05/22/2026
Did you know the placenta regulates iron?
This is one of my favorite papers (oldie but a goodie) to share with providers because it helps to reframe how we think about iron in pregnancy.
For decades, the dominant model was that the FETUS controlled how much iron it received. This review challenged that by providing evidence that maternal iron status and placental iron signaling play a more active role in regulating transfer.
Iron transport across the placenta is transcellular and unidirectional, meaning it goes one way...from mom to baby...through the syncytiotrophoblast cells.
Specific transporters, such as TFR1 (transferrin receptor I), bind maternal transferrin-bound iron in circulation...not unlike other cells in the maternal physiology...it can be stored as ferritin in the placenta, used for placental cell functions, or transferred to the baby.
When maternal iron is low, the placenta expresses more TFR1 to increase placental uptake of iron.
The placenta is selfish. When iron levels are low, it prioritizes iron for its own function, shifting less to the fetus by downregulating Ferroportin at the basement membrane and in fetal capillaries.
Other transporters, such as LPR1, PCFT, and FLVCR2, take up Fe2+/heme iron directly. This form of iron is transferred directly to the fetus. FLVCR1 directly transports heme iron to the fetal capillary regardless of placental iron status.
Why is this important clinically?
Iron form matters depending on who we are trying to support. Ideally, we are working on mom... if mom is healthy, baby is healthy... however, in cases of severe iron deficiency, we need to prioritize the baby.
Non-heme iron supports maternal/placental function, while heme iron is better for the baby.
We need both!
When working on iron deficiencies, we won't see ferritin levels begin to rise until all the buckets are full. Baby, placenta, and mom.
