Diabetes in pregnancy in associations with perinatal and postneonatal mortality in First Nations and non-Indigenous populations in Quebec, Canada: population-based linked birth cohort study

OBJECTIVE: Both pregestational and gestational diabetes mellitus (PGDM, GDM) occur more frequently in First Nations (North American Indians) pregnant women than their non-Indigenous counterparts in Canada. We assessed whether the impacts of PGDM and GDM on perinatal and postneonatal mortality may differ in First Nations versus non-Indigenous populations. DESIGN: A population-based linked birth cohort study. SETTING AND PARTICIPANTS: 17 090 First Nations and 217 760 non-Indigenous singleton births in 1996–2010, Quebec, Canada. MAIN OUTCOME MEASURES: Relative risks (RR) of perinatal and postneonatal death. Perinatal deaths included stillbirths and neonatal (0–27 days of postnatal life) deaths; postneonatal deaths included infant deaths during 28–364 days of life. RESULTS: PGDM and GDM occurred much more frequently in First Nations (3.9% and 10.7%, respectively) versus non-Indigenous (1.1% and 4.8%, respectively) pregnant women. PGDM was associated with an increased risk of perinatal death to a much greater extent in First Nations (RR=5.08[95% CI 2.99 to 8.62], p<0.001; absolute risk (AR)=21.6 [8.6–34.6] per 1000) than in non-Indigenous populations (RR=1.76[1.17, 2.66], p=0.003; AR=4.2[0.2, 8.1] per 1000). PGDM was associated with an increased risk of postneonatal death in non-Indigenous (RR=3.46[1.71, 6.99], p<0.001; AR=2.4[0.1, 4.8] per 1000) but not First Nations (RR=1.16[0.28, 4.77], p=0.35) infants. Adjusting for maternal and pregnancy characteristics, the associations were similar. GDM was not associated with perinatal or postneonatal death in both groups. CONCLUSIONS: The study is the first to reveal that PGDM may increase the risk of perinatal death to a much greater extent in First Nations versus non-Indigenous populations, but may substantially increase the risk of postneonatal death in non-Indigenous infants only. The underlying causes are unclear and deserve further studies. We speculate that population differences in the quality of glycaemic control in diabetic pregnancies and/or genetic vulnerability to hyperglycaemia’s fetal toxicity may be contributing factors.