Jennifer M Yamamoto1,2,3, Jamie L Benham4,5, Deborah Dewey5,6,7, J Johanna Sanchez8, Helen R Murphy9,10,11, Denice S Feig12,13,14, Lois E Donovan4,15,16. 1. Department of Medicine, Cumming School of Medicine, University of Calgary, Richmond Road Diagnostic and Treatment Centre, 1820 Richmond Road SW, Calgary, AB, T2T 5C7, Canada. jennifer.yamamoto@ucalgary.ca. 2. Department of Obstetrics and Gynecology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. jennifer.yamamoto@ucalgary.ca. 3. Alberta Children's Hospital Research Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. jennifer.yamamoto@ucalgary.ca. 4. Department of Medicine, Cumming School of Medicine, University of Calgary, Richmond Road Diagnostic and Treatment Centre, 1820 Richmond Road SW, Calgary, AB, T2T 5C7, Canada. 5. Department of Community Health Sciences, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. 6. Department of Paediatrics, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. 7. Owerko Centre at the Alberta Children's Hospital Research Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. 8. Sunnybrook Research Institute, Toronto, ON, Canada. 9. Wolfson Diabetes and Endocrine Clinic, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK. 10. Women's Health Academic Centre, Division of Women's and Children's Health, King's College London, London, UK. 11. Norwich Medical School, University of East Anglia, Norwich, UK. 12. Mount Sinai Hospital, Toronto, ON, Canada. 13. Lunenfeld-Tanenbaum Research Institute, Toronto, ON, Canada. 14. Department of Medicine, University of Toronto, Toronto, ON, Canada. 15. Department of Obstetrics and Gynecology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. 16. Alberta Children's Hospital Research Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.
Abstract
AIMS/HYPOTHESIS: We performed a systematic review and meta-analysis to determine whether exposure to maternal pre-existing diabetes in pregnancy is associated with neurocognitive or behavioural outcomes in offspring. METHODS: We searched MEDLINE, EMBASE, PsychINFO, the Cochrane Database of Systematic Reviews and Scopus for studies that examined any neurocognitive or behavioural outcomes in offspring of mothers with pre-existing diabetes in pregnancy in accordance with a published protocol (PROSPERO CRD42018109038). Title and abstract review, full-text review and data extraction were performed independently and in duplicate. Risk of bias was assessed using the Newcastle-Ottawa scale. Meta-analyses of summary measures were performed using random-effects models. RESULTS: Nineteen articles including at least 18,681 exposed and 2,856,688 control participants were identified for inclusion. Exposure to maternal pre-existing diabetes in pregnancy was associated with a lower pooled intelligence quotient in the offspring (pooled weighted mean difference -3.07 [95% CI -4.59, -1.55]; I2 = 0%) and an increased risk of autism spectrum disorders (effect estimate 1.98 [95% CI 1.46, 2.68]; I2 = 0%). There was also an increased risk of attention deficit/hyperactivity disorder (pooled HR 1.36 [95% CI 1.19, 1.55]; I2 = 0%), though this was based on only two studies. Although most studies were found to be high quality in terms of participant selection, in many studies, comparability of cohorts and adequacy of follow-up were sources of bias. CONCLUSIONS/ INTERPRETATION: There is evidence to suggest that in utero exposure to maternal pre-existing diabetes is associated with some adverse neurocognitive and behavioural outcomes. It remains unclear what the role of perinatal factors is and the degree to which other environmental factors contribute to these findings.
AIMS/HYPOTHESIS: We performed a systematic review and meta-analysis to determine whether exposure to maternal pre-existing diabetes in pregnancy is associated with neurocognitive or behavioural outcomes in offspring. METHODS: We searched MEDLINE, EMBASE, PsychINFO, the Cochrane Database of Systematic Reviews and Scopus for studies that examined any neurocognitive or behavioural outcomes in offspring of mothers with pre-existing diabetes in pregnancy in accordance with a published protocol (PROSPERO CRD42018109038). Title and abstract review, full-text review and data extraction were performed independently and in duplicate. Risk of bias was assessed using the Newcastle-Ottawa scale. Meta-analyses of summary measures were performed using random-effects models. RESULTS: Nineteen articles including at least 18,681 exposed and 2,856,688 control participants were identified for inclusion. Exposure to maternal pre-existing diabetes in pregnancy was associated with a lower pooled intelligence quotient in the offspring (pooled weighted mean difference -3.07 [95% CI -4.59, -1.55]; I2 = 0%) and an increased risk of autism spectrum disorders (effect estimate 1.98 [95% CI 1.46, 2.68]; I2 = 0%). There was also an increased risk of attention deficit/hyperactivity disorder (pooled HR 1.36 [95% CI 1.19, 1.55]; I2 = 0%), though this was based on only two studies. Although most studies were found to be high quality in terms of participant selection, in many studies, comparability of cohorts and adequacy of follow-up were sources of bias. CONCLUSIONS/ INTERPRETATION: There is evidence to suggest that in utero exposure to maternal pre-existing diabetes is associated with some adverse neurocognitive and behavioural outcomes. It remains unclear what the role of perinatal factors is and the degree to which other environmental factors contribute to these findings.
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