Maternal iron kinetics and maternal-fetal iron transfer in normal weight and overweight pregnancy

Abstract

Abstract Background Inflammation during pregnancy may aggravate iron deficiency by increasing serum hepcidin and reducing iron absorption. This could restrict iron transfer to the fetus, increasing risk for infant iron deficiency and its adverse effects. Objectives To assess whether iron bioavailability and/or iron transfer to the fetus is impaired in overweight/obese (OW) women with adiposity-related inflammation, compared to normal weight (NW), pregnant women. Design In this prospective study, we followed NW (n = 43) and OW (n = 40) pregnant women who were receiving iron supplements from the 14th gestational week to term and followed their infants to age six months. We administered 57Fe and 58Fe in test meals mid-2nd and mid-3rd trimester, and measured tracer kinetics throughout pregnancy and infancy. Results 38 NW and 36 OW completed the study to pregnancy week 36 and 30 NW and 27 OW mother infant pairs completed the study to six months postpartum. Both groups had comparable iron status, hemoglobin and serum hepcidin throughout pregnancy. Compared to the NW, the OW pregnant women had: 1) 43% lower fractional iron absorption in the 3rd trimester (P = 0.033) with median (IQR) 23.9 (11.4–35.7) and 13.5 (10.8–19.5) %; and 2) 17% lower maternal-fetal iron transfer from the first tracer (P = 0.051) with median (IQR) 4.8 (4.2–5.4) and 4.0 (3.6–4.6) %. Compared to the infants born to NW, infants born to OW had lower body iron stores (BIS) with median (IQR) 7.7 (6.3–8.8) and 6.6 (4.6–9.2) mg/kg body weight at age six months (P = 0.024). Prepregnancy BMI was a negative predictors of maternal-fetal iron transfer (β = –0.339, SE = 0.144, P = 0.025) and infant BIS (β = –0.237, SE = 0.026, P = 0.001). Conclusions Compared to NW, OW pregnant women fail to upregulate iron absorption in late pregnancy, transfer less iron to their fetus, and their infants have lower BIS. These impairments are associated with inflammation independent of serum hepcidin. The study was registered at clinicaltrials.gov (NCT02747316).