Adriëtte Oostvogels

This thesis describes the impact of maternal characteristics, in particular maternal prepregnancy body mass index (pBMI), ethnicity, socioeconomic status and family history of diabetes on offspring’s cardiometabolic profile. Moreover, the potential pathways underlying the association between maternal pBMI and offspring’s cardiometabolic profile, in particular those related to early pregnancy lipid profile and offspring’s postnatal growth, are described. This final chapter summarises the main findings of the research presented in this thesis, addresses some methodological considerations, reflects on the main findings, and presents suggestions for future research and possible implications for public health practice. Summary of the main findings Hypothesis 1: An adverse cardiometabolic profile at age 5-6 years is the result of maternal overweight before pregnancy, which acts through prenatal exposure to an atherogenic lipid profile. Women with overweight before pregnancy appeared to have higher triglycerides, free fatty acids, total cholesterol and apolipoprotein B compared to women with a normal weight. They also had a higher blood pressure during pregnancy. Moreover, their children had a higher body mass index (BMI), fat percentage, waist-to-height ratio, systolic and diastolic blood pressure, and metabolic score. Although, as expected, maternal early pregnancy lipids were positively associated with both body composition and lipid profile in childhood, the early pregnancy lipid profile did not mediate the association between pBMI and blood pressure course. Hypothesis 2: Children with a family history of diabetes on the maternal side of the family are more often overweight and have a more adverse glucose metabolism at age 5-6 years than children with a family history of diabetes on the paternal side of the family. No differences in body composition or glucose metabolism were found between children with either maternal or paternal family history of diabetes (FHD), although children with both maternal and paternal FHD had increased C-peptide levels compared to children with no maternal or paternal FHD. Thus, our hypothesis that a maternal FHD will have a more negative impact on offspring’s cardiometabolic health than a paternal family history, was rejected. 220 Chapter 9