Adriëtte Oostvogels

4 113 Maternal lipids and offspring’s lipids & glucose Discussion This explorative study examined the association between maternal lipid profile during early pregnancy and offspring’s lipid profile and glycaemic control at age 5-6 years, and the mediating role of offspring’s fat percentage in this association. We found sex-specific associations between maternal early pregnancy lipid profile and offspring’s lipid profile in childhood with, in general, stronger associations in girls. There was no indication that maternal early pregnancy lipid profile was associated with offspring’s glycaemic control. Also, offspring’s fat percentage had no mediating role in these associations. Recently, the Rhea Cohort also found associations between maternal TC and LDL and offspring’s TC in models corrected for maternal covariates and sex. 21 Correcting for birth weight (amongst others) attenuated these significant associations. We chose not to correct for birth weight since it is an intermediate factor in the studied associations, but correction for birth weight would not have altered our results (results not shown). 6-10 The associations in the Rhea Cohort were no longer significant after corrections, although the estimates of the beta coefficients did not markedly decrease. Therefore, the study sample in the Rhea Cohort might simply have been underpowered with 249 mother-child pairs. Similar associations as ours were earlier found between maternal lipids during pregnancy and offspring’s lipids measured in cord blood. 22 Cord TG levels were positively related with maternal TG levels and negatively with maternal HDL, but this study did not differentiate between boys and girls. The association between maternal and offspring TG is in line with our study; however, in girls, we found a positive association between maternal ApoA1 and offspring’s TG. Moreover, an animal study found higher cholesterol levels in male offspring of dams fed a high-fat diet during pregnancy and lactation. 13 Although we found no association between maternal lipids and offspring’s glycaemic control, animal studies found conflicting results. Exposure to a high-fat diet in utero and/or lactation were both positively 13 and negatively 15 associated with offspring’s insulin resistance (HOMA IR). Underlying mechanisms First, shared genetic or environmental factors could explain part of our associations, as these were mainly found between high biochemically linked lipid substrates. Studies on twins showed that the heritability of lipid levels is around 60%. 23 Although we were unable to correct for shared genetic background, we tried to account for shared environmental factors by correcting for ethnicity, socioeconomic status, sedentary behaviour, and saturated fat and fibre intake.