Previous studies have linked maternal pre-pregnancy obesity (BMI ≥30 kg/m2) with suboptimal neurodevelopment in her offspring; however, the literature is not entirely consistent. Whether these effects are muddled by maternal self-reports of pre-pregnancy weight and height, or are driven or amplified by the well often comorbid hypertensive and diabetic pregnancy and pre-pregnancy disorders, remains unclear. We examined whether maternal early pregnancy obesity is associated with developmental delay in her offspring, and if the associations are driven or amplified by diabetic and hypertensive pregnancy and pre-pregnancy disorders.
A total of 2504 mother-child dyads participated in the Prediction and Prevention of Pre-eclampsia and Intrauterine Growth Restriction (PREDO) study. Data on maternal early pregnancy obesity, pre-pregnancy, and gestational hypertension, pre-eclampsia, type 1 and gestational diabetes were derived from the Finnish Medical Birth Register. At the child’s mean age of 42.1 (SD = 8.2) months the mothers completed the Ages and Stages Questionnaire (ASQ) Third edition for developmental milestones.
Children of obese mothers had 1.81–2.74 (p-values <0.02) higher odds of failing to meet the development that is typical for a child’s age (developmental domain score ≤−2SD below the child’s age) on the communication, fine and gross motor, problem solving and personal/social skills and children of overweight mothers had 2.14 (p = 0.002) higher odds of failing to meet the development that is typical for the child’s age on communication skills. Odds of developmental delay were also higher for children of mothers with pre-eclampsia and gestational diabetes. The associations were robust to covariates and confounders, the effects of overweight/obesity and pre-eclampsia were not driven by the other disorders, and overweight/obesity and hypertensive and diabetic disorders did not show additive effects.
Maternal early pregnancy overweight, obesity, and pre-eclampsia are independently associated with neurodevelopmental delay in her offspring. Further studies unraveling the underlying mechanisms are warranted.
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The PREDO study would not have been possible without the dedicated contribution of the PREDO Study group members: A Aitokallio-Tallberg, A-M Henry, VK Hiilesmaa, T Karipohja, R Meri, S Sainio, T Saisto, S Suomalainen-Konig, V-M Ulander, T Vaitilo (Department of Obstetrics and Gynaecology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland), L Keski-Nisula, Maija-Riitta Orden (Kuopio University Hospital, Kuopio Finland), E Koistinen, T Walle, R Solja (Northern Karelia Central Hospital, Joensuu, Finland), M Kurkinen (Päijät-Häme Central Hospital, Lahti, Finland), P.Taipale. P Staven (Iisalmi Hospital, Iisalmi, Finland), J Uotila (Tampere University Hospital, Tampere, Finland). We also thank the PREDO cohort mothers, fathers, and children for their enthusiastic participation.
This work was supported by the Academy of Finland (K.R., grant numbers 284859, 2848591, 312670), (E.K., grant numbers 127437, 129306, 130326, 134791, 263924 and 274794), (H.L., grant numbers 121196, 134957, and 278941), (M.L.-P., grant number 12853241), (A.-K.P.); University of Helsinki Research Funds (M.L.-P.), (H.L.), British Heart Foundation (R.M.R.); Tommy’s (R.M.R.); European Commission (E.K., K.R., Horizon 2020 Award SC1-2016-RTD-733280 RECAP); Foundation for Pediatric Research (E.K.); Juho Vainio Foundation (E.K.); Novo Nordisk Foundation (E.K.); Signe and Ane Gyllenberg Foundation (K.R., E.K.); Sigrid Jusélius Foundation (E.K.); Finnish Medical Foundation (H.L.); Jane and Aatos Erkko Foundation (H.L.); Päivikki and Sakari Sohlberg Foundation (H.L.); and Doctoral Program of Psychology, Learning, and Communication, (P.G.).
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The authors declare that they have no conflict of interest.
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