Neonatal iron status is impaired by maternal obesity and excessive weight gain during pregnancy

Abstract

Objective Maternal iron needs increase 6-fold during pregnancy, but obesity interferes with iron absorption. We hypothesized that maternal obesity impairs fetal iron status. Study Design 316 newborns with risk factors for infantile iron deficiency anemia (IDA) were studied to examine obesity during pregnancy and neonatal iron status. Erythrocyte iron was assessed by cord blood hemoglobin (Hb), zinc protoporphyrin/heme (ZnPP/H) and reticulocyte-ZnPP/H and storage iron by serum ferritin. Results Women with body mass index ≥30 kg/m2, as compared with non-obese women, delivered larger offspring with higher reticulocyte-ZnPP/H, and lower serum ferritin concentrations (p<0.05 for both). With increasing BMI, estimated body iron was relatively lower (mg/kg) and the ratio of total Hb-bound iron (mg)/total body iron (mg) increased. Maternal diabetes compromised infant iron status, but multivariate analysis demonstrated that obesity was an independent predictor. Conclusions Obesity during pregnancy and excessive weight gain are independent risk factors for iron deficiency in the newborn.

Maternal Obesity Affects Inflammatory and Iron Indices in Umbilical Cord Blood

“…Currently, known risks for developing iron deficiency as an infant were tallied: maternal obesity (BMI ≥30 kg/m 2 ), maternal diabetes, minority status, Medicaid insurance, and fetal growth disturbance (small or large for gestational age). 13,25 Subjects were selected after electronic medical record evaluation for inclusion and exclusion criteria. All subject data were de-identified.…”

“…17,18 An additional study found that lower umbilical tissue iron content was linked to childhood wheezing, 19 but did not measure immune indices at birth. We previously found poorer umbilical cord blood iron status in the presence of maternal obesity or with GWG exceeding 18 kg 13 and also demonstrated that either poor umbilical cord iron status or GWG exceeding 18 kg predicted the development of eosinophilia during the first year of life. 20 Eosinophilia is used to predict the development of allergic asthma.…”

“…Obesity stimulates the iron pathway cytokines, including IL-1 β and IL-6, 10 and, in one study, also upregulated maternal hepcidin levels, 8 decreasing both maternal and fetal iron bioavailabity Fetal hepcidin levels 8 are likely regulated in a similar fashion to that in adults, with lower hepcidin reported in rat pups with gestational iron deficiency 11 and higher umbilical cord levels in human newborns after intrauterine infection. 12 We previously showed that maternal obesity and excess GWG interfered with fetal iron endowment, 13 but it is not known whether fetal hepcidin levels will mount an appropriate response and decline under low fetal iron conditions. Because iron status impacts fetal neurodevelopment and health, 14 it is important to understand the physiological regulation of fetal iron in maternal obesity and/or excess GWG.…”

Effects of Maternal Obesity on Fetal Programming: Molecular Approaches

“…Decreased placental expression of ferritin may negatively impact the rate of iron uptake from the maternal circulation and transfer to the fetal circulation. Human studies have shown evidence of impaired iron status in newborns of obese women (Phillips et al 2014) and in infants born to diabetic mothers (Siddappa et al 2004). Iron deficiency is known to be associated with impaired brain development (Lozoff et al 1991).…”

Wpływ otyłości u matki w czasie ciąży na ryzyko rozwoju autyzmu u dziecka

“…Niewłaściwy stan odżywienia organizmu w ciąży powoduje niedorozwój łożyska (mniejszy jego rozmiar i utrudniony przepływ krwi), co z kolei upośle-dza dowóz składników odżywczych do płodu i rzutuje na krótko-i długoterminowy rozwój neurologiczny i chorobowość dziecka [50]. Ponadto nadmierna masa ciała przed ciążą oraz duży jej przyrost w ciąży jest niezależnym czynnikiem ryzyka niedoborów żelaza (im wyższe BMI, tym mniejsze stężenia żelaza i ferrytyny) [51]. Żelazo jest waż-nym mikroelementem dla rozwoju układu nerwowego płodu i mielinizacji nerwów.…”