The importance of iron levels (often expressed as ferritin level) for those who are hypothyroid has been stated numerous times here. It is a mantra.
The need for adequate iron in pregnancy is well-known and widely accepted. Witness products like Pregaday, that many pregnant women are prescribed iron supplementation, etc. (Though many women find the usual iron supplements so unbearable they don't always take them. Understandable. Alternatives should be identified and prescribed.)
The impact of inadequate thyroid hormone on the offspring is also well-known and, at least in the extremes, well accepted.
This paper pulls things together and identifies low iron as a cause of low thyroid hormone levels which in turn can affect brain development. Further, the paper calls for monitoring of thyroid hormone levels in pregnant women who are iron deficient.
We all know the most likely end result, if acted on, would be the occasional TSH test. Better some recognition than none at all.
[Hypothyroxinemia is low thyroid hormone level in the blood. Hypothyroidism is inability of the thyroid to make enough thyroid hormone. Subtle distinction. But if the effect is due to low iron, maybe the thyroid is actually perfectly capable of producing enough?]
Thyroid. 2016 May 27. [Epub ahead of print]
Perinatal Iron Deficiency-Induced Hypothyroxinemia Impairs Early Brain Development Regardless of Normal Iron Levels in the Neonatal Brain.
Hu X1,2, Wang R3, Shan Z4, Dong Y5, Zheng H6, Jesse FF7, Rao E8, Takahashi E9, Li W10, Teng W11, Teng X12.
Both perinatal hypothyroxinemia and perinatal iron deficiency (ID) are associated with poor neurodevelopment in the offspring. Iron is an important component of thyroid peroxidase, a key enzyme in the synthesis of thyroid hormone (TH). Our previous study demonstrated that perinatal iron deficiency can lead to maternal hypothyroxinemia during pregnancy. The goal of this study was to determine whether perinatal ID associated hypothyroxinemia can cause brain defects prior to neonatal brain iron depletion.
We established two rat models to imitate the two common types of maternal ID [mild ID with anemia (ID+A) and ID without anemia (ID-A)], and iron limitation was initiated two weeks before pregnancy. Maternal and neonatal thyroid hormones in serum were analyzed at postnatal (P) day 0 and P10. Neonatal TH, as well as mRNA expression of some TH-responsive genes in the cerebral cortex and hippocampus were measured at P10. Serum iron and brain iron concentrations were analyzed by inductively coupled plasma mass spectrometry. Liver iron concentration was determined using graphite furnace atomic absorption spectroscopy. Hemoglobin was analyzed with an automated blood coagulation analyzer. Surface righting reflex and Vibrissae-evoked forelimb placing were measured to assess the sensory-motor behaviors.
We found that pre-pregnant mild ID resulted in maternal hypothyroxinemia, which lasted from gestation (G) day 13 to postnatal (P) day 10. Pre-pregnant mild ID decreased neonatal brain TT3 level at P10. Consistent with low TT3 level, the mRNA expression of some TH-responsive genes (Mbp, RC3, and Srg1) were significantly reduced in the neonatal cerebral cortex and hippocampus in both ID rat models at P10. Furthermore, ID rat pups at P10 showed retarded sensorimotor skills. No significant difference was found between the control and the ID pups in terms of iron concentrations in the neonatal brain at P10.
This study demonstrates that perinatal ID-associated hypothyroxinemia is sufficient to impair early brain development, regardless of whether the neonatal brain iron level is normal, and monitoring thyroid hormone level is indicated in ID pregnant women.
PMID: 27231981 [PubMed - as supplied by publisher]