22 Aug 2023
Publication statusPublished - Nov 2023

Bibliographical note

Funding Information:
We gratefully acknowledge all PANDORA Wave 1 study staff and participants, as well as Diabetes across the Lifecourse: Northern Australia Partnership investigators, partners, staff, Aboriginal and Torres Strait Islander Advisory Group and Clinical Reference Group, health professionals from Northern Territory Health hospitals and remote primary healthcare, Healthy Living NT and Aboriginal Community Controlled Health Organizations. Partnership investigators in addition to those listed as author include S Thomas, S Chitturi, S Eades, S Corpus, Z Lu, C Whitbread. We thank Professor Kerin O’Dea for her significant contributions over many years in the foundation of this program of work. We thank Elizabeth Death posthumously for her important work in establishing the PANDORA Wave 1 follow-up study, including working closely with lead investigators in writing the study protocol, drafting the ethics application, supervising the research team and collecting data. The views expressed in this publication are those of the authors and do not reflect the views of the National Health and Medical Research Council of Australia.

Funding Information:
This work was supported by the National Health and Medical Research Council of Australia (NHMRC Grant no. 1078333) and the Diabetes Australia Research Program (#Y16G-TITA). AT was supported by a NHMRC Postgraduate Scholarship (#114760), RACP NHMRC Woolcock Scholarship and NHMRC Hot North PhD Completion Scholarship. LJMB was supported by NHMRC Practitioner Fellowship no. 1078477 and NHMRC Investigator Grant no. 1194698. JAB was supported by NHMRC Career Development Fellowship. JES was supported by NHMRC Fellowship no. 1079438. ADHB was supported by a Viertel Senior Medical Research Fellowship and an NHMRC Senior Research Fellowship no. 1137563. AW was supported by a NHMRC Postgraduate Scholarship. The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript. Open Access funding enabled and organized by CAUL and its Member Institutions.

Publisher Copyright:
© 2023, The Author(s).


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