Louise Maple-Brown1,2, I-Lynn Lee1, Danielle Longmore1, Federica Barzi1, Christine Connors3, Jacqueline A Boyle1,4, Elizabeth Moore5, Cherie Whitbread1,2, Marie Kirkwood1, Sian Graham1, Vanya Hampton1, Alison Simmonds1, Paula Van Dokkum6, Joanna Kelaart6, Sujatha Thomas7, Shridhar Chitturi2, Sandra Eades8, Sumaria Corpus9, Michael Lynch10, Zhong X Lu11,12, Kerin O'Dea1,13, Paul Zimmet14, Jeremy Oats15, Harold D McIntyre16, Alex D H Brown17, Jonathan E Shaw8. 1. Wellbeing and Preventable Chronic Diseases Division, Menzies School of Health Research, Darwin, NT, Australia. 2. Endocrinology Department, Division of Medicine, Royal Darwin Hospital, Darwin, NT, Australia. 3. Remote Primary Health Care, Top End Health Services, Northern Territory Department of Health, Darwin, NT, Australia. 4. Monash Centre for Health Research and Implementation, School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia. 5. Public Health Unit, Aboriginal Medical Services Alliance, Darwin, NT, Australia. 6. Aboriginal Health Domain, Baker Heart and Diabetes Institute, Alice Springs, NT, Australia. 7. Division of Maternal and Child Health, Royal Darwin Hospital, Darwin, NT, Australia. 8. Clinical and Population Health, Baker Heart and Diabetes Institute, Melbourne, Australia. 9. Clinical Services, Danila Dilba Health Service, Darwin, NT, Australia. 10. Pathology Network, Top End Health and Hospital Services, Darwin, NT, Australia. 11. Biochemistry Department, Melbourne Pathology, Melbourne, VIC, Australia. 12. Department of Medicine, Monash University, Melbourne, Australia. 13. School of Health Sciences, University of South Australia, Adelaide, SA, Australia. 14. Department of Diabetes, Central Clinical School, Monash University, Melbourne, VIC, Australia. 15. Melbourne School of Population and Global Health, University of Melbourne, Melbourne, VIC, Australia. 16. Faculty of Medicine, Mater Medical Research Institute, University of Queensland, Brisbane, QLD, Australia. 17. Wardliparingga Aboriginal Research Unit, South Australian Health and Medical Research Institute, Adelaide, SA, Australia.
Abstract
BACKGROUND: In Australia's Northern Territory, 33% of babies are born to Indigenous mothers, who experience high rates of hyperglycemia in pregnancy. We aimed to determine the extent to which pregnancy outcomes for Indigenous Australian women are explained by relative frequencies of diabetes type [type 2 diabetes (T2DM) and gestational diabetes (GDM)]. METHODS: This prospective birth cohort study examined participants recruited from a hyperglycemia in pregnancy register. Baseline data collected were antenatal and perinatal clinical information, cord blood and neonatal anthropometry. Of 1135 women (48% Indigenous), 900 had diabetes: 175 T2DM, 86 newly diagnosed diabetes in pregnancy (DIP) and 639 had GDM. A group of 235 women without hyperglycemia in pregnancy was also recruited. RESULTS: Diabetes type differed for Indigenous and non-Indigenous women (T2DM, 36 vs 5%; DIP, 15 vs 7%; GDM, 49 vs 88%, p < 0.001). Within each diabetes type, Indigenous women were younger and had higher smoking rates. Among women with GDM/DIP, Indigenous women demonstrated poorer birth outcomes than non-Indigenous women: large for gestational age, 19 vs 11%, p = 0·002; neonatal fat 11.3 vs 10.2%, p < 0.001. In the full cohort, on multivariate regression, T2DM and DIP were independently associated (and Indigenous ethnicity was not) with pregnancy outcomes. CONCLUSIONS: Higher rates of T2DM among Indigenous women predominantly contribute to absolute poorer pregnancy outcomes among Indigenous women with hyperglycemia. As with Indigenous and minority populations globally, prevention or delay of type 2 diabetes in younger women is vital to improve pregnancy outcomes and possibly to improve the long-term health of their offspring.
BACKGROUND: In Australia's Northern Territory, 33% of babies are born to Indigenous mothers, who experience high rates of hyperglycemia in pregnancy. We aimed to determine the extent to which pregnancy outcomes for Indigenous Australian women are explained by relative frequencies of diabetes type [type 2 diabetes (T2DM) and gestational diabetes (GDM)]. METHODS: This prospective birth cohort study examined participants recruited from a hyperglycemia in pregnancy register. Baseline data collected were antenatal and perinatal clinical information, cord blood and neonatal anthropometry. Of 1135 women (48% Indigenous), 900 had diabetes: 175 T2DM, 86 newly diagnosed diabetes in pregnancy (DIP) and 639 had GDM. A group of 235 women without hyperglycemia in pregnancy was also recruited. RESULTS:Diabetes type differed for Indigenous and non-Indigenous women (T2DM, 36 vs 5%; DIP, 15 vs 7%; GDM, 49 vs 88%, p < 0.001). Within each diabetes type, Indigenous women were younger and had higher smoking rates. Among women with GDM/DIP, Indigenous women demonstrated poorer birth outcomes than non-Indigenous women: large for gestational age, 19 vs 11%, p = 0·002; neonatal fat 11.3 vs 10.2%, p < 0.001. In the full cohort, on multivariate regression, T2DM and DIP were independently associated (and Indigenous ethnicity was not) with pregnancy outcomes. CONCLUSIONS: Higher rates of T2DM among Indigenous women predominantly contribute to absolute poorer pregnancy outcomes among Indigenous women with hyperglycemia. As with Indigenous and minority populations globally, prevention or delay of type 2 diabetes in younger women is vital to improve pregnancy outcomes and possibly to improve the long-term health of their offspring.
Keywords:
Aboriginal; Indigenous Australian; birth cohort; diabetes in pregnancy; gestational diabetes; hyperglycemia in pregnancy; type 2 diabetes in pregnancy
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