Birgitte Bytoft1, Sine Knorr2, Zuzana Vlachova3, Rikke B Jensen4, Elisabeth R Mathiesen5, Henning Beck-Nielsen6, Claus H Gravholt2, Dorte M Jensen7, Tine D Clausen8, Erik L Mortensen9, Peter Damm10. 1. Center for Pregnant Women with Diabetes, Rigshospitalet, Copenhagen, Denmark Department of Obstetrics, Rigshospitalet, Copenhagen, Denmark Institute of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark birgitte.bytoft@regionh.dk. 2. Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark. 3. Department of Endocrinology, Odense University Hospital, Odense, Denmark Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark. 4. Institute of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark Department of Growth and Reproduction, Rigshospitalet, Copenhagen, Denmark. 5. Center for Pregnant Women with Diabetes, Rigshospitalet, Copenhagen, Denmark Institute of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark Department of Endocrinology, Rigshospitalet, Copenhagen, Denmark. 6. Department of Endocrinology, Odense University Hospital, Odense, Denmark. 7. Department of Endocrinology, Odense University Hospital, Odense, Denmark Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark Department of Gynecology and Obstetrics, Odense University Hospital, Odense, Denmark. 8. Department of Gynecology and Obstetrics, Nordsjaellands Hospital, Hilleroed, Denmark. 9. Section of Environmental Health, Department of Public Health and Center for Healthy Aging, University of Copenhagen, Copenhagen, Denmark. 10. Center for Pregnant Women with Diabetes, Rigshospitalet, Copenhagen, Denmark Department of Obstetrics, Rigshospitalet, Copenhagen, Denmark Institute of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Abstract
OBJECTIVE: Exposure to maternal diabetes in utero may have a negative impact on the developing brain. The objective was to examine long-term cognitive consequences of intrauterine hyperglycemia in adolescent offspring of women with type 1 diabetes and to ascertain a possible association with maternal HbA1c. RESEARCH DESIGN AND METHODS: Offspring of a prospectively followed cohort of women with type 1 diabetes (n = 277) participated in a follow-up examination at the age of 13-19 years. A control group from the background population was identified (n = 301). Cognitive function was evaluated using Reynolds Intellectual Assessment Scales and classified into indices of composite intelligence, verbal and nonverbal intelligence, and composite memory. Frequencies of reading and writing problems and attendance to classes for children with learning difficulties were assessed. RESULTS: Offspring of women with type 1 diabetes scored lower in all normalized and standardized intelligence indices compared with controls: composite intelligence (95.7 vs. 100, P = 0.001), verbal intelligence (96.2 vs. 100, P = 0.004), nonverbal intelligence (96.4 vs. 100, P = 0.008), and composite memory (95.7 vs. 100, P = 0.001). A higher frequency of diabetes-exposed offspring had parent-reported learning difficulties in primary school. Differences between groups remained after adjustment for confounders and potential mediators. We found no direct association between maternal HbA1c and offspring cognitive function in the exposed group. CONCLUSIONS: Adolescent offspring of women with type 1 diabetes had lower cognitive function compared with a control group, also after adjustment for confounders and potential mediators. These differences may reflect direct harmful effects of maternal diabetes on neurodevelopment in the offspring.
OBJECTIVE: Exposure to maternal diabetes in utero may have a negative impact on the developing brain. The objective was to examine long-term cognitive consequences of intrauterine hyperglycemia in adolescent offspring of women with type 1 diabetes and to ascertain a possible association with maternal HbA1c. RESEARCH DESIGN AND METHODS: Offspring of a prospectively followed cohort of women with type 1 diabetes (n = 277) participated in a follow-up examination at the age of 13-19 years. A control group from the background population was identified (n = 301). Cognitive function was evaluated using Reynolds Intellectual Assessment Scales and classified into indices of composite intelligence, verbal and nonverbal intelligence, and composite memory. Frequencies of reading and writing problems and attendance to classes for children with learning difficulties were assessed. RESULTS: Offspring of women with type 1 diabetes scored lower in all normalized and standardized intelligence indices compared with controls: composite intelligence (95.7 vs. 100, P = 0.001), verbal intelligence (96.2 vs. 100, P = 0.004), nonverbal intelligence (96.4 vs. 100, P = 0.008), and composite memory (95.7 vs. 100, P = 0.001). A higher frequency of diabetes-exposed offspring had parent-reported learning difficulties in primary school. Differences between groups remained after adjustment for confounders and potential mediators. We found no direct association between maternal HbA1c and offspring cognitive function in the exposed group. CONCLUSIONS: Adolescent offspring of women with type 1 diabetes had lower cognitive function compared with a control group, also after adjustment for confounders and potential mediators. These differences may reflect direct harmful effects of maternal diabetes on neurodevelopment in the offspring.
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