Minimizing neonatal hypothyroidism induced by lithium exposure through breast milk

Lithium-induced hypothyroidism in the neonate is a growing concern for lactating mothers. Maternal hypothyroidism in the postpartum period could lead to hypothyroidism in the infant via maternal compromised thyroid hormones (likely T4) in breast milk, and lithium in breast milk could have a direct effect on the neonatal thyroid axis over lithium carbonate direct administration.

We have studied the effects of lithium exposure on neonatal pups through two different modes of exposure: direct oral administration of lithium carbonate and indirect exposure of lithium from breast milk from dams. Furthermore, dams were supplemented with two different iodine dosages in both control and lithium-treated groups. We employed Enzyme-linked immunosorbent assay, inductively coupled plasma mass and atomic absorption spectrometry to assess hormone profiles and intrathyroidal elemental content.

Interestingly, lithium administered directly to pups from control mothers (average dose 900 mg/50 kg per day), did not affect their weight, thyroid hormones, blood urea, and intrathyroidal iodine content despite traces of lithium found in their blood and thyroid. The iodine pathway in the presence of lithium content in both thyroid follicular cells and lactocyte has been hypothesized. The results also demonstrate that lithium administration in lactating dams alters thyroid hormones (T4) and blood urea in both dams and pups, which could be reversed by iodine supplement. The mechanism for supplemented iodine uptake in the presence of lithium is hypothesized.

In future, supplementing iodine may be potentially useful in clinical practices to address the neonate concerns of lactating mothers and their infants either caused by prolonged lithium medication or maternal iodine deficiency.